Tick-host Interaction with Specific Reference to Host Immune System

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In case of livestock enterprises, 80% of the world cattle population is affected by the ticks and tick-borne diseases. Direct effects of ticks on animals include skin damage by opening of wounds that ultimately lead to secondary bacterial infections and paralysis, additionally causing toxicosis in some cases. Indirect losses of ticks are even more dangerous because they act as vectors of many disease, for example theileriosis and babesiosis. Ticks have the ability to survive without food for up to three years, however, they are unable to oviposit during this period because engorgement is required for this process. They affect their host by reducing milk production and growth rate, damaging hides and transmit lethal disease causing organisms that result in injuries and paralysis. Thus, it is demanding to have better understanding of the tick-host interaction and host immune system against feeding ticks.

Interaction between Ticks and Hosts:

Ticks take the blood meal through pool feeding and they have to puncture many blood vessels for the release of blood to feed on it. Slow and rapid feeding ticks cause different levels of damage to their hosts. A hematoma is formed gradually during the feeding of hard ticks. Degranulation and inflammation is mainly caused by the neutrophils which are attracted towards the site of feeding. Soft ticks, on the other hand, feed for a short period through deep penetration in the host’s skin and cause considerable blood loss even after the completion of blood meal. During the process of blood meal, laceration of blood vessels and small capillaries occurs, hemorrhages are formed and host cells are ruptured. This phenomenon increases the blood supply towards the site of feeding and ultimately leads to the activation of host’s defense mechanism that includes hemostasis (platelet aggregation and blood coagulation) and immune system. Blood flow from small vessels is arrested by platelet aggregation which is considered to be the most immediate defense system. It has been hypothesized that platelet aggregation might be the possible reason of evolution of arthropod’s salivary proteins than that of blood coagulation. Thus, coagulation is less significant in host’s defense mechanism against hematophagus arthropods.

Tick hosts have developed certain defensive mechanisms, thus ticks have to overcome this defense to complete a successful blood meal during the feeding period. The host defense mechanism against feeding ticks includes: (i) hemostasis, works to prevent blood loss and heals injuries caused during tick bites, (ii) innate immunity consisting of cascade complement and inflammatory response which are helpful to remodel the damaged tissues and have an antimicrobial effect and (iii) antigen specific acquired immunity which develops during the feeding of ticks due to prolonged feeding and repeated exposure of animals to ticks. However, coagulation is important during the process of ingestion of blood because many anti-coagulant inhibitors are responsible for maintenance of fluid form of blood. It must be considered that only 3-4 minutes are taken by the blood for coagulation after vascular damage. Argasid ticks take 30-60 minutes for feeding while the Ixodid ticks may take longer from a week or more. Thus, there is sufficient time for blood to be coagulated and play its pivotal role while feeding.

Host Immune Response Against Ticks:

The first report about the immunity of host against ticks was published in 1918 but very little was known during the period of 1918-1973 about the bovine host immunity against ticks. However, African bred Bos indicus cattle was known to be resistant against ticks as compared to British bred Bos taurus cattle. Immediately after the challenge of tick feeding, vasoactive amines (important part of basophils) arrive at the feeding site and increase the cellular density up to 80%. Basophil derived mediators play a very crucial role in the development of immunity in hosts against ticks, as described in many studies that (1) tissue histamine level was suggested to be twice in resistant animals than the susceptible animal, (2) tick mortality or withdrawal was observed after the injection of histamine at the tick attachment sites with an additional effect of interruption in tick feeding when histamine was added to the artificial media and (3) reduced resistance and skin reactivity was observed in animals when they were treated with histamine receptor antagonist.

Histopathologically, tick feeding sites have been observed to possess neutrophil infiltration accompanied by eosinophil response as the cutaneous cellular mechanism in naive animals. Pathological lesion is restricted to feeding site where a feeding cavity is formed that leads to hemorrhages with the advancement of feeding process. Neutrophils cause perivascular cuffing in the vessels of lower dermis. In addition, little degranulation is caused by the accumulation of basophils at the border of dermis and epidermis. Microscopically, intra-epidermal vesicles have been observed on feeding sites. Here, intense cellular response of leukocytes is observed adjacent to the hypostome of ticks that mainly consists of basophils. Interestingly, circulating leukocytes contain only 1% basophils because they are not normally found in the tissues of majority of vertebrates, however, they can increase up to 500% in the hosts parasitized by ticks. Specific immunological response involving antibodies and T-cells is responsible for accumulation of these cells in tissues.

Many authors believe that histamine has a secondary role in the host immunity against ticks because basophil derived mediators play a major role in immune response. Furthermore, the ticks also induce immunomodulation of the host immune response by various immune-modulators present in their salivary glands. Thus, a deep understanding of the biologically active molecules in the tick salivary glands can create many possibilities to investigate various strategies used by ticks to deter host resistance against ticks.


Published in: Volume 08 Issue 30

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