What is Dr. Zubair Khalid's research focus?

Dr. Zubair Khalid specializes in molecular virology, mRNA vaccine development, and computational biology, with a focus on avian pathogens like IBDV and Avian Reovirus.

Where is Dr. Zubair Khalid currently working?

Dr. Zubair Khalid is a Postdoctoral Research Associate at the University of Maryland (UMD), specifically within the Department of Animal and Avian Sciences.

Parascaris equorum in Foals: Equine Roundworm Pathogenesis, Treatment, and Control

Etiology and Taxonomy

Parascaris equorum is a large intestinal nematode belonging to the family Ascarididae. It is the primary ascarid parasite of equids, with foals and juvenile horses (typically under 18 months of age) serving as the principal hosts. Adult worms are robust, creamy white, and can reach lengths of 15 to 50 cm. The life cycle is direct, involving the ingestion of embryonated eggs from a contaminated environment. Larvae hatch in the small intestine, penetrate the intestinal wall, and migrate via the portal circulation to the liver and then to the lungs. After a tracheal migration, larvae are coughed up, swallowed, and return to the small intestine where they mature into adults. The prepatent period is approximately 10 to 15 weeks.

Epidemiology

Parascaris equorum has a cosmopolitan distribution, with prevalence highest in intensively managed foal populations. Infection pressure is driven by the extreme environmental resilience of ascarid eggs, which can remain viable for years in soil, bedding, and on stable surfaces. Foals acquire infection through ingestion of eggs from contaminated teats, feed, water, or by direct geophagia. Immunity develops with age, and adult horses rarely harbor patent infections. However, subclinical carrier mares can serve as a source of environmental contamination. Necropsy surveys have demonstrated that P. equorum remains common on small farms and in non-intensive management systems [1].

Pathogenesis

The pathogenesis of Parascaris equorum infection in foals is a function of both larval migration and adult worm burden. Hepatic migration causes traumatic hepatitis, characterized by focal hemorrhage, necrosis, and eosinophilic infiltration. These lesions may appear as white foci ("milk spots") on the liver capsule. Pulmonary migration induces a verminous pneumonia, with coughing, nasal discharge, and tachypnea. In heavy infections, the pulmonary phase can be severe and may predispose foals to secondary bacterial pneumonia.

Adult worms reside in the lumen of the small intestine, where they compete for nutrients and can cause mechanical obstruction. Large boluses of worms can precipitate intestinal impaction, intussusception, or rupture, which are life-threatening surgical emergencies. Chronic infection is associated with poor growth, rough hair coat, pot-bellied appearance, and recurrent colic. The host immune response is characterized by a Th2-type reaction with eosinophilia and elevated IgE levels.

Clinical Signs

Clinical signs of Parascaris equorum infection in foals are most pronounced in animals aged 2 to 8 months. Common presentations include:

Unthriftiness and poor weight gain
Rough, dull hair coat
Pot-bellied appearance
Intermittent colic
Coughing and nasal discharge (during larval migration)
Diarrhea or pasty feces
Inappetence

In cases of massive worm burdens, acute intestinal obstruction can occur, presenting as severe colic, abdominal distension, and shock. Respiratory signs may dominate in foals with heavy pulmonary larval migration.

Pathology

Gross pathological findings in foals with P. equorum infection include:

Liver: Focal white fibrotic nodules (milk spots) on the capsular and cut surfaces, representing sites of larval migration and granulomatous inflammation.
Lungs: Multifocal hemorrhagic and edematous areas, with verminous pneumonia evident on histology. Larvae may be found in bronchioles and alveoli.
Small intestine: Adult worms are present in the lumen, often in large numbers. The intestinal mucosa may be catarrhal or hemorrhagic. In obstructive cases, a tangled mass of worms can be found at the ileocecal junction or within the jejunum.

Histologically, hepatic lesions show eosinophilic infiltration, fibrosis, and granuloma formation. Pulmonary lesions feature alveolar hemorrhage, eosinophilic exudate, and bronchiolar epithelial hyperplasia.

Diagnostics

Antemortem diagnosis of Parascaris equorum infection relies primarily on fecal examination. The following diagnostic modalities are employed:

Fecal Flotation and Egg Counting

Standard fecal flotation using saturated salt or sugar solutions (specific gravity 1.20 to 1.25) is effective for detecting P. equorum eggs. Eggs are thick-shelled, round to oval, approximately 90 to 100 micrometers in diameter, with a characteristic brownish color and a single-cell morula. Quantitative techniques such as the McMaster counting chamber or modified Wisconsin method allow estimation of eggs per gram (EPG) of feces. A strong positive correlation exists between EPG and adult worm burden.

Fecal Egg Count Reduction Test (FECRT)

The FECRT is the standard method for detecting anthelmintic resistance in P. equorum populations. Fecal samples are collected on the day of treatment (Day 0) and 10 to 14 days post-treatment. A reduction in mean EPG of less than 90% (or less than 95% for macrocyclic lactones) is indicative of resistance. The FECRT has been widely used to document resistance to ivermectin, pyrantel, and fenbendazole in P. equorum [2, 3, 4, 5, 6].

Molecular Diagnostics

PCR-based assays targeting the internal transcribed spacer (ITS) regions of ribosomal DNA can confirm species identification and are useful for epidemiological studies. Quantitative PCR (qPCR) offers higher sensitivity than fecal flotation for detecting low-level infections. Molecular methods are also employed to detect single nucleotide polymorphisms (SNPs) associated with benzimidazole resistance in the beta-tubulin gene.

Necropsy and Worm Counts

Necropsy with total worm count remains the gold standard for quantifying adult worm burdens and for confirming treatment efficacy in experimental studies [7, 8, 9, 10]. The small intestine is opened longitudinally, and all visible worms are collected, counted, and identified.

Treatment

Treatment of Parascaris equorum infection in foals has become increasingly complicated due to the widespread emergence of anthelmintic resistance. The three major drug classes used are macrocyclic lactones (ivermectin, moxidectin), tetrahydropyrimidines (pyrantel pamoate), and benzimidazoles (fenbendazole, oxibendazole).

Macrocyclic Lactones

Ivermectin has historically been the drug of choice for P. equorum control. It is effective against both adult worms and migrating larvae [7, 8, 9]. However, resistance to ivermectin is now documented in multiple geographic regions, including Australia [2, 3], New Zealand [4], Italy [11, 6], and Sweden [5]. Sub-optimal efficacy, defined as less than 90% reduction in EPG, has been reported in numerous studies. Moxidectin, a second-generation macrocyclic lactone, may retain efficacy against some ivermectin-resistant isolates, but cross-resistance is common.

Tetrahydropyrimidines

Pyrantel pamoate is a nicotinic acetylcholine receptor agonist. It has demonstrated efficacy against macrocyclic lactone-resistant P. equorum isolates in some studies [12]. However, resistance to pyrantel has also been reported [3, 6]. The drug is administered orally at a dose of 6.6 mg/kg (as pyrantel base). Its efficacy should be confirmed by FECRT on each farm.

Benzimidazoles

Fenbendazole has been evaluated for larvicidal activity against P. equorum [10]. Resistance to fenbendazole is widespread, and its use as a single agent is often ineffective [3]. Oxibendazole may retain efficacy in some populations, but resistance is common.

Treatment Recommendations

Given the high prevalence of resistance, treatment decisions must be guided by farm-specific FECRT data. The following principles apply:

Use the lowest effective dose of a drug class that has demonstrated greater than 90% efficacy on the farm.
Rotate drug classes annually or biannually, but only if FECRT confirms susceptibility.
Avoid routine, interval-based deworming of all foals. Instead, employ targeted selective treatment (TST) based on individual EPG thresholds.
For foals with confirmed high worm burdens, combination therapy (e.g., ivermectin plus pyrantel) may be considered, although data on synergy are limited.

Anthelmintic Resistance

Anthelmintic resistance in Parascaris equorum is a global and growing problem. Resistance has been documented to all three major drug classes [13, 14]. The mechanisms of resistance include:

Macrocyclic lactones: Altered ligand-gated chloride channel subunits (GluCl, GABA-Cl) and increased drug efflux via P-glycoprotein transporters.
Tetrahydropyrimidines: Reduced affinity at nicotinic acetylcholine receptors.
Benzimidazoles: Single nucleotide polymorphisms (e.g., Phe200Tyr) in the beta-tubulin isotype 1 gene.

The clinical consequence of resistance is treatment failure, leading to persistent infection, poor growth, and risk of intestinal obstruction. Resistance is exacerbated by frequent, interval-based deworming with the same drug class, which selects for resistant alleles.

Control

Integrated control of Parascaris equorum in foals requires a multifaceted approach that combines strategic anthelmintic use with environmental management.

Pasture and Stable Management

Remove feces from paddocks and stables daily to reduce egg contamination.
Compost manure at temperatures exceeding 55 degrees Celsius to kill ascarid eggs.
Rotate pastures and avoid overstocking.
Use deep litter bedding systems with regular complete removal.

Diagnostic Surveillance

Conduct FECRT annually on each farm to monitor drug efficacy.
Perform fecal egg counts on all foals at 8 to 12 weeks of age to detect early infections.
Use TST protocols: treat only foals with EPG above a predetermined threshold (e.g., 200 EPG).

Quarantine and Biosecurity

Quarantine new arrivals for at least 14 days and perform fecal egg counts before introducing them to the resident herd.
Treat all incoming foals with a drug class known to be effective on the farm, and confirm efficacy with a post-treatment FECRT.

Refugia-Based Strategies

Maintain a proportion of the foal population untreated to preserve susceptible alleles. This can be achieved by leaving foals with low EPG values untreated.
Avoid treating all foals on the same day; stagger treatments to maintain environmental refugia.

Decision Tree for Parascaris equorum Management in Foals

The following Mermaid diagram outlines a clinical decision algorithm for managing P. equorum infection in foals on a farm.

flowchart TD
    A[Foal aged 2-8 months], > B[Perform fecal egg count]
    B, > C{EPG > 200?}
    C, >|Yes| D[Select anthelmintic based on recent FECRT]
    C, >|No| E[No treatment; monitor]
    D, > F[Administer treatment]
    F, > G[Perform post-treatment FECRT at Day 10-14]
    G, > H{EPG reduction > 90%?}
    H, >|Yes| I[Continue using same drug class]
    H, >|No| J[Switch to alternative drug class]
    J, > K[Confirm efficacy with repeat FECRT]
    I, > L[Implement integrated control: pasture hygiene, composting, quarantine]
    K, > L
    L, > M[Annual FECRT surveillance]

Conclusion

Parascaris equorum remains a significant pathogen of foals worldwide. The emergence of resistance to all major anthelmintic classes has rendered traditional interval-based deworming protocols ineffective and counterproductive. A modern approach to control must be grounded in diagnostic surveillance, targeted selective treatment, and rigorous environmental management. The FECRT is an indispensable tool for guiding drug selection and detecting resistance at the farm level. Continued research into alternative treatment modalities, including combination therapy and novel drug targets, is urgently needed.

References

[1] Kornaś S, Skalska M, Nowosad B. Occurrence of roundworm (Parascaris equorum) in horses from small farms based on necropsy. Wiad Parazytol. 2006. URL: https://pubmed.ncbi.nlm.nih.gov/17432627/

[2] Beasley A, Coleman G, Kotze AC. Suspected ivermectin resistance in a south-east Queensland Parascaris equorum population. Aust Vet J. 2015. URL: https://pubmed.ncbi.nlm.nih.gov/26313207/

[3] Armstrong SK, Woodgate RG, Gough S, et al. The efficacy of ivermectin, pyrantel and fenbendazole against Parascaris equorum infection in foals on farms in Australia. Vet Parasitol. 2014. URL: https://pubmed.ncbi.nlm.nih.gov/25224788/

[4] Bishop RM, Scott I, Gee EK, et al. Sub-optimal efficacy of ivermectin against Parascaris equorum in foals on three Thoroughbred stud farms in the Manawatu region of New Zealand. N Z Vet J. 2014. URL: https://pubmed.ncbi.nlm.nih.gov/24151853/

[5] Lind EO, Christensson D. Anthelmintic efficacy on Parascaris equorum in foals on Swedish studs. Acta Vet Scand. 2009. URL: https://pubmed.ncbi.nlm.nih.gov/19930608/

[6] Veronesi F, Moretta I, Moretti A, et al. Field effectiveness of pyrantel and failure of Parascaris equorum egg count reduction following ivermectin treatment in Italian horse farms. Vet Parasitol. 2009. URL: https://pubmed.ncbi.nlm.nih.gov/19201100/

[7] DiPietro JA, Lock TF, Todd KS Jr, et al. Efficacy of ivermectin in the treatment of induced Parascaris equorum infection in pony foals. J Am Vet Med Assoc. 1989. URL: https://pubmed.ncbi.nlm.nih.gov/2599956/

[8] French DD, Klei TR, Taylor HW, et al. Efficacy of ivermectin in oral drench and paste formulation against migrating larvae of experimentally inoculated Parascaris equorum. Am J Vet Res. 1989. URL: https://pubmed.ncbi.nlm.nih.gov/2774327/

[9] DiPietro JA, Lock TF, Todd KS Jr, et al. Evaluation of ivermectin for larvicidal effect in experimentally induced Parascaris equorum infections in pony foals. Am J Vet Res. 1988. URL: https://pubmed.ncbi.nlm.nih.gov/3247923/

[10] Vandermyde CR, DiPietro JA, Todd KS Jr, et al. Evaluation of fenbendazole for larvacidal effect in experimentally induced Parascaris equorum infections in pony foals. J Am Vet Med Assoc. 1987. URL: https://pubmed.ncbi.nlm.nih.gov/3610763/

[11] Veronesi F, Fioretti DP, Genchi C. Are macrocyclic lactones useful drugs for the treatment of Parascaris equorum infections in foals? Vet Parasitol. 2010. URL: https://pubmed.ncbi.nlm.nih.gov/20471177/

[12] Reinemeyer CR, Prado JC, Nichols EC, et al. Efficacy of pyrantel pamoate against a macrocyclic lactone-resistant isolate of Parascaris equorum in horses. Vet Parasitol. 2010. URL: https://pubmed.ncbi.nlm.nih.gov/20307936/

[13] von Samson-Himmelstjerna G. Anthelmintic resistance in equine parasites - detection, potential clinical relevance and implications for control. Vet Parasitol. 2012. URL: https://pubmed.ncbi.nlm.nih.gov/22100141/

[14] Reinemeyer CR. Anthelmintic resistance in non-strongylid parasites of horses. Vet Parasitol. 2012. URL: https://pubmed.ncbi.nlm.nih.gov/22078748/