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Food webs are theoretical abstractions of the complex linkages and interactions that are thought to occur in nature. Although few real food webs have actually been characterized scientifically, there is a large body of literature on the processes that contribute towards complexity and stability in webs. Food webs are generally thought of as ‘what eats what’ webs, but parasites are not usually incorporated into webs even though parasitism is a feeding strategy shared by a majority of species on earth (70%). This chapter examines major ideas on the roles of parasites in food webs, starting with Elton’s (1927) idea that parasites are analogous to predators. It describes some general patterns of parasite web structure (e.g., inverted pyramid of numbers and body size hypotheses) using both available published data and data from studies on food webs in freshwater streams in New Jersey.

This chapter explains the biological synergies of malnutrition, parasitic and infectious diseases, and immune response that are specific to HIV transmission, and widespread among poor populations in Africa, Asia, Latin America, and the transition countries. It draws on extensive medical literature that demonstrates that malnutrition, malaria, soil-transmitted helminths and other worms, schistosomiasis (and its genital lesions and inflammation, which resemble sexually transmitted diseases, or STDs), and other parasites increase HIV viral load and viral shedding, and hence increase the risk of HIV transmission.

We live in an environment that differs in many important respects from the environments in which our ancestors lived and to which they became more or less well adapted. We live in large, culturally diverse, and socioeconomically stratified communities of genetically unrelated individuals; we eat different foods; we are exposed to different sets of pathogens and toxins; and we have different patterns of physical activity than did our ancestors. These culturally constructed or man-made environmental changes have resulted in an epidemiologic transition. As deaths from famine and infectious diseases decreased, and life expectancy increased, the burden of disease has shifted to chronic, noncommunicable diseases such as diabetes, coronary heart disease, and stroke. These diseases, which are often referred to as Western diseases, are more appropriately thought of as man-made diseases. Changes in diet, particularly increases in the consumption of sucrose, high fructose corn syrup, and salt, have led to increases in obesity, diabetes, and hypertension. Reducing the prevalence of these diseases requires interventions that reduce risk factors in the entire population. According to the hygiene hypothesis, reduction in exposure to helminths and other pathogens has resulted in an increased risk of allergic and autoimmune diseases. This hypothesis has led to novel, helminth-based treatment of patients with these diseases. Finally, socioeconomic disparities in physiological capital and in psychosocial stresses have led to health disparities. Reducing socioeconomic disparities is the most promising approach to ameliorating health disparities.

A parasite is an organism that lives on or in a host and gets its food from or at the expense of its host. Worms or helminths either live as parasites or free of a host in aquatic and terrestrial environments. Parasites and worms are found worldwide but mainly in the tropics. It is estimated that 20% of immigrants from endemic countries may have helminthic infections at their arrival to the UK. These people could be asymptomatic, but tend to present with unexplained symptoms, especially gastrointestinal in nature or eosinophilia. Travellers to endemic countries tend to be newly infected and have greater immune response and pronounced eosinophilia in some but not all parasitic infections. Parasites that can cause disease in humans fall under three classes: protozoa, helminths, and Ectoparasites Protozoa are microscopic, one- celled organisms that can be free living or parasitic in nature. Transmission of protozoa that live in a human’s intestine to another human typically occurs through a faeco-oral route (for example, contaminated food or water, or person- to-person contact). Protozoa that live in the blood or tissue of humans are transmitted to other humans by an arthropod vector (for example, through the bite of a mosquito or sand fly). Helminths are large, multicellular organisms that are generally visible to the naked eye in their adult stages. Like protozoa, helminths can be either free living or parasitic. There are three main groups of helminths that parasitize humans: cestodes, trematodes, and nematodes. These are flat worms that comprise Echinococcus species: intestinal tapeworms and neurocysticercosis (Taenia solium) These are leaf- shaped, and they vary in length from a few millimetres to 8 cm. They include: ■ Liver fluke: Clonorchis sinensis, Fasciola hepatica ■ Intestinal fluke: Fasciola buski, Heterophyes heterophyes, ■ Lung fluke: Paragonimus westernmani ■ Blood flukes: Schistosoma species These are cylindrical in structure. Blood- sucking arthropods such as mosquitoes are considered as ectoparasites because they depend on blood meal for their survival. Narrowly speaking, ectoparasites include organisms like ticks, fleas, lice, and mites (scabies) that attach or burrow into the skin and remain there for relatively long periods of time (e.g. weeks to months).

Pathogens of every type can affect the eye— bacterial, fungal, viral, protozoal, and parasitic. The eye is a complex structure but for the purposes of categorizing infections it can be viewed as a series of layers, which are: ● Conjunctiva ● Cornea ● Vitreous humour ● Retina The bulk of acute conjunctivitis is viral— up to 90% of infection will be due to adenovirus. Enterovirus species can cause acute epidemic haemorrhagic conjunctivitis, e.g. coxsackie A 24 virus, enterovirus 70. Bacterial causes are more common in children than adults and include S. aureus, S. pneumoniae, and H. influenzae. Pseudomonas aeruginosa and other Gram negatives may cause conjunctivitis in contact lens wearers. It is sometimes possible to differentiate viral from bacterial disease clinically. Where viral conjunctivitis usually results in watery eyes and often comes in concert with a more generalized viral illness, bacterial infection usually occurs in the absence of systemic features and is more likely to be associated with purulent discharge or matting of the eyelids. Viral conjunctivitis does not require specific treatment save in the rare instances where herpes simplex virus is the causative agent—topical aciclovir can then be used. Bacterial infections, however, will resolve more rapidly with topical therapy. A wide range of preparations are available but topical chloramphenicol is the mainstay of treatment. Purulent conjunctivitis in the neonate is often a result of congenitally acquired N. gonorrhoeae or Chlamydia trachomatis infection. In these circumstances conjunctivitis can be the herald of systemic infection and it is therefore wise to treat both systemically and topically. Swabs can be sent for PCR and culture to identify the pathogen. Chlamydia can be treated with topical and oral azithromycin; gonococcal infection can be treated with topical chloramphenicol and a systemic cephalosporin chosen based on local sensitivity patterns. Sexually active adults can also occasionally suffer from these infections and should be treated similarly. Herpes simplex virus is a relatively common cause, usually inoculated directly into the eye by contaminated fingers. The classic presentation is with a unilateral dendritic ulcer, easily visualized on fluorescein dye staining. Herpes zoster virus can also affect the cornea—reactivation in the distribution of the ophthalmic branch of the trigeminal nerve (CN V) results in ophthalmic shingles.

An understanding of the main aspects and functions of the immune system is important, i.e. physical barriers, innate, humoral, and cell-mediated immunity (see Chapter 6, Basic Immunology), when caring for the immunocompromised patient. In adults, secondary immunodeficiency is much more common than primary, and is most often due to iatrogenic immunosuppression with drugs, e.g. corticosteroids, chemotherapy agents, immunosuppressive agents, ‘biological’ therapies. For example, treatment with corticosteroids for more than one month is enough to increase the risk of some fungal infections such as Candida and Pneumocystis jirovecii, such that PCP prophylaxis should be considered in patients receiving ≤ 20mg/day prednisolone for four or more weeks. Chemotherapy and immunosuppressive agents may cause profound immunosuppression. The degree and duration of immunosuppression following a transplant, and the conditioning regimen used before the transplant varies with respect to the type of transplant: heart and lung transplant recipients typically receive more significant immunosuppression, and so are at increased risk of opportunistic infection compared to other solid-organ transplant recipients. Infections (e.g. HIV), cancer, and autoimmune disorders and the treatment of these conditions can also affect the immune system. Other diseases are also considered immunosuppressive although the exact nature of this is less well defined, for example, poorly controlled diabetes mellitus increases the risk of candidal infections and common bacterial infections. Cirrhosis is also considered to be a relatively immunosuppressed state. Understanding the nature of immune defects in both primary and secondary immunodeficiency allows more accurate prediction of overall infection risk and risk of specific pathogens, allowing a rational approach to infection prevention and investigation when patients become unwell. The initial assessment of the immunocompromised host should be to identify why the patient is immunocompromised, how long they have been immunocompromised (is it a congenital or acquired immunodeficiency?), and whether there is potential for immune recovery. Clearly, a person with a congenital immunodeficiency will have lifelong susceptibility to specific infections, unlike an acquired deficiency due to chemotherapy or transplantation which may be transient. If the immunosuppression is due to a drug, is it possible to reduce or change the immunosuppression? If an infection is suspected, pre-immunosuppression infection screening results can help identify whether the current presentation represents reactivation of a latent infection or primary infection.

Parasites account for a significant burden of disease today, with 200 million people infected with malaria and more than 1.5 billion people infected with soil-transmitted helminths alone. This chapter explores the impact that parasitic infection has had on the evolution of Homo sapiens, as well as the impact that our species has had on the evolution of common parasites. It first establishes the long co-evolutionary history that exists between many parasite species and hominins by presenting both direct archaeological evidence for parasitic infection in humans from the Palaeolithic through to modern day, as well as indirect evidence that has been used to identify parasites that were likely passed down from hominin ancestors. It explores the major changes in parasite disease burden through our evolution as a result of biological, cultural and social changes. After establishing the significant time depth to human-parasite interactions it explores the co-evolutionary relationship between humans and their parasites by drawing on recent evidence gained from studies in immunology and genetics, identifying mechanisms that parasites use to alter human immune function to their benefit, human genes involved in parasite resistance and the intricate relationship between autoimmune diseases and parasitic infection. Finally, it reflects on how an evolutionary approach to parasitic infection can contribute to new approaches to the control of parasite transmission and treatment development.