Chapter 13 : Transmission and the Determinants of Transmission Efficiency

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Bacteria within the order would have little impact on human and veterinary medicine in the absence of the arthropod vector. Interestingly, the influence of primary infections with one sp. can influence the success of transovarial transmission of a second. This chapter details some fascinating trends observed regarding vertical and horizontal transmission. Biotic and abiotic factors determine the stability of any sylvatic or zoonotic transmission cycle. The chapter centers on a discussion of the attributes of successful pathogen transmission in the context of the vector's ability to modulate (i) the mammalian host's response during acquisition and transmission and (ii) microbial growth within the vector during the maintenance phase. The discussion in these two sections essentially defines the environment and competency of both the vector and mammalian host as determinants of transmission and transmission efficiency. The chapter ends with a survey of fluctuating ecological trends that can enhance or diminish the potency of vector-borne rickettsial zoonotic cycles. Even though acquisition rates were similar for each transmission experiment, intergenera transmission required cofeeding of multiple infected mites with uninfected mites. Rickettsial diseases have the potential to change the outcomes of war and prey on the unfortunate circumstances that arise from disaster.

Citation: Ceraul S. 2012. Transmission and the Determinants of Transmission Efficiency, p 391-415. In Palmer G, Azad A (ed), Intracellular Pathogens II: . ASM Press, Washington, DC. doi: 10.1128/9781555817336.ch13

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Small Interfering RNA
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Human Monocytic Ehrlichiosis
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Image of FIGURE 1

Tick-host-rickettsiae interaction. (A) Ticks secrete a number of antihemostatic and immunomodulatory substances into the bite site to increase blood flow and reduce immune activation to the tick during feeding. Rickettsiae are imbibed with the blood meal or transmitted to the host during this stage of the interaction. As rickettsiae enter the midgut lumen, they attach to the host cell (B) and induce phagocytosis so as to be enveloped in a vacuole that is rapidly degraded (C) to lie in direct contact with the cytoplasm. (D) Spotted fever group rickettsiae move between and within each host cell using actin tail polymerization. (E) Ticks respond to rickettsiae by mounting an innate immune response that involves antimicrobial peptide gene transcription. Recent work suggests that the rickettsial invasion process is limited by tick antimicrobial peptides. doi:10.1128/9781555817336.ch13.f1

Citation: Ceraul S. 2012. Transmission and the Determinants of Transmission Efficiency, p 391-415. In Palmer G, Azad A (ed), Intracellular Pathogens II: . ASM Press, Washington, DC. doi: 10.1128/9781555817336.ch13
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Image of FIGURE 2

Vectors of the . (A) tick. (B) Oriental rat flea, . (C) Body louse, . (D) Trombiculid larval mite (chigger). (Images A, B, and C from the Centers for Disease Control and Prevention Public Health Image Library. Image A modified from CDC image 10865; image B modified from CDC image 4633; image C modified from CDC image 9208. Image D from Wikipedia Commons. Photo credit: Luc Viatour; www.lucnix.be.) doi:10.1128/9781555817336.ch13.f2

Citation: Ceraul S. 2012. Transmission and the Determinants of Transmission Efficiency, p 391-415. In Palmer G, Azad A (ed), Intracellular Pathogens II: . ASM Press, Washington, DC. doi: 10.1128/9781555817336.ch13
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Image of FIGURE 3

Sylvatic and zoonotic transmission. Rickettsiae are transmitted in sylvatic cycles that involve a vector, in this case a tick, and their mammalian, reptilian, or avian hosts. Humans are accidentally infected when they encroach into the habitat where the sylvatic cycle exists. The cycle begins (1) and ends (4) when infected and uninfected ticks feed on large mammals. Horizontal transmission between infected and uninfected ticks can occur at this stage through cofeeding. Uninfected adults can also contract the pathogen by feeding on infected large mammals. If the bacterium is transmitted vertically (transovarial transmission), the egg clutch will be infected. Otherwise, uninfected egg masses will be oviposited. If transovarial transmission occurs, infected larvae will perpetuate pathogen transmission by feeding on small to medium-size hosts (2). Uninfected larvae can become infected at step 2 through cofeeding with infected larvae or by feeding on infected hosts. Infected larvae can also feed on humans (Z), representing the first point where humans can be infected. Transmission continues to uninfected hosts and ticks in the same manner at stage 3, perpetuating the pathogen in nature. Human infection can occur at Z and Z. Solid gray curved arrows follow the sylvatic cycle. The gray-to-white gradient curved arrows indicate accidental human infection. Solid gray straight arrows denote the infected path, while the open straight arrow denotes the uninfected path. (Portions of this figure adapted from images from the Centers for Disease Control and Prevention Public Health Image Library. Ticks modified from CDC image 6005; human modified from CDC image 3425; small mammals modified from CDC image 3381; large mammals modified from CDC image 3392.) doi: 10.1128/9781555817336.ch13.f3

Citation: Ceraul S. 2012. Transmission and the Determinants of Transmission Efficiency, p 391-415. In Palmer G, Azad A (ed), Intracellular Pathogens II: . ASM Press, Washington, DC. doi: 10.1128/9781555817336.ch13
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Image of FIGURE 4

Endosymbiotic rickettsial modulation of tick immune activation. Endosymbiotic rickettsiae like may recalibrate immune homeostatic norms, thereby increasing the sensitivity of ticks to secondary rickettsial infection. Primary rickettsial infections may increase the immunological sensitivity of ticks to secondary rickettsial infections. Although this hypothesis has not been tested, it is possible that by-products of replication like free peptidoglycan functionally saturate recognition proteins such as PGRP-LB, which normally prevents activation by degrading immunostimulatory peptidoglycan. Alternatively, rickettsiae may modulate host gene transcription or posttranslational modification of immune effectors to make them more potent. We hypothesize that endosymbiotic rickettsiae effectively lower the activation threshold (B) or increase basal homeostatic immune activity, bringing it closer to the activation threshold (C). Scenario A represents immune activation in ticks that possess no infection. Scenario D represents the immune activation that occurs when ticks possess a primary endosymbiont and imbibe a secondary rickettsia. We hypothesize that rapid and possibly sustained immune activation in scenario D limits infection of the ovary by a second rickettsia. Dashed lines represent immune activation threshold; solid lines represent baseline (constitutive) immune activity. doi:10.1128/9781555817336.ch13.f4

Citation: Ceraul S. 2012. Transmission and the Determinants of Transmission Efficiency, p 391-415. In Palmer G, Azad A (ed), Intracellular Pathogens II: . ASM Press, Washington, DC. doi: 10.1128/9781555817336.ch13
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Generic image for table

List of rickettsial diseases

The following sources were used to compile this table: .

Reservoirs are identified through isolation or detection in field-collected samples.

Exposed animals are those that serve as host for ticks but may not contract the rickettsiae. When no information was available the blocks were left blank.

Detection method.

Citation: Ceraul S. 2012. Transmission and the Determinants of Transmission Efficiency, p 391-415. In Palmer G, Azad A (ed), Intracellular Pathogens II: . ASM Press, Washington, DC. doi: 10.1128/9781555817336.ch13
Generic image for table

List of rickettsial diseases

The following sources were used to compile this table: .

Reservoirs are identified through isolation or detection in field-collected samples.

Exposed animals are those that serve as host for ticks but may not contract the rickettsiae. When no information was available the blocks were left blank.

Detection method.

Citation: Ceraul S. 2012. Transmission and the Determinants of Transmission Efficiency, p 391-415. In Palmer G, Azad A (ed), Intracellular Pathogens II: . ASM Press, Washington, DC. doi: 10.1128/9781555817336.ch13

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