Infections with extracellular trypanosomes require control by efficient innate immune mechanisms and can result in the destruction of the mammalian humoral immune system

Salivarian trypanosomes are extracellular parasites that affect humans, livestock, and game animals around the world. Through co-evolution with the mammalian immune system, trypanosomes have developed defense mechanisms that allow them to thrive in blood, lymphoid vessels, and tissue environments such as the brain, the fat tissue, and testes. Trypanosomes have developed ways to circumvent antibody-mediated killing and block the activation of the lytic arm of the complement pathway. Hence, this makes the innate immune control of the infection a crucial part of the host-parasite interaction, determining infection susceptibility, and parasitemia control. Indeed, trypanosomes use a combination of several independent mechanisms to avoid clearance by the humoral immune system. First, perpetuated antigenic variation of the surface coat allows to escape antibody-mediated elimination. Secondly, when antibodies bind to the coat, they are efficiently transported toward the endocytosis pathway, where they are removed from the coat proteins. Finally, trypanosomes engage in the active destruction of the mammalian humoral immune response. This provides them with a rescue solution in case antigenic variation does not confer total immunological invisibility. Both antigenic variation and B cell destruction pose significant hurdles for the development of anti-trypanosome vaccine strategies. However, developing total immune escape capacity and unlimited growth capabilities within a mammalian host is not beneficial for any parasite, as it will result in the accelerated death of the host itself. Hence, trypanosomes have acquired a system of quorum sensing that results in density-dependent population growth arrest in order to prevent overpopulating the host. The same system could possibly sense the infection-associated host tissue damage resulting from inflammatory innate immune responses, in which case the quorum sensing serves to prevent excessive immunopathology and as such also promotes host survival. In order to put these concepts together, this review summarizes current knowledge on the interaction between trypanosomes and the mammalian innate immune system, the mechanisms involved in population growth regulation, antigenic variation and the immuno-destructive effect of trypanosomes on the humoral immune system. Vaccine trials and a discussion on the role of innate immune modulation in these trials are discussed at the end

Features of Highly Pathogenic Avian Influenza (HPAI) H5N1 in Domestic Poultry

H5 and H7 subtypes are associated with the highly pathogenic form of AI (HPAI), which are extremely virulent, causing up to 100% mortality in domestic poultry. This virulence and ability to cause systemic infection have been attributed to the multibasic cleavage motif in their hemagglutinin molecule, which are recognized by subtilisin-like endoproteases that are virtually present in every tissue, making them capable of replicating in multiple tissue; hence, lesions are multisystemic (i.e., nervous, circulatory, respiratory, integumentary, musculoskeletal, hemopoietic, gastrointestinal, reproductive systems). The myriads of lesion that accompanied outbreaks of HPAI in domestic poultry as seen in Nigeria from 2006 to 2016 are as a result of the above findings. A critical look at the Nigerian HPAI situation not only revealed the general clinic-pathologic features in domestic poultry and factors that support the persistence of the virus in the environment but also gave insight to the flow of the virus in the country. A situation whereby poultry are kept in free-range, multispecies, multiage holdings with low biosecurity supports the spread of HPAI. Also, the live bird markets (LBMs) that have been fed by this unorganized poultry structure have consistently been the nidus for HPAI detection, be it in 2008 after the virus was thought to have been eradicated or in 2015, when the virus resurfaced in Lagos. It is proposed that all factors enhancing the propensity of the virus to remain in poultry should be giving the attention required. Therefore, it is important that the strict biosecurity measures that ensure prevention of HPAI incursion into poultry premises after 2008 are revamped while improving on the organization of the poultry and product supply chain in the country

First molecular detection of Sarcocystis suihominis in a domestic pig of Nigeria

Sarcocystis are Apicomplexan protozoa with a dixenous life cycle that includes a predator and a prey as definitive and intermediate hosts, respectively. Domestic and wild pigs are intermediate hosts of S. suihominis, with formation of sarcocysts in their muscles, while humans and non-human primates act as final hosts. After ingesting raw or undercooked sarcocyst-infested pork, signs of gastroenteritis including inappetence, nausea, vomiting, and diarrhea may develop in humans. Moreover, excretion of infective forms with human feces leads to dissemination of the parasite in the environment. In this study, macroscopic sarcocysts of white color, oval shape, and a diameter of approximately 3–8 mm were found in the skeletal muscle of a slaughtered domestic pig (Sus scrofa domesticus) destined for human consumption in an abattoir of Makurdi, Benue State, Nigeria. Sarcocyst DNA was used as template to PCR amplify the near-complete length of the 18S rRNA gene and a fragment of the cytochrome c oxidase subunit 1 (cox-1) gene. Amplicons were sequenced and used to construct phylogenetic trees with selected available Sarcocystis spp. sequences. In both cases, the placement of the analyzed sequences with S. suihominis was strongly supported, confirming the species identity of this macroscopic sarcocyst-forming parasite. This constitutes the first molecular identification of S. suihominis in Nigeria and the African continent. Proximity between pigs and humans, and poor sanitary conditions frequently encountered in pig farms of Nigeria might favor the dissemination of this zoonotic parasite, posing a threat to public health.12 month embargo; first published 23 February 2024This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]