Porcine Coccidiosis – Investigations on the Cellular Immune Response against Isospora suis

Abstract

Porcine neonatal coccidiosis is caused by the protozoan Isospora suis and affects mainly piglets in the first three weeks of life. High morbidity with diarrhoea and reduced weight gain lead to economic losses, affecting pig-breeding worldwide. Infection causes damage of the mucosal surface in the jejunum and ileum and transient non-haemorrhagic diarrhoea. Secondary infections with other enteric pathogens may lead to increased mortality. Despite its economic and veterinary importance, the immunology of porcine isosporosis is still poorly understood. A striking feature of the infection is the rapidly increasing age resistance prohibiting the development of clinical disease in piglets older than 3-4 weeks irrespective of the immune status. It can be hypothesised that the development of the innate immune system in the first weeks of life and subsequently its interplay with the adaptive immune system is closely related to this phenomenon. Infections with I. suis induce migration of TcR-gammadelta(+) cells to the gut during primary infection and lead to induction of IFN-gamma production by TcR-gammadelta(+) cells and CD4(+) T-helper cells in blood and various lymphoid tissues. Like in other coccidial infections both innate as well as adaptive response mechanisms are activated during infection. They might be both not completely developed in the first weeks of life and therefore leaving a time frame for successful infection.

Experimentally confirmed toltrazuril resistance in a field isolate of Cystoisospora suis

“…While mean fecal consistencies remained below 1.2 in group Wien-20, all other groups developed increased mean fecal scores after infection, indicating enteritis as a consequence of parasite replication [50]. Diarrhea was observed in all groups except group Wien-20, but prevalences and numbers of diarrhea days were generally low.…”

Clinical cystoisosporosis associated to porcine cytomegalovirus (PCMV, Suid herpesvirus 2 ) infection in fattening pigs

“…It has been suggested that PCMV infection might exacerbate porcine respiratory disease complex (PRDC) [27] and other diseases in growers due to its immunosuppressive effect [25,28,29]. PCMV mainly affects the immune function of T lymphocytes and macrophages [28,29] and it is assumed that resistance to C. suis and other coccidia is mainly based on cellmediated immunity [7,30]. Recent research has shown that PCMV induces changes in the transcriptome of the porcine thymus involving immune-related signalling pathways [29] and the micro-RNA expression of infected macrophages, mainly involved in immune and metabolic processes [28].…”

Vaccination against parasites – status quo and the way forward

“…Isospora suis ) causes intestinal infections which may cause transient diarrhoea mostly in the second week of life. Due to the peculiarities of the porcine neonatal immune system (see below) and the strong age resistance to C. suis in piglets older than three weeks [46, 47], it is currently assumed that only pigs older than six weeks can mount an appropriate immune response. For this and other reasons vaccination of piglets against C. suis is not considered feasible.…”

“…At the time of birth the porcine immune system is poorly developed (for review see [47]); intestinal Peyer’s patches contain almost no immune cells and the gut epithelium and subepithelial tissues are only completely populated with T- and B-cells and antigen-presenting cells at about six weeks of age, leaving ample time for pathogens to establish and reproduce. At the same time, the gut microbiota are establishing and infections with pathogens at a very early age may have a number of consequences beyond transient parasite infection.…”

“…C. suis as a member of the Apicomplexa, which have a strictly intracellular development in the host, was assumed to be under the control of the cellular immune system, mainly NK cells, CD4 + and CD8 + T-cells, while antibodies are probably not protective [47]. Phenotyping of cells after primary infection revealed that several subpopulations of T-cells (especially γδ-T cells and, T H cells) were decreased in peripheral organs (blood, spleen) but increased in the jejunum upon infection), and after challenge infection (5 months after primary infection) these cell populations also produced interferon-γ (which is crucial for the defence against apicomplexan parasites) and were able to proliferate upon antigen stimulation [8, 48, 49].…”