Neurological trypanosomiasis in quinapyramine sulfate-treated horses—a breach of the blood–brain barrier?

Abstract

Trypanosoma evansi infection typically produces wasting disease, but it can also develop into a neurological or meningoencephalitis form in equids. Trypanosomiasis in horses was treated with quinapyramine sulfate, and all the 14 infected animals were recovered clinically. After clinical recovery, four animals developed a neurological form of the disease at various intervals. Two of these animals treated with diminazene aceturate recovered temporarily. Repeated attempts failed to find the parasite in the blood or the cerebrospinal fluid (CSF), but all of the animals were positive in enzyme-linked immunosorbent assay. The calculation of the antibody index (AI) in the serum and the CSF and polymerase chain reaction (PCR) analysis of the CSF and brain tissue were carried out to confirm the neuro-infection. We found PCR and AI analyses of the CSF to be useful tools in the diagnosis of the neurological form of trypanosomiasis when the organism cannot be found in the blood or CSF. The increased albumin quotient is indicative of barrier leakage due to neuroinflammation. The biochemical changes in the CSF due to nervous system trypanosomiasis include increases in the albumin quotient, total protein, and urea nitrogen. It seems to be the first report on relapse of the nervous form of trypanosomiasis in equids even after quinapyramine treatment in endemic areas.

The animal trypanosomiases and their chemotherapy: a review

“…1) include both animal ( T. b. brucei, T. b. evansi, T. b. equiperdum ) and human ( T. b. rhodesiense, T. b. gambiense ) infective subspecies. Unlike T. vivax (most strains at least) or T. congolense, T. brucei group trypanosomes are found in both the vascular system and in other tissues, and can parasitize the brain in experimental infections (Moulton, 1986; Grab and Kennedy, 2008; Coles et al 2015); descriptions of this clinical condition in field settings are limited, other than for equids, which are particularly susceptible to T. brucei (Tuntasuvan et al 1997; Ranjithkumar et al 2014). As the most widely used drugs to treat animal trypanosomes (diminazene and isometamidium) do not cross the blood–brain barrier, the presence of parasites in sites other than the bloodstream represents a potentially important issue for treatment of T. brucei .…”

“…The compound was applied to treat cattle infected with trypanosomes until 1976, when it was withdrawn from many areas due to emergence of widespread resistance (Connor, 1992). The drug was subsequently reintroduced in 1984 to treat T. b. evansi in camels and horses (Peregrine, 1994), and is still used today (Ranjithkumar et al 2014). In horses with acute infections of T. brucei spp.…”

Important hemoprotozoan diseases of livestock: Challenges in current diagnostics and therapeutics: An update

“…Among them, PCR has the maximum application [ 28 , 29 ]. Several PCR-based diagnostic assays have been developed which include the use of species-specific primers, single and nested PCRs [ 30 ], and real-time PCR [ 31 ]. Tandem repeat domain of GM6 (cytoskeletal protein) has diagnostic value and its usefulness as seroepidemiological studies of surra has been evaluated among water buffaloes [ 32 ].…”

Production and preliminary evaluation of Trypanosoma evansi HSP70 for antibody detection in Equids

“…The numbers of surra outbreaks and severity is escalating radically over the last few years . In equines, the parasite is reported to breach blood brain barrier and show marked ataxia, blindness, circling, hyper-excitability, depression and gradual onset of paralysis of hind quarters (Rodrigues et al 2009;Ranjithkumar et al 2013). The clinical signs of trypanosomosis in general are indicative but are not sufficiently patho-gnomonic and have to be confirmed by laboratory methods.…”