Intermediate Host Transmission Dynamics

Overview

This app allows you to explore transmission dynamics for parasites. Specifically, this app focuses on parasites with indirect life cycles which used intermediate hosts to complete their life cycle. Parasites are an extremely diverse group of organisms that can cause disease in plants and animals. Any organism that lives on or in another organism and derives its nutrients from that organism at the host’s expense can be considered a parasite. However, we are going to focus on classic parasitic diseases of vertebrates which are commonly caused by helminths and protozoa. There are an estimated 75,000 to 300,000 parasitic helminths of vertebrate hosts compared to the approximately 66,200 species of vertebrates described i.e. fish, reptiles, amphibians, birds, and mammals (Dobson et al. 2008).

In addition to the abundant species diversity of parasites, there is a lot of variation in reproductive strategies. Life cycles of parasites are broadly categorized as direct or indirect. Parasites with direct life cycles only require one host to reach sexual maturity and produce progeny. Compared to parasites with indirect life cycles which require at least one intermediate host to complete their life cycle. Some parasites with indirect life cycles require more than one intermediate host for development.

To learn more about the model in detail read the description in the “Model” tab and then do the tasks described in the “What to do” tab.

Learning Objectives

The Model

Model Overview and Background Information

In this model we will only be looking at a simple indirect life cycle with 2 species (a host and an intermediate host), using the basic SIR compartmental model.

The model has the following compartments:

Assumptions:

We assume that once an intermediate host is infected, it stays infected until it dies. Therefore, recovered intermediate hosts are not included in the model. Additionally, we assume the time scale for this model is short enough that we can ignore the birth and death rates for definitive hosts. This is likely an appropriate assumption as long as our simulation is only a couple years. This model would not be good for chronic parasitic infections that persist for a long time e.g. echinococcosis, chronic schistosomiasis, and paragonimiasis (Manfras et al. 2002; Olveda et al. 2014; Walker and Zunt 2005).

The processes being modeled are:

We envision this model being flexible allowing hosts to represent a wide range of definitive and intermediate hosts with the one caveat that intermediate hosts are not intended to represent vectors, like mosquitoes, which can act as intermediate hosts for parasites.

Model Diagram

The flow diagram and the set of ordinary differential equations (ODE) which are used to implement this model are as follows:

Flow diagram for this model.

Flow diagram for this model.

Model Equations

\[\dot S_h = - S_h b_i I_i + w R_h\] \[\dot I_h = S_h b_i Ii - g I_h\] \[\dot R_h = g I_h - w R_h\] \[\dot E = p I_h - c E\] \[\dot S_i = (m-n) S_i - b_e S_i E\] \[\dot I_i = S_i b_e I_h - n I_i\]

What to do

The tasks below are described in a way that assumes everything is in units of MONTHS (rate parameters, therefore, have units of inverse months). If any quantity is not given in those units, you need to convert it first (e.g. if it says a year, you need to convert it to 12 months).

Task 1

In the first task we are going to use Dracunculus medinensis as an example. This parasitic nematode is the causative agent of Dracunculiasis also know as the Guinea worm. Humans are infected through the consumption of water containing infected copepods, the intermediate host. You can read more about Guinea worm and see a diagram of its life cycle on this CDC website.

Task 2

In the scenario above the death rate of the intermediate host was set at 0.083, which is equivalent to a year lifespan. Copepods typically lifespan can be anywhere from 150 days to a year (Kurtz 2007).

Task 3

For the following tasks we will be using Taenia multiceps as an example. T. multiceps is a type of tapeworm that infects dogs and requires a rabbit or ruminant intermediate host. This not to be confused with Dipylidium caninum, the flea tapeworm, which is commonly associated with domestic dogs and requires a flea as intermediate host and is transmitted to the dog via ingestion of the infected flea. Anthelmintics, or dewormers, are commonly used to control worm burdens and shedding in pets and livestock. In this scenario we will explore how host shedding impacts transmission dynamics. You can read more about T. multiceps and see a diagram of its life cycle on this CDC website.

Using anthelmintics is a common why to reduce the worm burden in a host and the number of eggs being shed into the environment. Fecal egg counts are often used to assess the effectiveness of a drug and determine if resistance is presence. Parasites should be considered susceptible to a drug if there is a 90% reduction in eggs compared to a pretreatment fecal egg count (McKenna 1990).

Task 4

In addition to reducing worm burdens and shedding, treating with anthelmintics can shorten the infectious period and increase the recovery rate. While, treatments can increase the recovery rate drugs like steroids, which are immunosuppressive can prolong the recovery rate.

Task 5

For this task we are going to use two examples, Toxoplasma gondii and Heterakis gallinarum. Both parasites have a direct and indirect life cycle. For the purpose of this exercise we will only look at the indirect life cycle. T. gondii is a protozoa and the causative agent of Toxoplasmosis. Felines are the definitive host and small rodents are the intermediate hosts. Oocysts can survive in the environment for up to 90 days (Lindsay, Blagburn, and Dubey 2002). Compared to H. gallinarum, a nematode which serves as a vector for a protozoal disease in turkeys called Histomoniasis. Poultry are the definitive host of H. gallinarum and earthworms serve as the paratentic host, or an intermediate host that is not required for development but essential for completing the life cycle and transmitting the parasite to the definitive host. While 90% of the eggs survive 20 to 40 days in the environment, a small proportion can survive up to 2 years (Thapa et al. 2017).

What effect does increasing the duration a parasite persists in the environment have on the number of susceptible intermediate hosts? Why do you see an initial decrease in susceptible intermediate hosts then an increase? (Hint: Look at the number of parasites in the environment. As the number of parasites in the environment decreases the number of susceptible intermediate hosts increases as new individuals are born).

Task 6

Up onto this point we have not changed the rate of waning immunity and have assumed that once an infected host recovers, they have a lasting protective immunity. However, in reality it is very common for a host to loss its protection against reinfection as time progresses. In this scenario we will observe the effects that waning immunity has on outbreak dynamics. It may be necessary to shorten the duration of the simulation time from 5 years to half year to visualizes the graphs well.

Task 7

We are going to use the previous example of T. gondii in the next task to assess the effects of transmission from an intermediate host to host on outbreak dynamics. There have been many parasites that have been studied because of their ability to modify a host’s behavior to increase transmission. T. gondii is one such parasite that has been documented to alter rodent behavior to decrease their fear of felines and make them more prone to predation which increases transmission potential (Vyas et al. 2007).

The number of infected hosts increases as transmission rate increases and the time at which peak infection occurs decreases. Vaccines typically target transmission. Compare your results to those in task 3 where you altered the rate pathogens are shed into the environment. Does decreasing the transmission rate have more of impact on the number of infected hosts than decreasing parasite shedding?

Task 8

In the following task we are going to look at the effects the number of parasites in the environment has on transmission dynamics. Environmental stages are extremely important and typically where the parasites are most vulnerable to degradation due to abiotic factors like temperature and precipitation. Additionally, favorable environmental conditions can decrease the development time required to become infective which can increase the rate of transmission.

Why do you think the initial number of parasites in the environment has little effect in the overall total of parasites in the environment? Think about the life cycle of a parasite. They require the definitive host for sexual reproduction. The physiologic processes in the host impact the number of parasites being shed in the environment. Increasing the rate of parasites shed into the environmental increases the number of parasites and the number of infected hosts. Increasing the environmental transmission to intermediate hosts increases the number of infected hosts but not the number of parasites in the environment.

Further Information

References

Dobson, Andy, Kevin D. Lafferty, Armand M. Kuris, Ryan F. Hechinger, and Walter Jetz. 2008. “Homage to Linnaeus: How Many Parasites? How Many Hosts?” Proceedings of the National Academy of Sciences.

Kurtz, Joachim. 2007. “Evolutionary Ecology of Immune Defence in Copepods.” Journal of Plankton Research 29 (January): i27–i38. https://doi.org/10.1093/plankt/fbl063.

Lindsay, D. S., B. L. Blagburn, and J. P. Dubey. 2002. “Survival of Nonsporulated Toxoplasma Gondii Oocysts Under Refrigerator Conditions.” Veterinary Parasitology 103 (4): 309–13.

Manfras, Burkhard J., Stefan Reuter, Thomas Wendland, and Peter Kern. 2002. “Increased Activation and Oligoclonality of Peripheral Cd8+ T Cells in the Chronic Human Helminth Infection Alveolar Echinococcosis.” Infection and Immunity 70 (3): 1168–74.

McKenna, P. B. 1990. “The Detection of Anthelmintic Resistance by the Faecal Egg Count Reduction Test: An Examination of Some of the Factors Affecting Performance and Interpretation.” New Zealand Veterinary Journal 38 (4): 142–47.

Olveda, David U., Remigio M. Olveda, Donald P. McManus, Pengfei Cai, Thao N. P. Chau, Alfred K. Lam, Yuesheng Li, Donald A. Harn, Marilyn L. Vinluan, and Allen G. P. Ross. 2014. “The Chronic Enteropathogenic Disease Schistosomiasis.” International Journal of Infectious Diseases 28: 193–203.

Thapa, Sundar, Stig M. Thamsborg, Nicolai V. Meyling, Suraj Dhakal, and Helena Mejer. 2017. “Survival and Development of Chicken Ascarid Eggs in Temperate Pastures.” Parasitology 144 (9): 1243–52.

Vyas, Ajai, Seon-Kyeong Kim, Nicholas Giacomini, John C. Boothroyd, and Robert M. Sapolsky. 2007. “Behavioral Changes Induced by Toxoplasma Infection of Rodents Are Highly Specific to Aversion of Cat Odors.” Proceedings of the National Academy of Sciences 104 (15): 6442–7.

Walker, M. D., and Joseph R. Zunt. 2005. “Neuroparasitic Infections: Cestodes, Trematodes, and Protozoans.” In Seminars in Neurology, 25:262. 3. NIH Public Access.