Coccidiosis, caused by
Eimeria protozoa, is a major parasitic disease impacting livestock and poultry worldwide (
Saeed and Alkheraije, 2023). Infection occurs when animals ingest sporulated oocysts from contaminated feed or water, with each
Eimeria species targeting specific intestinal epithelial cells
(Haug et al., 2008). After ingestion, sporozoites are released in the duodenum and invade the intestinal epithelium, starting a life cycle with asexual (merogony) and sexual (gametogony) phases (
Conway and McKenzie, 2007). Asexual reproduction produces merozoites that spread the infection, while sexual reproduction forms gametes that fuse into zygotes and develop into oocysts. This rapid cycle allows a single oocyst to produce millions of parasites within 4 to 5 days
(Pattison et al., 2007). Pathogenic
Eimeria infections cause hemorrhagic enteritis, bloody diarrhea, malabsorption, emaciation and stunted growth (
Awais et al., 2012;
Ram et al., 2019; Kaur et al., 2019). These pathological changes reduce feed efficiency, delay sexual maturity and lower production, leading to economic losses through both mortality and subclinical effects. Disease severity depends on host, parasite and environmental factors (
Reid, 1990). Its prevalence varies globally, reaching up to 98% in goats and 86% in calves and sheep in England and the USA (
Keeton and Navarre, 2018), nearly 100% in Malaysian goats
(Paul et al., 2020), 78 to 79% in Ethiopian and Iranian goats and sheep
(Dau et al., 2021; Barre et al., 2023; Hatam-Nahavandi et al., 2023), 28.6% in India (
Bangoura and Bardsley, 2020) and 39.8% in Amazonian livestock
(Paul et al., 2020). Management traditionally relies on synthetic anticoccidials, vaccination and plant-derived products. While coccidiocides and ionophores are cost-effective and widely used, rising drug resistance and regulatory restrictions, such as the Europian Union’s ban on prophylactic additives (Council Directive 2011/50/EU), have prompted alternative approaches
(Chapman et al., 2010). Vaccination with wild-type or attenuated
Eimeria strains offers partial protection and plant-based natural products are gaining attention as sustainable feed additives, though challenges remain in standardization, safety, mechanism elucidation and cost-effectiveness
(Gokila et al., 2014; Yang et al., 2015; Murshed et al., 2023).
The rising global prevalence of coccidiosis and increased interest in natural therapies have driven research into plant-derived anticoccidial agents. Phytochemicals show promise as supplements to conventional treatments by providing immunomodulatory, anti-inflammatory and direct antimicrobial effects. The present review explores herb-based alternatives targeting coccidial infections, emphasizing anti-inflammatory, antidiarrheal, anti-ulcer and immunomodulatory actions. Evaluating traditional ethnobotanical knowledge offers valuable insights for developing plant-based strategies, potentially reducing dependence on synthetic anticoccidial drugs.
Source of literature and selection process
Coccidia infections cause diarrhea, ulcers, inflammation and immunosuppression in animals. The present study reviews plants with immunomodulatory, anti-inflammatory, anti-ulcer and anti-diarrheal properties, focusing on those cited in traditional Indian literature and validated by
in vitro and
in vivo studies. Although not yet tested directly against coccidiosis, these plants show potential as future phytotherapeutic agents. The present review integrates traditional Ayurvedic knowledge with modern research, considering only relevant English-language studies and excluding repetitive or unrelated data.
Sources of evidence
This review draws on both traditional and modern scientific sources. Key references include
The Ayurvedic Pharmacopoeia of India, which details validated formulations and therapeutic uses, alongside contemporary studies sourced from Google Scholar, PubMed and Scopus. By combining traditional knowledge with evidence-based research, 48 medicinal plants were identified as promising candidates for potential treatment of coccidial infections.
Screening process and evidence mapping
After screening and removing duplicates, 48 medicinal plants from Indian traditional texts previously untested for anticoccidial activity were identified for their anti-inflammatory, antidiarrheal, anti-ulcer and immunomodulatory properties (Table 1). Their scientific relevance was verified through databases like Google Scholar, PubMed and Scopus, including only English-language articles with supportive evidence. Plants without data on these properties were excluded. Fig 1 shows the selection and screening workflow, while targeted keywords ensured retrieval of relevant literature for each activity.
Development of coccidial infection
Coccidiosis starts when animals ingest sporulated oocysts containing sporocysts and sporozoites. In the gut, the oocyst wall breaks, releasing sporozoites that invade intestinal cells. These sporozoites multiply asexually, producing many merozoites and repeat this cycle several times. Later, sexual stages form male and female gametes, which combine to create new oocysts that are passed in the feces (
Saif, 2009). The life cycle of coccidia with environmental transmission and host-dependent developmental stages is shown in Fig 2.
Conceptual Framework for anti-coccidial activity of selected plants
Based on current literature, the intestinal epithelium and gut-associated immune components play a pivotal role in host–pathogen interactions during
Eimeria infection. The major sites and mechanisms involved in the pathogenesis and potential intervention points are summarized and the mechanistic flowchart of plants exhibiting anti-coccidial effects is shown in Fig 3.
Invasion of intestinal epithelium and nutrient absorption
The intestinal epithelium, responsible for nutrient absorption, is also the site where
Eimeria parasites invade and reproduce
(Shivaramaiah et al., 2014). The invasive sporozoites enter gut cells, multiply asexually (merogony) producing around 1,000 merozoites per sporozoite, repeating 2 to 4 cycles depending on the species. These merozoites then enter the sexual phase (gametogony), forming gametes that fuse into zygotes and develop into unsporulated oocysts, which are shed in feces (
Lillehoj, 1998). This cycle damages the gut lining, weakens the host and aids parasite transmission.
Mucosal and cellular immune mechanisms
After
Eimeria infection, the intestinal epithelium not only absorbs nutrients but also activates immune defenses
(Shivaramaiah et al., 2014). Gut-associated lymphoid tissue, including Peyer’s patches, cecal tonsils and lamina propria lymphocytes, processes antigens, produces antibodies and stimulates B cells, T cells, Natural killer (NK) cells and dendritic cells (
Lillehoj, 1998;
Dalloul and Lillehoj, 2006). Additional defenses include mucus, antimicrobial peptides and a healthy gut microbiota
(Zhao et al., 2001). Cell-mediated immunity, especially CD4+ and CD8+ T cells producing Interferon-gamma (IFN-γ), is crucial for parasite elimination
(Kim et al., 2019; Arstila et al., 1994; Lillehoj and Choi, 1998). Intraepithelial lymphocytes and NK cells provide early local defense, while dendritic cells bridge innate and adaptive immunity, activating T cells, reducing oocyst shedding and enhancing protection (
Lillehoj, 1989;
Cornelissen et al., 2009; Schnitzer et al., 2010; del Cacho et al., 2012;
Sheridan et al., 2013; Shoaib et al., 2017).
Cytokine and chemokine regulation of immune dynamics
Cytokines and chemokines are crucial for immunity against
Eimeria, affecting both protection and disease severity
(Hong et al., 2006). Early responses of IFN-γ and IL-10 enhance resistance, while delayed responses increase susceptibility
(Bremner et al., 2021). IFN-γ inhibits parasite growth and promotes Th1 type response
(Dimier et al., 1998) and pro-inflammatory cytokines like IL-1β and IL-18 trigger inflammation and further IFN-γ production
(Hong et al., 2006; Dalloul et al., 2007). IL-2 activates T and NK cells against
E. acervulina (Ding et al., 2004) and IL-6 supports B cell differentiation and antibody production
(Hong et al., 2006). IL-10 controls inflammation but can suppress Th1 responses, aiding parasite survival
(Rothwell et al., 2004). TNF-α recruits neutrophils and drives tissue inflammation during primary infection
(Zhang et al., 1995), while chemokines such as MIP-1β and K203 guide immune cells to infection sites for effective gut defense
(Laurent et al., 2001).
Microbial dysbiosis and compromised gut integrity
The gut microbiota is vital for immune balance, metabolism and protection against pathogens.
Eimeria tenella infection disrupts the cecal microbial community, causing dysbiosis
(Huang et al., 2018; Macdonald et al., 2017). Beneficial bacteria like
Lactobacillus and
Faecalibacterium decline, while harmful bacteria such as
Clostridium and Escherichia-Shigella increase
(Chen et al., 2020; Cui et al., 2017). Loss of
Faecalibacterium, a major butyrate producer, weakens mucosal integrity and anti-inflammatory responses, worsening gut damage and delaying recovery
(Chen et al., 2020).
