CASE NOTES


Discussion paper – Cattle Nematodes on the Mid-North Coast of NSW

Jim Kerr, District Veterinarian, Tocal

Posted Flock & Herd March 2016

INTRODUCTION

Investigation of weight loss in cattle in the Taree and Gloucester districts of NSW sometimes implicates gastrointestinal worms as a likely cause.  In younger cattle, faecal egg counts with larval differentiation are relied upon for such a diagnosis. In adult cattle with negligible or zero faecal egg counts, elevated serum pepsinogen levels are occasionally the basis for the diagnosis, coupled with a subsequent response to drenching.  

Ostertagia ostertagi (the small brown stomach worm) has been identified as the most important roundworm of cattle in temperate regions (Love & Hutchinson, 2007), and is commonly nominated as the parasitic cause for elevated serum pepsinogen levels (NSW DPI 2015, Hutchinson 2009).

In summer rainfall areas, however, Haemonchus placei is reported to be the most significant species of cattle nematode (Love & Hutchinson, 2007; Radostits et al, 2007).  Worm-testing in recent years by the LHPA/LLS and Pfizer has confirmed that Haemonchus placei and Cooperia spp are the predominant roundworms of cattle in the Gloucester and Taree districts, with Ostertagia often at negligible levels (Refer to Appendix 1). Some references suggest that Haemonchus spp (not just Haemonchus contortus) may also cause elevated pepsinogen levels through abomasal damage. This paper describes a number of issues associated with cattle nematodes in the Taree/Gloucester region, including the possibility that elevated pepsinogen levels in cattle weight loss cases may sometimes indicate Haemonchus placei infestations. 

DISCUSSION

The NSW DPI Vet Lab Manual (viewed online 2015) describes the diagnostic use of pepsinogen as follows:

In adult cattle, estimations of serum or plasma pepsinogen concentrations are considered a useful indicator of abomasal damage and of value in the diagnosis of type II ostertagiasis.

Pepsinogen is produced in the gastric mucosa as the inactive precursor of pepsin. Abomasal damage results in increased blood pepsinogen concentration. The assay measures the presence of pepsinogen through the ability of the test serum or plasma to breakdown a protein substrate to peptide fragments. Results are compared with a tryrosine standard, and expressed in terms of U/L of tyrosine.

Pepsinogen level (U/L) Interpretation

< 5 No significant abomasal damage
5-10 Minor damage*
10-15 Moderate damage
> 15 Major abomasal damage

* Levels of 5 or greater are considered indicative of damage sufficient to cause production losses

Hutchinson (2009) and the NSW DPI Vet Lab Manual (viewed 2015) warn that although elevated serum pepsinogen levels in adult cattle may reflect abomasal mucosa damage caused by larval stages of Ostertagia ostertagi, they should be interpreted with caution and used on a herd rather than individual animal basis.

Additionally, Radostits et al (2007) report that ‘older immune cattle may show elevated values when grazing contaminated pasture, even though few incoming larvae are able to establish.’

In the following weight loss cases in individual adult cattle (Table 1), however, elevated pepsinogen was the only significant abnormality detected by blood testing, and interpreted as suggestive of worm infestation despite zero faecal egg counts in 7 of the 9 cases.  Those animals suffering diarrhoea are denoted by an asterisk *.  The diarrhoea cases had variously been investigated for other causes of diarrhoea including pestivirus, BJD, salmonella, yersinia, and liver fluke with negative results.

  

While these cases seem to support the diagnostic validity of pepsinogen in some weight loss cases (supported by an apparent response to drenching, summarised in Table 2) it should be noted that estimation of serum pepsinogen levels in adult cattle cohorts not suffering weight loss was not undertaken in any of these cases (i.e. no control group for comparison).

Table 1: Faecal egg counts and serum pepsinogen levels in Mid North Coast cattle weight loss cases
Animal Faecal egg count (epg) Larval differentiation Pepsinogen U/L
(Normal 0.0 – 5.0 U/L)
Gloucester bull 2012 0 27.2
Gloucester bull 2013 0 15.9
Nabiac bull 2015 0 13.6
Stroud bull 2015* 0 12.8
Gloucester bull # 1 2015* 60 77% Trichostrongylus
23% Ostertagia
66.8
Gloucester bull # 2 2015 0 12.2
Gloucester bull # 3 2015 15.4
Gloucester cow 2015 2380 100% Haemonchus 18.3
Kempsey cow 2015* 0 125.4

While causes for abomasal damage other than parasite burdens have to be considered when interpreting pepsinogen levels, cases which feature an apparent response to anthelminthics provide some confidence that elevated pepsinogen can indeed reflect a nematode infestation.

Table 2: Pepsinogen levels in cattle before and after drenching
Pepsinogen at 1st sampling Pepsinogen at post-drench sampling
Animal ID Date FEC (epg) Pepsinogen U/L (Norm 0-5 U/L) Date FEC Pepsinogen U/L (Norm 0-5 U/L)
Gloucester bull 2012 12.09.2012 0 27.2 16.10.12 10.3
Gloucester bull 2013 30.07.2013 0 15.9 26.08.13 9.8
01.10.13 9.7
11.11.13 6.3
Gloucester bull # 1 2015 10.06.2015 60
77% trich
23% ostertagia
66.8 03.08.15 0 34.1
20.08.15 28.4
Kempsey cow 23.11.2015 0 125.4 18.01.16 35.5

Pepsinogen levels become elevated when there is damage to the gastric glands in the mucosa of the abomasum. Such damage is known to occur with type 1 and type 2 ostertagiosis when 4th stage ostertagia larvae emerge from the gastric glands. Type 2 ostertagiosis features the emergence of large numbers of L4 larvae which have remained dormant in the gastric glands awaiting more suitable environmental conditions outside the animal to complete their development to egg laying adults.  This strategy of inhibited  development is known as hypobiosis

Hypobiosis can also be a feature of the life cycle of Haemonchus worms (Junquera, 2014), and Radostits et al. (2007) report that plasma pepsinogen levels rise during haemonchosis.  Besier (2015), however, reports that hypobiotic infestations of Haemonchus contortus in sheep is a “routine but largely invisible phenomenon in summer rainfall regions”.  If the hypobiotic phase of Haemonchus placei infestations in cattle similarly causes few clinical signs, then weight loss cases in adult cattle characterised by elevated pepsinogen and zero worm egg counts would be difficult to attribute to Haemonchus infestations. However, the same is reportedly true of the hypobiotic phase of Ostertagia ostertagi: the abomasal damage, weight loss and diarrhoea do not occur during the hypobiotic pre-Type 2 phase of the infestation (Radostits et al, 2007). 

Unfortunately, only two of the cases summarised in this paper have been subject to histological examination of the abomasum to clarify the nature of the abomasal infestation and/or damage. In the case described as ‘Gloucester cow’ (Table 1 and Table 3, below), which seemed to strongly suggest an elevated pepsinogen level due to a Haemonchus placei infestation, the abomasum no longer had any evidence of parasitic infestation after repeated drenching (see Table 3), and turned out to possess a healing ulcer.  In the case recorded as ‘Gloucester bull # 3 2015’ (Table 1), the lab reported “There is a parasitic abomasitis present with intraglandular nematodes which we don't see that often. It looks relatively mild, however it is difficult to correlate histological severity with functional effects. I cannot tell whether or not these are inhibited Ostertagia larvae.”

CONCLUSION

Overall, the most significant pepsinogen elevations occurred in animals which also displayed pronounced diarrhoea (‘Kempsey cow’ and ‘Gloucester bull # 1 2015’ in Table 1), which suggests ostertagiosis as a more likely cause than haemonchus.  Additionally, ‘Gloucester bull # 1 2015’ did have a small number of ostertagia eggs in a faecal sample which lacked any haemonchus eggs, even though worm testing of younger animals on that property returned a breakdown of 82% Haemonchus, 8% Cooperia, 7% ostertagia, 2% trichostrongylus, and 1% Oesophagostamum.

Perhaps the afflicted cattle are particularly prone to ostertagia infestations, even if that parasite appears to be present only at low or negligible levels on the property.  With bull investigations featuring zero egg counts, there is also the possibly misleading factor that they may have arrived carrying a worm burden (possibly inhibited) with a different distribution to that on the property which bought them. More work needs to be done to resolve the questions raised in this paper, preferably featuring planned rather than opportunistic sampling.

“The macrocyclic lactones are well absorbed when administered PO or parenterally; the pour-on formulations exhibit greater variability.” (Vercruysse & Claerebout, 2007)

“Topical administration (i.e., pour-on formulations) is more convenient but results are more variable between animals than when administration is SC or PO. Grooming behavior of cattle has a major influence on the plasma disposition of topical macrocyclic lactones. Undesirable subtherapeutic concentrations in both treated and untreated cattle may contribute to development of drug resistance” (Vercruysse & Claerebout, 2007).

Case # 1:

‘Gloucester bull 2012’ (Tables 1 and 2) had been treated twice with pour-on drench for worms + liver fluke (abamectin + triclabendazole) in the months immediately before being sampled on 12th September 2012.  His pepsinogen at the September sampling was 27.2 U/L.  Injectable ivermectin was subsequently given due to the suspicion that the pour-ons had failed, and his pepsinogen had dropped to 10.3 U/L when re-tested several weeks later on 16th October 2012.

Case # 2: Gloucester cow

14.05.15 17.05.15 27.05.15 02.06.15 10.06.15 25.06.15 08.07.15 04.08.15
WormTest 2380 epg
100% Haemonchus
1440 epg
100% Haemonchus
480 epg
100% Haemonchus
0 epg Killed Wingham abattoir
No evidence of parasites
Old abomasal ulcer
Drench applied Doramectin pour-on Moxidectin pour-on Abamectin, levamisole, oxfendazole + Co & Se oral drench 
Pepsinogen 18.3 U/L

In the case described below (Wards River yearlings), a significant haemonchus burden (at least 8 fatalities in a group of 40 yearlings) was successfully treated with moxidectin pour-on. Initial wormtest results for the first heifer sampled and then 10 of her cohorts were as follows:

Strongyle epg Haemonchus % Trichostrongylus % Cooperia % Oesphagostomum %
Heifer # 1 (pre-drench) 32000 (PCV 8%) 94% 2% 4%
Cohorts 1-10 (pre-drench) 4858 (average) 84% 2% 4% 10%
Heifer # 2 (post-drench) 4720 100%


After drenching with moxidectin pour-on, worm-testing was undertaken to check that the treatment had been effective. Eight of the 10 animals sampled returned zero egg counts, but two animals returned disappointing egg counts of 4720 (Heifer # 2, PCV 15%) and 460 epg.  

These two animals were so anaemic as to be recumbent, so were covered with a tarpaulin overnight after drenching to keep them warm.  Presumably the tarpaulin rubbed off some of the pour-on, reducing the amount absorbed. As Cooperia spp and Nematodirus spp are less susceptible to the macrocyclic lactones than the other common cattle nematodes (Vercruysse and Claerebout, 2014), it is perhaps not surprising that the larval differentiation for heifer # 2 after drenching was 100% Cooperia. What is less clear, however, is why the removal of the Haemonchus burden seems to have created an environment which favoured proliferation of the Cooperia population in that heifer, given that they occupy different locations in the gut (abomasum for Haemonchus vs. intestine for Cooperia). Because Haemonchus infestation causes a significant rise in abomasal pH (Radostits et al, 2007), perhaps the subsequent reduction in abomasal pH after removing a significant population of Haemonchus might positively affect the intestinal environment for Cooperia?

REFERENCES

  1. Besier RB 2015, ‘Hypobiosis in sheep worms in Australia – is it present and is it a problem?’, WormMail.2015-01-29, ed. S Love, NSW DPI.
  2. Hutchinson GW, 2009. Nematode Parasites of Small Ruminants, Camelids and Cattle Diagnosis with Emphasis on Anthelmintic Efficacy and Resistance Testing. Australia-New Zealand Diagnostic Standard Procedures (ANZDSPs). Accessed July 2015 www.scahls.org.au/Procedures/Pages/ANZSDPs.aspx
  3. Junquera P, 2014.  Haemonchus spp, parasitic roundworms of CATTLE, SHEEP and GOATS. Biology, prevention and control. Haemonchus contortus, Haemonchus placei. Haemonchosis. Viewed December 2014
  4. parasitipedia.net/index.php?option=com_content&view=article&id=2634&Itemid=2912
  5. NSW Dept of Primary Industries (Agriculture) Vet Lab Manual, viewed June 2015
  6. www.dpi.nsw.gov.au/agriculture/vetmanual/specimens-by-disease-syndrome/diseases_of_livestock/pepsinogen_estimations_from_serum_or_plasma
  7. Radostits OM, Gay CC, Hinchcliff KW and Constable PD 2007, Veterinary Medicine.  A textbook of the diseases of cattle, horses, sheep, pigs and goats.  10th Edition. Saunders Elsevier, Philadelphia.
  8. Vercruysse J and Claerebout E 2014, ‘Macrocyclic lactones’, The Merck Veterinary Manual, viewed Feb 2016
  9. www.merckvetmanual.com/mvm/pharmacology/anthelmintics/macrocyclic_lactones.html

Appendix 1:

18 Mobs FEC Sampled Nov 11 to Mar 13 (Pfizer field data)
 {Dungog, Stroud, Kimbriki, Gloucester, Barrington, Stroud Hill, Wingham, Giro, Stratford}

 


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