Equine piroplasmosis is caused by a protozoan parasite, either Babesia. equi (formerly known as Theileria equi) or Babesia caballi. Due to its prevalence in recent U.S. outbreaks, B. equi is the focus of this article.

The recent insidious emergence of piroplasmosis, a tick-borne disease, is a striking reminder of the vigilance required to remain free of the class of infectious diseases that include persistence in their pathogenesis. Pathogen persistence is the ability of an infectious organism to remain in the host long-term, even for life, in the absence of easily detectable clinical disease. A critical outcome of persistence is infected populations that are clinically silent reservoirs for transmission.

Infection of equine erythrocytes by B. equi leads to variable levels of anemia, fever, anorexia, malaise and icterus (jaundice). Although death is possible following infection of a naïve horse, it has not been reported in the current U.S. infections.

The reasons for clinically silent transmission of B. equi are not well understood. Possibilities include missed diagnosis due to the non-specificity of clinical signs; the contributions of parasite virulence and the horse’s ability to control parasite replication; the roles of infection prevalence within horses and transmission of competent tick populations; and the overall health status of newly infected horses. These parameters likely contribute collectively to transmission dose and clinical outcome of initial infection.

Although the host-parasite-vector parameters responsible for the level of clinical disease are not well understood, factors likely responsible for re-emergence of B. equi infections in the United States are better defined. The historical widespread use of the complement fixation test (CFT) for serological screening of horses moving internationally likely allowed for entrance of infected horses into countries considered free of infection and/or disease. Equine immunoglobulin IgG(T) does not fix complement via the classical pathway and therefore contributes to false-negative CFT results. Movement of infected horses into areas with transmission-competent ticks may lead to additional infections.

Transition to the use of cELISA and polymerase chain reaction (PCR) testing has enhanced detection of clinically silent, persistently infected horses. An important component of infection and disease control in a low-prevalence country such as the United States is treatment of persistently infected horses with the intent of eliminating B. equi and removing transmission risk. While a number of drugs have been tested, the majority of data have been derived using imidocarb dipropionate (ID). Published data clearly show that ID is an effective anti-babesial chemotherapeutic that reduces B. equi parasitemias associated with acute and persistent infections.

However, controversy exists concerning the ability of ID to completely eliminate B. equi from persistently infected horses. Several reasons exist for this controversy. Past use of the CFT to measure the expected decrease in anti- B. equi antibody following parasite removal may have given false-negative results, and since several different recommended ID doses and treatment protocols have been used, some may have led to ID-resistant strains. Alternatively, there may be naturally occurring strains or sub-populations of B. equi that are resistant to elimination by ID.

Further complicating assessment of chemotherapeutic efficacy in the complete elimination of B. equi persistence is the potential of persistence-specific antibody titers, even in the absence of stimulating antigen. Antigen-independent models have been proposed to explain the persistence of long-term antibody titers. These models include memory B lymphocytes with special “memory” qualities that need fewer signals to mature to plasma cells and/or the presence of long-lived, antibody-producing plasma cells. A possible outcome of persistent antibody titers is finding treated horses that are PCR-negative but antibody-positive for B. equi, suggesting parasite elimination but antibody persistence. Should such data be forthcoming, consideration must be given to changing the premise that specific antibody titers always indicate B. equi infection and transmission risk.

Management options available to owners of B. equi and/or B. caballi infected horses are evolving and variable depending on location. Knowing that ticks are required for natural transmission allows for tick-free quarantine as one option. The implementation of this option is related to the practicality of maintaining a tick-free environment and knowledge of the transmission capacity of local ticks. Next, historical and recent data indicate that ID treatment will remove transmission risk from some infected horses; however, a clear understanding of the meaning of the presence of specific antibody in a treated, PCR-negative horse must be defined.

There are at least two explanations for an ID-treated, PCR-negative, antibody-positive horse. First is that a specific antibody may be the result of the length of the infection and long-lived memory B lymphocytes and plasma cells. Second is that it has been hypothesized that in PCR-negative, antibody-positive horses, parasites are sequestered in, for instance, capillary beds or bone marrow. With time the parasites will emerge in the peripheral blood, and such a horse will re-convert to PCR-positive and remain a transmission risk. It is the opinion of this author that the collective data indicating ID treatment for complete removal of B. equi and or B. caballi from infected horses are worthy of consideration in non-endemic countries.

The final word on ID treatment must await the defining of the transmission risk of treated horses that are PCR-negative but possess persisting specific antibody.

Knowles, Donald, DVM, DAVP