{"id":706,"date":"2016-11-04T03:34:53","date_gmt":"2016-11-04T03:34:53","guid":{"rendered":"https:\/\/courses.lumenlearning.com\/microbiology\/?post_type=chapter&#038;p=706"},"modified":"2016-11-10T05:45:51","modified_gmt":"2016-11-10T05:45:51","slug":"virulence-factors-of-eukaryotic-pathogens","status":"publish","type":"chapter","link":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/chapter\/virulence-factors-of-eukaryotic-pathogens\/","title":{"raw":"Virulence Factors of Eukaryotic Pathogens","rendered":"Virulence Factors of Eukaryotic Pathogens"},"content":{"raw":"<div class=\"textbox learning-objectives\">\r\n<h3>Learning Objectives<\/h3>\r\n<ul>\r\n \t<li>Describe virulence factors unique to fungi and parasites<\/li>\r\n \t<li>Compare virulence factors of fungi and bacteria<\/li>\r\n \t<li>Explain the difference between protozoan parasites and helminths<\/li>\r\n \t<li>Describe how helminths evade the host immune system<\/li>\r\n<\/ul>\r\n<\/div>\r\nAlthough fungi and parasites are important pathogens causing infectious diseases, their pathogenic mechanisms and virulence factors are not as well characterized as those of bacteria. Despite the relative lack of detailed mechanisms, the stages of pathogenesis and general mechanisms of virulence involved in disease production by these pathogens are similar to those of bacteria.\r\n<h2>Fungal Virulence<\/h2>\r\nPathogenic fungi can produce virulence factors that are similar to the bacterial virulence factors that have been discussed earlier in this chapter. In this section, we will look at the virulence factors associated with species of <em>Candida<\/em>, <em>Cryptococcus, Claviceps,<\/em> and <em>Aspergillus<\/em>.\r\n\r\n<strong><em>Candida albicans<\/em><\/strong> is an opportunistic fungal pathogen and causative agent of oral thrush, vaginal yeast infections, and cutaneous candidiasis. <em>Candida<\/em> produces adhesins (surface glycoproteins) that bind to the phospholipids of epithelial and endothelial cells. To assist in spread and tissue invasion, <em>Candida<\/em> produces proteases and phospholipases (i.e., exoenzymes). One of these proteases degrades keratin, a structural protein found on epithelial cells, enhancing the ability of the fungus to invade host tissue. In animal studies, it has been shown that the addition of a protease inhibitor led to attenuation of <em>Candida<\/em> infection.[footnote]K. Fallon et al. \"Role of Aspartic Proteases in Disseminated <em>Candida albicans<\/em> Infection in Mice.\" <em>Infection and Immunity<\/em> 65 no. 2 (1997):551\u2013556.[\/footnote] Similarly, the phospholipases can affect the integrity of host cell membranes to facilitate invasion.\r\n\r\nThe main virulence factor for <strong><em>Cryptococcus<\/em><\/strong>, a fungus that causes pneumonia and meningitis, is capsule production. The polysaccharide glucuronoxylomannan is the principal constituent of the <em>Cryptococcus<\/em> capsule. Similar to encapsulated bacterial cells, encapsulated <em>Cryptococcus<\/em> cells are more resistant to phagocytosis than nonencapsulated <em>Cryptococcus<\/em>, which are effectively phagocytosed and, therefore, less virulent.\r\n\r\nLike some bacteria, many fungi produce exotoxins. Fungal toxins are called <strong>mycotoxin<\/strong><strong>s<\/strong>. <em>Claviceps purpurea<\/em>, a fungus that grows on rye and related grains, produces a mycotoxin called ergot toxin, an alkaloid responsible for the disease known as <strong>ergotism<\/strong>. There are two forms of ergotism: gangrenous and convulsive. In <strong>gangrenous ergotism<\/strong>, the ergot toxin causes vasoconstriction, resulting in improper blood flow to the extremities, eventually leading to gangrene. A famous outbreak of gangrenous ergotism occurred in Eastern Europe during the 5th century AD due to the consumption of rye contaminated with <em>C. purpurea<\/em>. In <strong>convulsive ergotism<\/strong>, the toxin targets the central nervous system, causing mania and hallucinations.\r\n\r\nThe mycotoxin <strong>aflatoxin<\/strong> is a virulence factor produced by the fungus <strong><em>Aspergillus<\/em><\/strong>, an <strong>opportunistic pathogen<\/strong> that can enter the body via contaminated food or by inhalation. Inhalation of the fungus can lead to the chronic pulmonary disease <strong>aspergillosis<\/strong>, characterized by fever, bloody sputum, and\/or asthma. Aflatoxin acts in the host as both a <strong>mutagen<\/strong> (a substance that causes mutations in DNA) and a <strong>carcinogen<\/strong> (a substance involved in causing cancer), and has been associated with the development of <strong>liver cancer<\/strong>. Aflatoxin has also been shown to cross the blood-placental barrier.[footnote]C.P. Wild et al. \"In-utero exposure to aflatoxin in west Africa.\" <em>Lancet<\/em> 337 no. 8757 (1991):1602.[\/footnote] A second mycotoxin produced by <em>Aspergillus<\/em> is <strong>gliotoxin<\/strong>. This toxin promotes virulence by inducing host cells to self-destruct and by evading the host\u2019s immune response by inhibiting the function of phagocytic cells as well as the pro-inflammatory response. Like <em>Candida<\/em>, <em>Aspergillus<\/em> also produces several proteases. One is <strong>elastase<\/strong>, which breaks down the protein elastin found in the connective tissue of the lung, leading to the development of lung disease. Another is <strong>catalase<\/strong>, an enzyme that protects the fungus from hydrogen peroxide produced by the immune system to destroy pathogens.\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Think about It<\/h3>\r\n<ul>\r\n \t<li>List virulence factors common to bacteria and fungi.<\/li>\r\n \t<li>What functions do mycotoxins perform to help fungi survive in the host?<\/li>\r\n<\/ul>\r\n<\/div>\r\n<h2>Protozoan Virulence<\/h2>\r\nProtozoan pathogens are unicellular eukaryotic parasites that have virulence factors and pathogenic mechanisms analogous to prokaryotic and viral pathogens, including adhesins, toxins, antigenic variation, and the ability to survive inside phagocytic vesicles.\r\n\r\nProtozoans often have unique features for attaching to host cells. The protozoan <strong><em>Giardia lamblia<\/em><\/strong>, which causes the intestinal disease giardiasis, uses a large adhesive disc composed of microtubules to attach to the intestinal mucosa. During adhesion, the flagella of <em>G. lamblia<\/em> move in a manner that draws fluid out from under the disc, resulting in an area of lower pressure that facilitates adhesion to epithelial cells. <em>Giardia<\/em> does not invade the intestinal cells but rather causes inflammation (possibly through the release of cytopathic substances that cause damage to the cells) and shortens the intestinal villi, inhibiting absorption of nutrients.\r\n\r\nSome protozoans are capable of <strong>antigenic variation<\/strong>. The obligate intracellular pathogen <strong><em>Plasmodium falciparum<\/em><\/strong> (one of the causative agents of <strong>malaria<\/strong>) resides inside red blood cells, where it produces an adhesin membrane protein known as PfEMP1. This protein is expressed on the surface of the infected erythrocytes, causing blood cells to stick to each other and to the walls of blood vessels. This process impedes blood flow, sometimes leading to organ failure, anemia, jaundice (yellowing of skin and sclera of the eyes due to buildup of bilirubin from lysed red blood cells), and, subsequently, death. Although PfEMP1 can be recognized by the host\u2019s immune system, antigenic variations in the structure of the protein over time prevent it from being easily recognized and eliminated. This allows malaria to persist as a chronic infection in many individuals.\r\n\r\nThe virulence factors of <strong><em>Trypanosoma brucei<\/em><\/strong>, the causative agent of <strong>African sleeping sickness<\/strong>, include the abilities to form <strong>capsules<\/strong> and undergo <strong>antigenic variation<\/strong>. <em>T. brucei<\/em> evades phagocytosis by producing a dense glycoprotein coat that resembles a bacterial capsule. Over time, host antibodies are produced that recognize this coat, but <em>T. brucei<\/em> is able to alter the structure of the glycoprotein to evade recognition.\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Think about It<\/h3>\r\n<ul>\r\n \t<li>Explain how antigenic variation by protozoan pathogens helps them survive in the host.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<h2>Helminth Virulence<\/h2>\r\nHelminths, or parasitic worms, are multicellular eukaryotic parasites that depend heavily on virulence factors that allow them to gain entry to host tissues. For example, the aquatic larval form of <strong><em>Schistosoma mansoni<\/em><\/strong>, which causes <strong>schistosomiasis<\/strong>, penetrates intact skin with the aid of proteases that degrade skin proteins, including elastin.\r\n\r\nTo survive within the host long enough to perpetuate their often-complex life cycles, helminths need to evade the immune system. Some helminths are so large that the immune system is ineffective against them. Others, such as adult <strong>roundworms<\/strong> (which cause <strong>trichinosis<\/strong>, <strong>ascariasis<\/strong>, and other diseases), are protected by a tough outer cuticle.\r\n\r\nOver the course of their life cycles, the surface characteristics of the parasites vary, which may help prevent an effective immune response. Some helminths express polysaccharides called <strong>glycans<\/strong> on their external surface; because these glycans resemble molecules produced by host cells, the immune system fails to recognize and attack the helminth as a foreign body. This \"<strong>glycan gimmickry<\/strong>,\" as it has been called, serves as a protective cloak that allows the helminth to escape detection by the immune system.[footnote]I. van Die, R.D. Cummings. \"Glycan Gimmickry by Parasitic Helminths: A Strategy for Modulating the Host Immune Response?\" <em>Glycobiology<\/em> 20 no. 1 (2010):2\u201312.[\/footnote]\r\n\r\nIn addition to evading host defenses, helminths can actively suppress the immune system. <em>S. mansoni<\/em>, for example, degrades host antibodies with <strong>proteases<\/strong>. Helminths produce many other substances that suppress elements of both innate nonspecific and adaptive specific host defenses. They also release large amounts of material into the host that may locally overwhelm the immune system or cause it to respond inappropriately.\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Think about It<\/h3>\r\n<ul>\r\n \t<li>Describe how helminths avoid being destroyed by the host immune system.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Key Concepts and Summary<\/h3>\r\n<ul>\r\n \t<li>Fungal and parasitic pathogens use pathogenic mechanisms and virulence factors that are similar to those of bacterial pathogens<\/li>\r\n \t<li>Fungi initiate infections through the interaction of adhesins with receptors on host cells. Some fungi produce toxins and exoenzymes involved in disease production and capsules that provide protection of phagocytosis.<\/li>\r\n \t<li>Protozoa adhere to target cells through complex mechanisms and can cause cellular damage through release of cytopathic substances. Some protozoa avoid the immune system through antigenic variation and production of capsules.<\/li>\r\n \t<li>Helminthic worms are able to avoid the immune system by coating their exteriors with glycan molecules that make them look like host cells or by suppressing the immune system.<\/li>\r\n<\/ul>\r\n<\/div>\r\n<div class=\"textbox exercises\">\r\n<h3>Multiple Choice<\/h3>\r\nWhich of the following is a major virulence factor for the fungal pathogen <em>Cryptococcus?<\/em>\r\n<ol style=\"list-style-type: lower-alpha;\">\r\n \t<li>hemolysin<\/li>\r\n \t<li>capsule<\/li>\r\n \t<li>collagenase<\/li>\r\n \t<li>fimbriae<\/li>\r\n<\/ol>\r\n[reveal-answer q=\"595019\"]Show Answer[\/reveal-answer]\r\n[hidden-answer a=\"595019\"]Answer b. Capsule is a major virulence factor for the fungal pathogen <em>Cryptococcus<\/em>.[\/hidden-answer]\r\n\r\nWhich of the following pathogens undergoes antigenic variation to avoid immune defenses?\r\n<ol style=\"list-style-type: lower-alpha;\">\r\n \t<li><em data-effect=\"italics\">Candida<\/em><\/li>\r\n \t<li><em data-effect=\"italics\">Cryptococcus<\/em><\/li>\r\n \t<li><em data-effect=\"italics\">Plasmodium<\/em><\/li>\r\n \t<li><em data-effect=\"italics\">Giardia<\/em><\/li>\r\n<\/ol>\r\n[reveal-answer q=\"842714\"]Show Answer[\/reveal-answer]\r\n[hidden-answer a=\"842714\"]Answer c.\u00a0<em>Plasmodium<\/em> undergoes antigenic variation to avoid immune defenses.[\/hidden-answer]\r\n\r\n<\/div>\r\n<div class=\"textbox exercises\">\r\n<h3>Fill in the Blank<\/h3>\r\n<em>Candida<\/em> can invade tissue by producing the exoenzymes __________ and __________.\r\n\r\n[reveal-answer q=\"626001\"]Show Answer[\/reveal-answer]\r\n[hidden-answer a=\"626001\"]<em>Candida<\/em> can invade tissue by producing the exoenzymes <strong>protease<\/strong> and <strong>phospholipase<\/strong>.[\/hidden-answer]\r\n\r\nThe larval form of <em>Schistosoma mansoni<\/em> uses a __________ to help it gain entry through intact skin.\r\n\r\n[reveal-answer q=\"503881\"]Show Answer[\/reveal-answer]\r\n[hidden-answer a=\"503881\"]The larval form of Schistosoma mansoni uses a <strong>protease<\/strong> to help it gain entry through intact skin.[\/hidden-answer]\r\n\r\n<\/div>\r\n<div class=\"textbox key-takeaways\">\r\n<h3>Think about It<\/h3>\r\n<ol>\r\n \t<li>Describe the virulence factors associated with the fungal pathogen <em>Aspergillus.<\/em><\/li>\r\n \t<li>Explain how helminths evade the immune system.<\/li>\r\n<\/ol>\r\n<\/div>","rendered":"<div class=\"textbox learning-objectives\">\n<h3>Learning Objectives<\/h3>\n<ul>\n<li>Describe virulence factors unique to fungi and parasites<\/li>\n<li>Compare virulence factors of fungi and bacteria<\/li>\n<li>Explain the difference between protozoan parasites and helminths<\/li>\n<li>Describe how helminths evade the host immune system<\/li>\n<\/ul>\n<\/div>\n<p>Although fungi and parasites are important pathogens causing infectious diseases, their pathogenic mechanisms and virulence factors are not as well characterized as those of bacteria. Despite the relative lack of detailed mechanisms, the stages of pathogenesis and general mechanisms of virulence involved in disease production by these pathogens are similar to those of bacteria.<\/p>\n<h2>Fungal Virulence<\/h2>\n<p>Pathogenic fungi can produce virulence factors that are similar to the bacterial virulence factors that have been discussed earlier in this chapter. In this section, we will look at the virulence factors associated with species of <em>Candida<\/em>, <em>Cryptococcus, Claviceps,<\/em> and <em>Aspergillus<\/em>.<\/p>\n<p><strong><em>Candida albicans<\/em><\/strong> is an opportunistic fungal pathogen and causative agent of oral thrush, vaginal yeast infections, and cutaneous candidiasis. <em>Candida<\/em> produces adhesins (surface glycoproteins) that bind to the phospholipids of epithelial and endothelial cells. To assist in spread and tissue invasion, <em>Candida<\/em> produces proteases and phospholipases (i.e., exoenzymes). One of these proteases degrades keratin, a structural protein found on epithelial cells, enhancing the ability of the fungus to invade host tissue. In animal studies, it has been shown that the addition of a protease inhibitor led to attenuation of <em>Candida<\/em> infection.<a class=\"footnote\" title=\"K. Fallon et al. &quot;Role of Aspartic Proteases in Disseminated Candida albicans Infection in Mice.&quot; Infection and Immunity 65 no. 2 (1997):551\u2013556.\" id=\"return-footnote-706-1\" href=\"#footnote-706-1\" aria-label=\"Footnote 1\"><sup class=\"footnote\">[1]<\/sup><\/a> Similarly, the phospholipases can affect the integrity of host cell membranes to facilitate invasion.<\/p>\n<p>The main virulence factor for <strong><em>Cryptococcus<\/em><\/strong>, a fungus that causes pneumonia and meningitis, is capsule production. The polysaccharide glucuronoxylomannan is the principal constituent of the <em>Cryptococcus<\/em> capsule. Similar to encapsulated bacterial cells, encapsulated <em>Cryptococcus<\/em> cells are more resistant to phagocytosis than nonencapsulated <em>Cryptococcus<\/em>, which are effectively phagocytosed and, therefore, less virulent.<\/p>\n<p>Like some bacteria, many fungi produce exotoxins. Fungal toxins are called <strong>mycotoxin<\/strong><strong>s<\/strong>. <em>Claviceps purpurea<\/em>, a fungus that grows on rye and related grains, produces a mycotoxin called ergot toxin, an alkaloid responsible for the disease known as <strong>ergotism<\/strong>. There are two forms of ergotism: gangrenous and convulsive. In <strong>gangrenous ergotism<\/strong>, the ergot toxin causes vasoconstriction, resulting in improper blood flow to the extremities, eventually leading to gangrene. A famous outbreak of gangrenous ergotism occurred in Eastern Europe during the 5th century AD due to the consumption of rye contaminated with <em>C. purpurea<\/em>. In <strong>convulsive ergotism<\/strong>, the toxin targets the central nervous system, causing mania and hallucinations.<\/p>\n<p>The mycotoxin <strong>aflatoxin<\/strong> is a virulence factor produced by the fungus <strong><em>Aspergillus<\/em><\/strong>, an <strong>opportunistic pathogen<\/strong> that can enter the body via contaminated food or by inhalation. Inhalation of the fungus can lead to the chronic pulmonary disease <strong>aspergillosis<\/strong>, characterized by fever, bloody sputum, and\/or asthma. Aflatoxin acts in the host as both a <strong>mutagen<\/strong> (a substance that causes mutations in DNA) and a <strong>carcinogen<\/strong> (a substance involved in causing cancer), and has been associated with the development of <strong>liver cancer<\/strong>. Aflatoxin has also been shown to cross the blood-placental barrier.<a class=\"footnote\" title=\"C.P. Wild et al. &quot;In-utero exposure to aflatoxin in west Africa.&quot; Lancet 337 no. 8757 (1991):1602.\" id=\"return-footnote-706-2\" href=\"#footnote-706-2\" aria-label=\"Footnote 2\"><sup class=\"footnote\">[2]<\/sup><\/a> A second mycotoxin produced by <em>Aspergillus<\/em> is <strong>gliotoxin<\/strong>. This toxin promotes virulence by inducing host cells to self-destruct and by evading the host\u2019s immune response by inhibiting the function of phagocytic cells as well as the pro-inflammatory response. Like <em>Candida<\/em>, <em>Aspergillus<\/em> also produces several proteases. One is <strong>elastase<\/strong>, which breaks down the protein elastin found in the connective tissue of the lung, leading to the development of lung disease. Another is <strong>catalase<\/strong>, an enzyme that protects the fungus from hydrogen peroxide produced by the immune system to destroy pathogens.<\/p>\n<div class=\"textbox key-takeaways\">\n<h3>Think about It<\/h3>\n<ul>\n<li>List virulence factors common to bacteria and fungi.<\/li>\n<li>What functions do mycotoxins perform to help fungi survive in the host?<\/li>\n<\/ul>\n<\/div>\n<h2>Protozoan Virulence<\/h2>\n<p>Protozoan pathogens are unicellular eukaryotic parasites that have virulence factors and pathogenic mechanisms analogous to prokaryotic and viral pathogens, including adhesins, toxins, antigenic variation, and the ability to survive inside phagocytic vesicles.<\/p>\n<p>Protozoans often have unique features for attaching to host cells. The protozoan <strong><em>Giardia lamblia<\/em><\/strong>, which causes the intestinal disease giardiasis, uses a large adhesive disc composed of microtubules to attach to the intestinal mucosa. During adhesion, the flagella of <em>G. lamblia<\/em> move in a manner that draws fluid out from under the disc, resulting in an area of lower pressure that facilitates adhesion to epithelial cells. <em>Giardia<\/em> does not invade the intestinal cells but rather causes inflammation (possibly through the release of cytopathic substances that cause damage to the cells) and shortens the intestinal villi, inhibiting absorption of nutrients.<\/p>\n<p>Some protozoans are capable of <strong>antigenic variation<\/strong>. The obligate intracellular pathogen <strong><em>Plasmodium falciparum<\/em><\/strong> (one of the causative agents of <strong>malaria<\/strong>) resides inside red blood cells, where it produces an adhesin membrane protein known as PfEMP1. This protein is expressed on the surface of the infected erythrocytes, causing blood cells to stick to each other and to the walls of blood vessels. This process impedes blood flow, sometimes leading to organ failure, anemia, jaundice (yellowing of skin and sclera of the eyes due to buildup of bilirubin from lysed red blood cells), and, subsequently, death. Although PfEMP1 can be recognized by the host\u2019s immune system, antigenic variations in the structure of the protein over time prevent it from being easily recognized and eliminated. This allows malaria to persist as a chronic infection in many individuals.<\/p>\n<p>The virulence factors of <strong><em>Trypanosoma brucei<\/em><\/strong>, the causative agent of <strong>African sleeping sickness<\/strong>, include the abilities to form <strong>capsules<\/strong> and undergo <strong>antigenic variation<\/strong>. <em>T. brucei<\/em> evades phagocytosis by producing a dense glycoprotein coat that resembles a bacterial capsule. Over time, host antibodies are produced that recognize this coat, but <em>T. brucei<\/em> is able to alter the structure of the glycoprotein to evade recognition.<\/p>\n<div class=\"textbox key-takeaways\">\n<h3>Think about It<\/h3>\n<ul>\n<li>Explain how antigenic variation by protozoan pathogens helps them survive in the host.<\/li>\n<\/ul>\n<\/div>\n<h2>Helminth Virulence<\/h2>\n<p>Helminths, or parasitic worms, are multicellular eukaryotic parasites that depend heavily on virulence factors that allow them to gain entry to host tissues. For example, the aquatic larval form of <strong><em>Schistosoma mansoni<\/em><\/strong>, which causes <strong>schistosomiasis<\/strong>, penetrates intact skin with the aid of proteases that degrade skin proteins, including elastin.<\/p>\n<p>To survive within the host long enough to perpetuate their often-complex life cycles, helminths need to evade the immune system. Some helminths are so large that the immune system is ineffective against them. Others, such as adult <strong>roundworms<\/strong> (which cause <strong>trichinosis<\/strong>, <strong>ascariasis<\/strong>, and other diseases), are protected by a tough outer cuticle.<\/p>\n<p>Over the course of their life cycles, the surface characteristics of the parasites vary, which may help prevent an effective immune response. Some helminths express polysaccharides called <strong>glycans<\/strong> on their external surface; because these glycans resemble molecules produced by host cells, the immune system fails to recognize and attack the helminth as a foreign body. This &#8220;<strong>glycan gimmickry<\/strong>,&#8221; as it has been called, serves as a protective cloak that allows the helminth to escape detection by the immune system.<a class=\"footnote\" title=\"I. van Die, R.D. Cummings. &quot;Glycan Gimmickry by Parasitic Helminths: A Strategy for Modulating the Host Immune Response?&quot; Glycobiology 20 no. 1 (2010):2\u201312.\" id=\"return-footnote-706-3\" href=\"#footnote-706-3\" aria-label=\"Footnote 3\"><sup class=\"footnote\">[3]<\/sup><\/a><\/p>\n<p>In addition to evading host defenses, helminths can actively suppress the immune system. <em>S. mansoni<\/em>, for example, degrades host antibodies with <strong>proteases<\/strong>. Helminths produce many other substances that suppress elements of both innate nonspecific and adaptive specific host defenses. They also release large amounts of material into the host that may locally overwhelm the immune system or cause it to respond inappropriately.<\/p>\n<div class=\"textbox key-takeaways\">\n<h3>Think about It<\/h3>\n<ul>\n<li>Describe how helminths avoid being destroyed by the host immune system.<\/li>\n<\/ul>\n<\/div>\n<div class=\"textbox key-takeaways\">\n<h3>Key Concepts and Summary<\/h3>\n<ul>\n<li>Fungal and parasitic pathogens use pathogenic mechanisms and virulence factors that are similar to those of bacterial pathogens<\/li>\n<li>Fungi initiate infections through the interaction of adhesins with receptors on host cells. Some fungi produce toxins and exoenzymes involved in disease production and capsules that provide protection of phagocytosis.<\/li>\n<li>Protozoa adhere to target cells through complex mechanisms and can cause cellular damage through release of cytopathic substances. Some protozoa avoid the immune system through antigenic variation and production of capsules.<\/li>\n<li>Helminthic worms are able to avoid the immune system by coating their exteriors with glycan molecules that make them look like host cells or by suppressing the immune system.<\/li>\n<\/ul>\n<\/div>\n<div class=\"textbox exercises\">\n<h3>Multiple Choice<\/h3>\n<p>Which of the following is a major virulence factor for the fungal pathogen <em>Cryptococcus?<\/em><\/p>\n<ol style=\"list-style-type: lower-alpha;\">\n<li>hemolysin<\/li>\n<li>capsule<\/li>\n<li>collagenase<\/li>\n<li>fimbriae<\/li>\n<\/ol>\n<div class=\"qa-wrapper\" style=\"display: block\"><span class=\"show-answer collapsed\" style=\"cursor: pointer\" data-target=\"q595019\">Show Answer<\/span><\/p>\n<div id=\"q595019\" class=\"hidden-answer\" style=\"display: none\">Answer b. Capsule is a major virulence factor for the fungal pathogen <em>Cryptococcus<\/em>.<\/div>\n<\/div>\n<p>Which of the following pathogens undergoes antigenic variation to avoid immune defenses?<\/p>\n<ol style=\"list-style-type: lower-alpha;\">\n<li><em data-effect=\"italics\">Candida<\/em><\/li>\n<li><em data-effect=\"italics\">Cryptococcus<\/em><\/li>\n<li><em data-effect=\"italics\">Plasmodium<\/em><\/li>\n<li><em data-effect=\"italics\">Giardia<\/em><\/li>\n<\/ol>\n<div class=\"qa-wrapper\" style=\"display: block\"><span class=\"show-answer collapsed\" style=\"cursor: pointer\" data-target=\"q842714\">Show Answer<\/span><\/p>\n<div id=\"q842714\" class=\"hidden-answer\" style=\"display: none\">Answer c.\u00a0<em>Plasmodium<\/em> undergoes antigenic variation to avoid immune defenses.<\/div>\n<\/div>\n<\/div>\n<div class=\"textbox exercises\">\n<h3>Fill in the Blank<\/h3>\n<p><em>Candida<\/em> can invade tissue by producing the exoenzymes __________ and __________.<\/p>\n<div class=\"qa-wrapper\" style=\"display: block\"><span class=\"show-answer collapsed\" style=\"cursor: pointer\" data-target=\"q626001\">Show Answer<\/span><\/p>\n<div id=\"q626001\" class=\"hidden-answer\" style=\"display: none\"><em>Candida<\/em> can invade tissue by producing the exoenzymes <strong>protease<\/strong> and <strong>phospholipase<\/strong>.<\/div>\n<\/div>\n<p>The larval form of <em>Schistosoma mansoni<\/em> uses a __________ to help it gain entry through intact skin.<\/p>\n<div class=\"qa-wrapper\" style=\"display: block\"><span class=\"show-answer collapsed\" style=\"cursor: pointer\" data-target=\"q503881\">Show Answer<\/span><\/p>\n<div id=\"q503881\" class=\"hidden-answer\" style=\"display: none\">The larval form of Schistosoma mansoni uses a <strong>protease<\/strong> to help it gain entry through intact skin.<\/div>\n<\/div>\n<\/div>\n<div class=\"textbox key-takeaways\">\n<h3>Think about It<\/h3>\n<ol>\n<li>Describe the virulence factors associated with the fungal pathogen <em>Aspergillus.<\/em><\/li>\n<li>Explain how helminths evade the immune system.<\/li>\n<\/ol>\n<\/div>\n\n\t\t\t <section class=\"citations-section\" role=\"contentinfo\">\n\t\t\t <h3>Candela Citations<\/h3>\n\t\t\t\t\t <div>\n\t\t\t\t\t\t <div id=\"citation-list-706\">\n\t\t\t\t\t\t\t <div class=\"licensing\"><div class=\"license-attribution-dropdown-subheading\">CC licensed content, Shared previously<\/div><ul class=\"citation-list\"><li>OpenStax Microbiology. <strong>Provided by<\/strong>: OpenStax CNX. <strong>Located at<\/strong>: <a target=\"_blank\" href=\"http:\/\/cnx.org\/contents\/e42bd376-624b-4c0f-972f-e0c57998e765@4.2\">http:\/\/cnx.org\/contents\/e42bd376-624b-4c0f-972f-e0c57998e765@4.2<\/a>. <strong>License<\/strong>: <em><a target=\"_blank\" rel=\"license\" href=\"https:\/\/creativecommons.org\/licenses\/by\/4.0\/\">CC BY: Attribution<\/a><\/em>. <strong>License Terms<\/strong>: Download for free at http:\/\/cnx.org\/contents\/e42bd376-624b-4c0f-972f-e0c57998e765@4.2<\/li><\/ul><\/div>\n\t\t\t\t\t\t <\/div>\n\t\t\t\t\t <\/div>\n\t\t\t <\/section><hr class=\"before-footnotes clear\" \/><div class=\"footnotes\"><ol><li id=\"footnote-706-1\">K. Fallon et al. \"Role of Aspartic Proteases in Disseminated <em>Candida albicans<\/em> Infection in Mice.\" <em>Infection and Immunity<\/em> 65 no. 2 (1997):551\u2013556. <a href=\"#return-footnote-706-1\" class=\"return-footnote\" aria-label=\"Return to footnote 1\">&crarr;<\/a><\/li><li id=\"footnote-706-2\">C.P. Wild et al. \"In-utero exposure to aflatoxin in west Africa.\" <em>Lancet<\/em> 337 no. 8757 (1991):1602. <a href=\"#return-footnote-706-2\" class=\"return-footnote\" aria-label=\"Return to footnote 2\">&crarr;<\/a><\/li><li id=\"footnote-706-3\">I. van Die, R.D. Cummings. \"Glycan Gimmickry by Parasitic Helminths: A Strategy for Modulating the Host Immune Response?\" <em>Glycobiology<\/em> 20 no. 1 (2010):2\u201312. <a href=\"#return-footnote-706-3\" class=\"return-footnote\" aria-label=\"Return to footnote 3\">&crarr;<\/a><\/li><\/ol><\/div>","protected":false},"author":17,"menu_order":5,"template":"","meta":{"_candela_citation":"[{\"type\":\"cc\",\"description\":\"OpenStax Microbiology\",\"author\":\"\",\"organization\":\"OpenStax CNX\",\"url\":\"http:\/\/cnx.org\/contents\/e42bd376-624b-4c0f-972f-e0c57998e765@4.2\",\"project\":\"\",\"license\":\"cc-by\",\"license_terms\":\"Download for free at http:\/\/cnx.org\/contents\/e42bd376-624b-4c0f-972f-e0c57998e765@4.2\"}]","CANDELA_OUTCOMES_GUID":"","pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":[],"pb_section_license":""},"chapter-type":[],"contributor":[],"license":[],"class_list":["post-706","chapter","type-chapter","status-publish","hentry"],"part":680,"_links":{"self":[{"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/pressbooks\/v2\/chapters\/706","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/wp\/v2\/users\/17"}],"version-history":[{"count":3,"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/pressbooks\/v2\/chapters\/706\/revisions"}],"predecessor-version":[{"id":1641,"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/pressbooks\/v2\/chapters\/706\/revisions\/1641"}],"part":[{"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/pressbooks\/v2\/parts\/680"}],"metadata":[{"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/pressbooks\/v2\/chapters\/706\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/wp\/v2\/media?parent=706"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/pressbooks\/v2\/chapter-type?post=706"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/wp\/v2\/contributor?post=706"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/courses.lumenlearning.com\/suny-mcc-microbiology\/wp-json\/wp\/v2\/license?post=706"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}