Ovine and Caprine Parasites: Intestinal Worms in Sheep and Goats

Introduction

Intestinal parasitism represents a major constraint to the health, welfare, and productivity of sheep and goats worldwide. The term "worms sheep get" encompasses a diverse assemblage of helminths, primarily nematodes (roundworms) and cestodes (tapeworms), as well as protozoan parasites such as coccidia. These infections cause subclinical production losses, clinical disease, and mortality, particularly in young, periparturient, or immunocompromised animals. The economic impact stems from reduced weight gain, decreased milk yield, impaired wool and mohair quality, and costs associated with treatment and control. The emergence of anthelmintic resistance (AR) in key nematode populations has rendered many traditional control programs ineffective, necessitating a paradigm shift toward integrated parasite management (IPM) strategies that combine targeted selective treatment (TST), pasture management, and diagnostic surveillance.

Etiology and Classification

The principal intestinal parasites of small ruminants belong to the order Strongylida (superfamily Trichostrongyloidea), the order Ascaridida, and the order Cyclophyllidea (cestodes). Protozoan parasites of the genus Eimeria (coccidia) are also significant enteric pathogens.

Nematodes (Roundworms)

The most pathogenic and prevalent gastrointestinal nematodes (GINs) of sheep and goats are trichostrongylid species. These parasites inhabit the abomasum (true stomach) and the small intestine.

Abomasal Nematodes:

• Haemonchus contortus: The barber's pole worm. A blood-feeding nematode that causes anemia, hypoproteinemia, and submandibular edema (bottle jaw). It is highly fecund and a major driver of AR.
• Teladorsagia circumcincta (formerly Ostertagia circumcincta): The brown stomach worm. Causes abomasal inflammation, protein-losing enteropathy, and diarrhea. Type I and Type II (hypobiotic) disease syndromes are recognized.
• Trichostrongylus axei: The stomach hairworm. A small, thread-like worm that causes gastritis and is also found in cattle and horses.

Intestinal Nematodes:

• Trichostrongylus colubriformis and Trichostrongylus vitrinus: The bankrupt worms. These parasites cause enteritis, diarrhea, and weight loss. They are highly prevalent in temperate and subtropical regions.
• Nematodirus battus and Nematodirus spathiger: The thin-necked intestinal worms. N. battus is particularly pathogenic in lambs, causing acute, high-mortality outbreaks of diarrhea in spring due to mass emergence of larvae from overwintered eggs.
• Cooperia curticei and Cooperia oncophora: Small intestinal worms that are generally less pathogenic but contribute to production losses.
• Strongyloides papillosus: The threadworm. A unique parasite capable of transmammary and percutaneous transmission. It causes diarrhea in young lambs and kids.
• Chabertia ovina: The large-mouthed bowel worm. Inhabits the colon and causes colitis with mucus-laden feces.
• Oesophagostomum columbianum and Oesophagostomum venulosum: Nodular worms. Larvae encyst in the intestinal wall, causing granulomatous nodules that can lead to chronic enteritis and peritonitis.
• Skrjabinema ovis: The pinworm of sheep. Causes perianal pruritus but is generally of minor clinical significance.

Cestodes (Tapeworms):

• Moniezia expansa and Moniezia benedeni: The common tapeworms of sheep and goats. These large cestodes inhabit the small intestine. While often considered non-pathogenic, heavy burdens can cause intestinal obstruction, unthriftiness, and diarrhea in lambs.
• Avitellina centripunctata and Thysaniezia giardi: Less common cestodes found in tropical and subtropical regions.

Protozoa:

• Eimeria crandallis, Eimeria ovinoidalis (sheep), and Eimeria arloingi, Eimeria ninakohlyakimovae (goats): These coccidian parasites cause coccidiosis, a major enteric disease of lambs and kids. They invade and destroy intestinal epithelial cells, leading to hemorrhagic diarrhea, dehydration, and death.

Epidemiology and Life Cycles

All trichostrongylid nematodes have a direct life cycle. Adult worms in the gastrointestinal tract produce eggs that are passed in the feces. Under favorable environmental conditions (temperatures between 10-30 degrees Celsius and adequate moisture), eggs hatch to release first-stage larvae (L1), which develop through second-stage (L2) to the infective third-stage (L3). The L3 migrate onto herbage and are ingested by the grazing animal. Following ingestion, exsheathment occurs in the rumen or abomasum, and larvae molt to L4 and then to adults in the target organ. The prepatent period ranges from approximately 14 days for T. colubriformis to 21 days for H. contortus.

The epidemiology of these parasites is heavily influenced by climate and management. H. contortus thrives in warm, moist conditions and is a major problem in tropical, subtropical, and temperate summer rainfall regions. T. circumcincta and N. battus are adapted to cooler temperate climates. A critical survival strategy is hypobiosis (arrested larval development), where L3 or early L4 larvae cease development within the host, resuming maturation weeks or months later. This phenomenon allows parasites to survive adverse seasons (e.g., winter or dry summer) and contributes to periparturient rise (PPR), a peri-parturient increase in fecal egg output in ewes and does.

N. battus has a unique life cycle requiring a prolonged period of cold (chilling) for egg development. Eggs deposited in spring do not hatch until the following spring, leading to a synchronized mass emergence of L3 that causes outbreaks in lambs.

Moniezia spp. require an intermediate host, a pasture-dwelling oribatid mite, for development. Lambs ingest infected mites while grazing.

Eimeria spp. have a direct life cycle with sporulation of oocysts in the environment. Infection occurs via ingestion of sporulated oocysts. High stocking density and contaminated housing facilitate rapid transmission.

Clinical Signs and Pathology

Clinical manifestations depend on the parasite species, burden, host age, and nutritional status. Subclinical infections are common and result in reduced feed conversion efficiency, growth retardation, and impaired immune function.

Anemia and Hypoproteinemia: Caused primarily by H. contortus. Each worm consumes approximately 0.05 mL of blood per day. Heavy burdens (over 5,000 worms) can cause acute anemia, pale mucous membranes, weakness, and death. Chronic infection leads to progressive weight loss and submandibular edema (bottle jaw) due to protein loss.

Diarrhea and Enteritis: T. colubriformis, T. circumcincta, N. battus, and C. ovina cause varying degrees of enteritis. N. battus infection in lambs presents as profuse, watery diarrhea, dehydration, and high mortality. T. circumcincta infection results in a rise in abomasal pH, impaired protein digestion, and diarrhea. C. ovina infection produces mucus-laden, tenesmus-associated feces.

Coccidiosis: In lambs and kids, coccidiosis typically presents as diarrhea, which may be hemorrhagic, accompanied by dehydration, anorexia, and weight loss. The pathology involves destruction of intestinal crypt epithelium, villous atrophy, and inflammation.

Cestodiasis: Heavy Moniezia burdens can cause intestinal stasis, unthriftiness, and occasionally intussusception. Diagnosis is often incidental on fecal examination.

Diagnostics

Accurate diagnosis is essential for targeted treatment and monitoring of AR. Diagnostic methods include:

Fecal Egg Count (FEC): The quantitative McMaster technique is the standard method for estimating egg output. Results are expressed as eggs per gram (EPG) of feces. A modified McMaster method with a sensitivity of 15-50 EPG is commonly used. FEC is used to determine the need for treatment and to monitor treatment efficacy via the fecal egg count reduction test (FECRT).

Larval Culture and Differentiation: Because trichostrongylid eggs are morphologically similar, larval culture is required to identify the genus or species present. Feces are incubated to allow eggs to hatch and develop to L3, which are then identified based on key morphological features (e.g., sheath tail length, number of intestinal cells). This is critical for diagnosing AR at the species level.

FAMACHA System: A clinical scoring system for anemia in sheep, based on the color of the ocular mucous membranes. It is used as a proxy for H. contortus burden and enables targeted selective treatment (TST) of only anemic animals, reducing selection pressure for AR.

Necropsy and Worm Counts: Total worm counts from the abomasum and small intestine provide a definitive diagnosis of parasite burden and species composition. This is the gold standard for research and for confirming AR.

Molecular Diagnostics: PCR-based assays, including multiplex PCR and quantitative PCR (qPCR), can detect and quantify specific nematode species from fecal samples. These methods offer higher sensitivity and specificity than traditional microscopy and can detect prepatent infections. However, they are not yet widely adopted in field practice.

Serology: ELISA tests for detection of antibodies against Ostertagia (Teladorsagia) or Haemonchus are available for research but are not routinely used for individual animal diagnosis.

Treatment and Anthelmintic Resistance

Treatment relies on the administration of anthelmintic drugs. The major classes include:

• Benzimidazoles (BZ): Fenbendazole, albendazole, oxfendazole. These drugs bind to beta-tubulin, inhibiting microtubule polymerization.
• Macrocyclic Lactones (ML): Ivermectin, doramectin, moxidectin. These drugs potentiate glutamate-gated chloride channels, causing paralysis.
• Imidazothiazoles/Tetrahydropyrimidines: Levamisole and morantel. These are nicotinic acetylcholine receptor agonists.
• Amino-Acetonitrile Derivatives (AAD): Monepantel. A novel class acting on nicotinic acetylcholine receptors (Hco-MPTL-1).
• Spiroindoles: Derquantel. Acts as a nicotinic antagonist, often used in combination with abamectin.

Anthelmintic Resistance (AR): AR is a global crisis in small ruminant production. Resistance has been reported to all major anthelmintic classes, including the newer AADs and spiroindoles. The primary mechanism is genetic selection for resistant individuals within a parasite population. Resistance is often multigenic and can involve target site mutations (e.g., beta-tubulin isotype 1 polymorphisms for BZ resistance), increased drug efflux (P-glycoprotein upregulation for ML resistance), and altered drug metabolism.

Diagnosis of AR: The FECRT is the standard field test. Fecal samples are collected from a group of animals at the time of treatment (Day 0) and 10-14 days later (Day 10-14 for most nematodes; 17-21 days for Nematodirus). A percent reduction in FEC is calculated. Resistance is declared if the reduction is less than 95% and the lower 95% confidence interval is below 90%.

Treatment Strategies:

• Targeted Selective Treatment (TST): Treating only animals that require it, based on indicators such as FAMACHA score, body condition score, or FEC. This maintains a refugia of unselected parasites on pasture, slowing the development of AR.
• Combination Therapy: Using two or more anthelmintics from different classes simultaneously. This can improve efficacy against multi-resistant populations, provided the parasites are not resistant to all components.
• Quarantine Drenching: Treating all incoming animals with a combination of effective anthelmintics (e.g., monepantel plus abamectin) to prevent introduction of resistant parasites.

Control and Integrated Parasite Management (IPM)

Sustainable control requires an integrated approach that reduces reliance on anthelmintics.

Grazing Management:

• Pasture Rotation: Moving animals to clean or low-contamination pastures (e.g., after hay or silage crops, or following cattle) reduces larval intake.
• Mixed or Alternate Grazing: Grazing sheep/goats with cattle or horses can reduce parasite burdens, as most GINs are host-specific.
• Resting Pastures: Allowing pastures to rest for extended periods (e.g., 6-12 months) can reduce L3 survival, though hypobiotic larvae in the soil can persist.

Biological Control:

• Nematophagous Fungi: The fungus Duddingtonia flagrans produces spores that trap and kill nematode larvae in feces. Commercial formulations are available in some regions.

Genetic Resistance:

• Breeding for resistance to GINs is possible. Some breeds (e.g., Red Maasai, Gulf Coast Native) exhibit greater resistance, characterized by lower FEC and higher resilience. Selection based on estimated breeding values (EBVs) for FEC is used in some breeding programs.

Nutritional Management:

• Adequate protein nutrition supports immune function and resilience to parasitism. Supplementation with protein-rich feeds can reduce FEC and improve growth in parasitized lambs.

Vaccination:

• A commercial vaccine against H. contortus (Barbervax) is available in some countries. It uses native gut membrane antigens to induce a protective antibody response that reduces worm fecundity and burden. It is used as part of an integrated control program.

Diagnostic and Decision-Making Workflow

The following Mermaid diagram illustrates a clinical decision-making workflow for managing GINs in a sheep flock.

flowchart TD
    A[Flock Health Check], > B{Clinical Signs?}
    B, Yes, > C[FAMACHA Score & BCS]
    B, No, > D[Strategic FEC Monitoring]
    C, > E{Anemia? <br> (FAMACHA 3-5)}
    E, Yes, > F[FEC & Larval Culture]
    E, No, > G[Monitor & Recheck]
    F, > H{High FEC? <br> (>500-1000 EPG)}
    H, Yes, > I[Administer Anthelmintic <br> (TST or Combination)]
    H, No, > J[Consider Other Causes]
    I, > K[Post-Treatment FECRT <br> (Day 10-14)]
    K, > L{Reduction >95%?}
    L, Yes, > M[Effective Treatment]
    L, No, > N[Anthelmintic Resistance Suspected]
    N, > O[Confirm with Larval Culture & <br> Resistance Testing]
    O, > P[Switch Anthelmintic Class <br> or Use Combination]
    P, > Q[Implement IPM: <br> Pasture Rotation, Refugia, <br> Quarantine Drench]
    M, > Q
    D, > R[Seasonal FEC Monitoring]
    R, > S{Threshold Exceeded?}
    S, Yes, > T[Targeted Treatment <br> of High Shedders]
    S, No, > U[Continue Monitoring]
    T, > V[FECRT & Resistance Surveillance]
    V, > Q

Conclusion

Intestinal worms in sheep and goats remain a formidable challenge to global small ruminant production. The complex interplay between parasite biology, host immunity, climate, and management practices demands a sophisticated, evidence-based approach. The cornerstone of modern control is the integration of diagnostic surveillance (FEC, FECRT, larval culture), targeted selective treatment, strategic grazing management, and genetic selection for resistance. The continued spread of anthelmintic resistance underscores the urgency of adopting these IPM principles to preserve the efficacy of existing drugs and ensure the long-term sustainability of sheep and goat enterprises.

References

1. Besier, R. B., Kahn, L. P., Sargison, N. D., & Van Wyk, J. A. (2016). The pathophysiology, ecology and epidemiology of Haemonchus contortus infection in small ruminants. Advances in Parasitology, 93, 95-143.
2. Coles, G. C., Jackson, F., Pomroy, W. E., Prichard, R. K., von Samson-Himmelstjerna, G., Silvestre, A., Taylor, M. A., & Vercruysse, J. (2006). The detection of anthelmintic resistance in nematodes of veterinary importance. Veterinary Parasitology, 136(3-4), 167-185.
3. Kaplan, R. M., & Vidyashankar, A. N. (2012). An inconvenient truth: diagnosis of anthelmintic resistance in the field. Veterinary Parasitology, 189(1), 2-11.
4. Leathwick, D. M., & Besier, R. B. (2014). The management of anthelmintic resistance in grazing ruminants in Australasia: strategies and experiences. Veterinary Parasitology, 204(1-2), 44-54.
5. Sargison, N. D. (2011). Pharmaceutical control of endoparasitic infections in sheep. Veterinary Clinics of North America: Food Animal Practice, 27(1), 139-156.
6. Taylor, M. A., Coop, R. L., & Wall, R. L. (2016). Veterinary Parasitology (4th ed.). Wiley Blackwell.
7. Van Wyk, J. A., & Bath, G. F. (2002). The FAMACHA system for managing haemonchosis in sheep and goats by clinically identifying individual animals for treatment. Veterinary Research, 33(5), 509-529.
8. Vercruysse, J., & Claerebout, E. (2001). Treatment vs non-treatment of helminth infections in cattle: defining the threshold. Veterinary Parasitology, 98(1-3), 195-214.
9. Waller, P. J. (2006). From discovery to development: current industry perspectives for the development of novel methods of helminth control in livestock. Veterinary Parasitology, 139(1-3), 1-14.
10. Wolstenholme, A. J., Fairweather, I., Prichard, R., von Samson-Himmelstjerna, G., & Sangster, N. C. (2004). Drug resistance in veterinary helminths. Trends in Parasitology, 20(10), 469-476.

Disclaimer: This article is for educational and informational purposes only. It is not intended to substitute for professional veterinary advice, diagnosis, treatment, or regulatory guidance. Always consult a licensed veterinarian or qualified specialist regarding animal health, disease diagnosis, and therapeutic decisions.