Congenital Tick Borne Diseases: Is This An Alternative Route of Transmission of Tick-Borne Pathogens In Mammals?

Tick-borne diseases (TBDs) have become a popular topic in many medical journals. Besides the obvious participation of ticks in the transmission of pathogens that cause TBD, little is written about alternative methods of their spread. An important role is played in this process by mammals, which serve as reservoirs. Transplacental transfer also plays important role in the spread of some TBD etiological agents. Reservoir species take part in the spread of pathogens, a phenomenon that has extreme importance in synanthropic environments. Animals that accompany humans and animals migrating from wild lands to urban areas increase the probability of pathogen infections by ticks This article provides an overview of TBDs, such as tick-borne encephalitis virus (TBEV), and TBDs caused by spirochetes, α-proteobacteria, γ-proteobacteria, and Apicomplexa, with particular attention to reports about their potential to cross the maternal placenta. For each disease, the method of propagation, symptoms of acute and chronic phase, and complications of their course in adults, children, and animals are described in detail. Additional information about transplacental transfer of these pathogens, effects of congenital diseases caused by them, and the possible effects of maternal infection to the fetus are also discussed. The problem of vertical transmission of pathogens presents a new challenge for medicine. Transfer of pathogens through the placenta may lead not only to propagation of diseases in the population, but also constitute a direct threat to health and fetal development. For this reason, the problem of vertical transmission requires more attention and an estimation of the impact of placental transfer for each of listed pathogens.

Hepatic tissue changes in rats due to chronic invasion of Babesia microti.

The etiological agents of babesiosis are intraerythrocytic parasites of the genus Babesia, which are transmitted by ticks. The course of disease is characterized by variable severity. The risk of a complicated course of babesiosis occurs in premature infants, the elderly, splenectomized patients and other immunocompromised patients. Severe cases of this disease can lead to multiple organ dysfunction. The study focuses on the impact assessment of chronic Babesia microti invasion on the morphology and ultrastructure of rat liver. The analyzed material was comprised of liver samples collected from Wistar rats infected with a reference strain of B. microti (ATCC 30221). None of the livers collected from rats with babesiosis was enlarged. The histopathological analyses showed signs of intensive inflammatory processes, especially in the perivascular areas. The hepatic mononuclear phagocyte system was characterized by increased activity. The ultrastructral analyses confirmed disintegration of hepatocytes with vacuolization in the perivascular areas. In addition, the perisinusoidal space (space of Disse) had irregular structure. In some areas, the space of Disse was enlarged or compressed. The morphological and ultrastructural analyses of rat liver with chronic babesiosis caused by B. microti showed significant pathological changes in perivascular areas which may be the cause of hepatic dysfunction.