micro 13-16, & 22
List and explain Koch's postulates.
1. The same pathogen must be present in every case of the disease. 2. The pathogen must be isolated from the diseased host and grown in pure culture. 3. The pathogen from the pure culture must cause the disease when it is inoculated into a healthy, susceptible laboratory animal. 4. The pathogen must be isolated from the inoculated animal and must be shown to bethe original organism. EXCEPTIONS TO KOCH'S POSTULATES Many rickettsial and viral pathogens cannot be cultured on artificial media because they multiply only within cells. (i.e. The bacterium Treponema pallidum know to cause syphilis, or Mycobacterium leprae known to cause leprosy). In a number of situations, a human host exhibits certain signs and symtoms that are associated only with a certain pathogen and its disease. for example, the pathogens responsible for diphtheria and tatanus cause distinguishing signs and symptoms that only organisms that produce their respective diseases. But some infectious diseases are not as clear-cut and provide another exception to Koch's postulates. For example, nephritis (inflammation of the kidneys) can involve any of several different pathogens, all of which cause the same signs and symptoms. Thus, it is often difficult to know which particular microorganism is causing a disease. Other infectious diseases that sometimes have poorly defined etiologies are pneumonia, meningitis, and peritonitis (inflammation of the peritoneum, the membrane that lines the abdomen and covers the organs within them). Still another exception to Koch's postulates results because some pathogens can cause several disease conditions. Mycobacterium tuberculosis, for example, is implicated in diseases of the lungs, skin, bones, and internal organs. Streptococcus puogenes can cause sore throat, scarlet fever, skin infections (such as erysipelas), and osteomyelitis (inflammation of bone), among other diseases. When clinical signs and symptoms are used tofether with laboratory methods, these infections can usually be distinguished from infections of the same organs by other pathogens. KEY CONCEPTS *According to Koch's postulates, a specific infectious disease is caused by a specific microbe. *Koch's postulates help determine the etiology of disease, the first step in treatment and prevention. * Microbiologists uses these steps to identify causes of emerging diseases. 1. Microorganisms are isolated from a diseased or dead animal 2a. The microorganisms are grown in pure culture. 2b. The microorganisms are identified. 3. The microorganisms are injected into a healthy laboratory animal. 4. Disease is reproduced in a laboratory animal. 5a. The microorganisms are isolated from this animal and grown in pure culture. 5b. Microorganisms are identified.
Differentiate physical from chemical factors, and list examples of each.
453-455
Describe the role of normal microbiota in innate resistance.
455-456
Classify phagocytic cells, and describe the roles of granulocytes and monocytes.
460
Define and explain phagocyte and phagocytosis.
460
Explain the different stages of inflammation.
463
Describe the cause and effects of fever.
464-466
Describe two of the three pathways of activating complement and describe the 3 outcomes.
466-470
Compare and contrast the actions of -IFN and -IFN with -IFN.
471-473
Describe the role of transferrins and antimicrobial peptides in innate immunity.
473
*Review anatomy of CNS, PNS, meninges, BBB
616
Differentiate meningitis from encephalitis including diagnosis and treatment.
616-617
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Bacterial meningitis caused by H. influenzae
618
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Bacterial meningitis caused by N. meningitidis
618
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Bacterial meningitis caused by L. monocytogenes
619
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Bacterial meningitis caused by S. pneumoniae
619
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Tetanus
621
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Botulism
622-625
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Leprosy
625
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Rabies
628-630
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Arboviral encephalitis
630-632
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Cryptococcosis.
632
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of African trypanosomiasis
633
Discuss mode of transmission, etiology, disease symptoms, treatment, and preventive measures of Prion diseases
636
List the distinguishing characteristics of the two classes of parasitic helminths, and give an example of each.
A number of parasitic animals spend part or all of their lives in humans. Most of these animals belong to two phyla: Platyhelminthes (flatworms) and Nematoda (roundworms). These worms are commonly called helminths. Helminths are multicellular eukaryotic animals that generally possess digestive, circulatory, nervous, excretory, and reproductive systems. Parasitic helminths must be highly specialized to live inside their hosts. The following generalizations distinguish parasitic helminths from their free-living relatives: 1. They may lack a digestive system. They can absorb nutrients from the host's food, body fluids, and tissues. 2. Their nervous sustem is reduced. They do not need an extensive nervous system because they do not have to search for food or respond much to their environment. The environment within a host is fairly constant. 3. Their means of locomotion is occasionally reduced of completely lacking. Because they are transferred from host to host, they do not need to search actinely for a suitable habitat. 4. Their reproductive system is often complex. An individual produces large numbers of eggs, by which a suitable host is infected. Platyhelminths: The classes of parasitic flatworms include the trematodes and cestodes. Trematodes, or flukes, often have flat, leaf-shaped bodies with a ventral sucker and an oral sucker. The suckers hold the organism in place. Flukes obtain food by absorbing it through their nonliving outer covering, called the cuticle. Flukes are given common names according to the tissue of the definitive host in which the adults live (i.e. lung fluke, liver fluke, blood fluke). The Asian liver fluke Clonorhis is occasionally seen in immigrants in the US, but it cannot be transmitted because its intermediate hosts are not in the US. Cestodes, or tapeworms, are intestinal parasites. The head, or scolex (plural: scoleces), has suckers for attaching to the intestinal mucosa of the definitive host; sone species also have small hooks for attachment. Tapeworms do not ingest the tissues of their hosts; in fact, they completely lack a digestive system. To obtain nutrients from the small intestine, they absorb food through their cuticle. The body consists of segments called proglottids. Proglottids are continually produced by the ceck region of the scolex, as long as the scoles is attached and alive. Each mature proglottid contains both male and female reproductive organs. The proglottids farthest away from the scolex are the mature ones containing eggs. Mature proglottids are essentially bags of eggs, each of which is infective to the proper intermediate host. Nematodes: Members of the Phylum Nematoda, the roundworms, are cylindrical and tapered at each end. Toucdworms have a complete difestive system, consisting of a mouth, an intestine, and an anus. Most species are dioecios. Males are smaller than females and have one or two hardened spicules on their posterior ends. Spicules are used to guid sperm to the female's genital pore.Some species of nematodes are free-living in soil and water, and others are parasites on plants and animals. Intestinal round worms are the most common causes of chronic infectious diseases. The most common are Ascaris, hookworms, and whipworms. Nematode infeions of humans can be divded into two categories: those in which the egg is infective, and those in which the larva is infective. Trichinellosis is caused by a nematode that the host acquires by eating existed larvae in undercooked meat of infected animals. The nematode, Dirofilaria initial, is spread from host to host through the bites of Aedes mosquitoes. It primarily affects dogs and cats, but it can infest human skin, conjunctiva or lungs. Larvae injected by the mosquito migrate to various organs, where they might mature into adults. The parasitic worm is called a heartworm because the adult stage is often in the animals hosts heart, where he can kill its host through congestive heart failure .
Define viral species.
A viral species is a group of viruses sharing the same genetic information and ecological niche (host range). Specific epithets for viruses are not used. Thus, viral species are designated by descriptive common names, such as human immunodeficiency virus (HIV), with subspecies (if any) designated by a number (HIV-1).
Outline the mechanisms of action of A-B toxins, membrane-disrupting toxins, and superantigens
A-B toxins were the first toxins to be studied in intensively and are so named because they consist of two parts designated A and B, both of which are polypeptides. Most exotoxins are A-B toxins. The A part is the active enzyme component, and the B part is the binding component. 1. In the first step, the A-B toxin is released from the bacterium. 2. The B component attaches to a host cell receptor. 3. The plasma membrane of the host cell invaginate's ( folds inward) at the point where that A-B exotoxin and plasma receptor make contact, and the exotoxin enters the cell by receptor - mediated endocytosis 4. The A-B exotoxin and receptor are enclosed by a pinched-off portion of the membrane. 5. The A-B components of the exotoxin separate. The A component alters the function of the host cell, often by inhibiting protein synthesis. The B component is released from the host cell, and the receptor is inserted into the plasma membrane for reuse. Membrane disrupting toxins cause lysis of host cells by disrupting their plasma membranes. Some do this by forming protein channels in the plasma membrane; others disrupt the phospholipid portion of the membrane. The cell losing exotoxin of Staphylococcus aureus is an example of an exotoxin that forms protein channels, whereas that of the clostridium perfringens is an example of an exotoxin that disrupts the phospholipid. Membrane disrupting toxins contribute to virulence by killing hosts cells, especially phagocytes, and by aiding the escape of bacteria from sacs within the phagocytes into the host cells cytoplasm. Leukocidins- substances produced by some bacteria that can destroy neutrophils and macrophages. Hemolysin- an enzyme that lyses red blood cells Streptolysin- a hemolytic enzyme-produced by streptococci Superantigens are antigens that provoke a very intense immune response. They are bacterial proteins. Through a series of interactions with various cells of the immune system superantigens non-specifically stimulate the proliferation of immune cells called T cells. These cells are types of white blood cells (lymphocytes) that act against foreign organisms and tissues and regulate the activation and proliferation of other cells of the new system. In response to superantigens, T cells are stimulated to release enormous amounts of chemical called cytokines. Cytokines are small protein molecules produced by various body cells, especially T cells, that regulate immune response and mediate cell to cell communication. Excessively high levels of cytokines release by T cells into the bloodstream and give rise to a number of symptoms including fever, nausea, vomiting, diarrhea, and sometimes shock and even death bacterial super antigens include the staphylococcal toxins that cause food poisoning and toxic shock syndrome.
Define herd immunity.Z
Acute disease- a disease in which symptoms develope rapidly but last for only a short time. (influenza) Chronic disease- an illness that develops slowly and is likely to continue or recur for long periods. ( Infectious momonucleosis, tuberculosis, and hepatitis B) subacute disease- a disease with symptoms that are intermediate between acute and chronic. (sclerosing panencehalitis, a rare brain disease characterized by diminished intellectual function and loss of nervous function). Latent disease- a disease characterized by a period of no symptoms when the pathogen is inactive. (shingles). Herd immunity- the presence of immunity in most of a population. Vaccination can provide). Local infection- an infection in which pathogens are limited to a small area of the body. ( boils and abcesses). Systemic (generalized) infection- microorganisms or their products are spread throughout the body by the blood or lymph. (measles) Focal infections- a systemic infections in one place. (teeth, tonsils, or sinuses). Sepsis- The presence of a toxin or pathogenic organism in blood and tissue. (sepsis is a toxic inflammatory condition arising from the spread of microbes, especially bacteria or their toxins, from a focus of infection). Septicemia- The proliferation of pathogens in the blood, accompanied by fever, sometimes causes organ damage. (also called blood poisoning, is a systemic infection arising from the multiplication of pathogens in the blood. Bacteremia- a condition in which there are bacteria in the blood. Toxemia- the presence of toxins in the blood. Viremia- the presence of viruses in the blood. Primary infection- an acute infection that causes the initial illness. Secondary infection- an infection caused by an opportunistic microbe after a primary infection has weakened the host's defenses. (sometimes more dangerous then the primary infection). Subclinical (inapparent) infection- an infection that does not cause a noticeable illness; also called inapparent infection. (Poliovirus and hepititis A virus, for example, can be carried by people who never develop the illness).
Using examples, explain how microbes adhere to host cells.
Adherence (adhesion)- attachment of a microbe or phagocyte to anothers plasma membrane or other surface. its a necessary step in pathogenicity. Adhesins- a carbohydrate-specific binding protein that projects from prokaryotic cells; used for adherence, also called an ligand. ( the attachment between pathogen and host is accomplished by means of surface molecules on the pathogen called adhesins or ligands that bind specifically to complementary surface receptors on the cells of certain host tissues. Adhesins may be located on a microbe's gylcocaly or on other microbial surface structures, such as pili, fimbriae, and flagella. The majority of adhesins on the microorganisms studied so far are glycoproteins or lipoproteins. The receptors on host cells are typically sugars, such as mannose. Adhesins on different strains of the same species of pathogen can vary in structure. Different cells of the same host can also have different receptors that vary in structure. If adhesins, receptors, or bothe can be altered to interface with adherence, infection can often be prevented ( or at least controlled). Streptococcus mutans, a bacterium that plays a key role in tooth decay, attaches to the surface of teerh by its glycocalyx. An enzyme produced by S. mutans, called glucosyltransferase, converts glucose (derived from sucrose or table sugar) into a sticky polysaccharide called dextran, which forms the glycocalyx. Actinomyces bacterial cells have fimbraie that adhere to the glycocalyx of S. mutans. The combination of S. mutans, Actinomyces, and dextran make up dental plaque and contribute to dental caries (tooth decay). Microbes have the ability to come together in masses, cling to surfaces, and take in and share available nutrients. These communities, which constitute masses of microbes and their extracellular products that can attach to living and nonliving surfaces, are called biofilms. Examples of biofilms include the dental plaque on teeth, the algae on the walls of swimming pools, and the scum that accumulates on shower doors. A biofilm forms when microbes adhere to a particular surface that is typicallu moist and contains organic matter. The first microbes to attach are usually bacteria. Once they adhere to the surface, they multiply and secrete a glycocalyx that further attaches the bacteria to each other and to the surface. they can be several layers thick, and they are resistant to disinfectants and antibiotics.
Define oncogene and transformed cell.
Almost anything that can alter the genetic material of a eukaryotic cell that has potential to make a normal cell cancerous. These canser-causing alteration to cellular DNA affect parts of the genome called oncogenes. Oncongenes were first identified in cancer-causing viruses and were thought to be part of the normal viral genome. However, American microbioligist J. Michael Bishop and Harold E. Varmus recived the 1989 Nobel prize in Medicine for providing that the cancer-including genes carried by viruses is derived from animal cells. Bishop and Varmus showed that the cancer-causing src gene is avian sarcoma viruses is derived from a normal part of chicken genes. Oncogenes can be activated to abnormal funtioning by a variety of agents, including mutagenic chemicals, high-energy radiation, and viruses. Viruses capable of including tumors in animals are called oncogenic viruses, or oncoviruses. Approximatley 10% of cancers are known to be virus-induced. An outstanding feature of all oncogenic viruses is that their genetic material intefrates into the host cell's DNA and replicates along with the host cell's chromosome. This mechanism is similar to the phenonenon of lysogeny in bacteria, and it can alter the host cell's characteristics in the same way. Tumor cells undergo transformation; that is, they acquire properties that are distinct from the properties of uninfected cells or from infected cells that do not form tumors. After veing transformed by biruses, many tumor cells contain a virusspecific antigen on their cell surface, called tumor-specific transplantation antigen (TSTA), or an antigen in their nucleus, called the T antigen. Transformed cells tend to be less round than normal cells. and they tend to exhibit certain chromosomal abnormalities, such as unusual numbers of chromosomes and fragmented chromosomes.
Define arthropod vector.
Anthropods are animal's characterized by segmented bodies, hard external skeletons, and jointed legs. With nearly one million species, this is the largest phylum in the animal kingdom. Although arthropods are not microbes themselves, we will briefly describe them here because a few suck the blood of humans and other animals and can transmit microbial diseases while doing so. Arthropods that carry pathogenic microorganisms are called vectors. Scabies and pediculosis are diseases that are caused by arthropods. Representative classes of arthropods include the following: * Arachnida (eight legs): spiders, mites, ticks * Crustacea (four antennae): crabs, crayfish * Insecta (six legs): bees, flies, lice
Describe how bacteriophages and animal viruses are cultured.
Bacteriophages can be grown either in suspensions of bateria in liquid media or in bacterial cultures on solid media. The use of solid media makes possible the plaque method for detecting and counting viruses. A sample of bacteriophage is mixed with host bacteria and melted agar. The agar containing the bacteriophages and host bacteria is then poured into a Petri plate containing a hardened layer of agar growth medium. The virus-bacteria mixture solidifies into a thin top layer that contains a layer of bacteria approximately one cell thick. Each virus infects a bacterium, multiplies, and releases several hundred new viruses. These newly produced viruses infect other bacteria in the immediate vicinity, and more new viruses are produced. Following several viral multiplication cycles, all the bacteria in the area surrounding the original virus are destroyed. This Produces a number of clearings, or plaques, visible against a lawn of bacterial growth on the surface of the agar. While the plaques from, uninfected bacteria elsewhere in the Petri plate multiply rapidly and produce a turbid background. In the laboratory, three methods are commonly used for culturing animal viruses. These methods involve using living animals, embryonated eggs, or cell cultures. 1. In living animals : Some animal viruses can be cultured only in living animals, such as mice, rabbits, and guinea pigs. Most experiiments to study the immune system's response to viral infections must also be performed in birally infected libe animals. Animal inoculation may be used as a diagnostic procedure for idetifying and isolating a virus from a clinical specimen. After the animal is inoculated with the specimen, the animal is observed for signs of disease or is killed so that infected tissues can be examined for the virus. Some human viruses cannot be grown in animals or can be grown bur do not cause disease. The lack of natural animal models for AIDS has slowed our understanding of its disease process and prbented experimentation with drugs that inhibit growth of the birus in vivo. In Embryonated Eggs: If the virus will grow in an embyonated egg, this can be a fairly convenient and inexpensive form of host for many animal viruses. A hole is drilled in the shell of the embryonated egg, and a viral suspension or suspected virus containing tissue is injected into the fluid of the egg. There are several membranes in an egg, and the virus is injected near the one most appropriate for its growth. Viral growth is signaled by the death of an embryo, by embryo cell damage, or by the formation of typical pocks or lesions on the egg membranes. This method was once the most widely used method of viral isolation and growth, and it is still used to grow viruses for some vaccines. For this reason, you may be asked if you are allergic to eggs before receiving a vaccination, because egg proteins may be present in the viral vaccine preparations. In Cell Cultures: cell cultures have replaced embryonated eggs as the preferred type of growth medium for many viruses. Cell cultures consist of cells grown in culture media in the laboratory. Because these cultures are generally rather homogeneous collections of cells and can be propagated and handled much like bacterial cultures, they are more convenient to work with then whole animals or embryonated eggs. Cell culture lines are started by treating a slice of animal tissue with enzymes that separate the individual cells. The cells are suspended in a solution that provides the osmotic pressure, nutrients, and growth factors needed for the cells to grow. Normal cells tend to adhere to the glass or plastic container and reproduce to form a monolayer. Viruses infecting much such a monolayer sometimes cause the cells of the monolayer to deteriorate as they multiply. The cell deterioration, called cytopathic effect (CPE). CPE can be detected and counted in much the same way as plaques caused by bacterial phages on a lawn of bacteria and repeat produced as PFU/ml. Primary cell lines, derived from tissue slices, tend to die out after only a few generations. Certain cell lines, called diploid cell lines, developed from human embryos can be maintained for about 100 generations and are widely used for culturing viruses that require a human host. Cell lines developed from embryonic human cells are used to coach her rabies virus for a rabies vaccine called human diploid culture vaccine. When viruses are routinely grown in a laboratory, continuous cell lines are used. These are transformed cancerous cells that can be maintained through an indefinite number of generations, and they are sometimes called immortal cell lines. One of these, the HeLa cell line, was isolated from the cancer of a woman (Henrietta Lacks) Who died in 1951.
Compare and contrast the lytic and lysogenic cycles of bacteriophages.
Bacteriophages can multiply by two alternative mechanisms: lytic cycle and the lysogenic cycle. Then lytic cycle ends with the lysis and death of the host cell, where is the host cell remains alive in the lysogenic cycle. The Lytic Cycle (T-even bacteriophages): The virions of T-even bacteriophages are large, complex, and nonenveloped, with a characteristic head-and-tail structure. The lenhth of DNA contained in these cacteriophages is only about 6% of that contained in E. coli, yet the phage has enough DNA for over 100 genes. the multiplication cycle of these phages, like that of all viruses, occurs in five distint stages: attachment, penetration, biosynthesis, maturation, and release. 1. Attachment: After a chance collision between phage particles and bacteria, attachment, or adsorption, occur. 2. Penetration: After attachment, the T-even bacteriophage injects irs DNA (nucleic acid) into the bacterium. to do this, the Bacteriophage's tail releases an enzyme, phage lysozyme, which breaks down a portion of the bacterial cell wall. 3. Biosynthesis: Once the bacteriophage DNA has reached the cytoplasm of the host cell. the biosynthesis of viral nucleic acid and protein occurs. Host protein sunthesis is stopped by virusinduced degradation of the host DNA, viral proteins that interfere with the transcription, or the repression of translation. 4. Maturation: Inthe next sequence of events, maturation occurs. In this process, bacteriophage DNA and capsids are assembled into complete virions. the viral components essentially assemble into a viral particle spontaneously, eliminatinf the need for many nonstructural fenes and fene products. 5. Release: The final stage of viral multiplication is the release of virions from the host cell. The term lysis isgenerally used for this stage in the multiplication of T-even phages because in this case, the plasma membrane actually breaks open (lyses). Lysozyme, which is encoded by a phage gene, is synthesized within the cell. This enzyme causes the bacterial cell wall to break sown, and the newly produced bacteriophages are released frome the hostcell. Bacteriophage Lambda: The Lysogenic Cycle Incontrast to T-even bacteriophages, som viruses do not cause lysis and death of the host cell when they multiply. These lysogenic phages (also called temperate phages) may indeed proceed through a lytic cycle, but they are also capable of incorporating their DNA into the host cell's DNA to begin a lysogenic cycle. In lysogeny, the phage remains latent (inactive). The participating bacterial host cells are known as lysogenic cells. We will use the bacteriophage lambda, a well-studied lysogenic phage, as an example of the lysogenic cycle. 1. Upon penetration into an E. coli cell, 2. the originally linear phage DNA forms a circle. 3A. This circle can multiply and be transcribed, 4A. leading to the production of new phage and to cell lysis ( the lytic cycle). 3B. Alternatively, the circle can recombine with and become part of the circular bacterial DNA ( the lysogenic cycle). The inserteed phage DNA is now called a prophage. Most of the prophage fenes are repressd by two repressor proteins that are the products of phage genes that would otherwise direct the synthesis and release of new virions are turned off, in much the same way that the fenes of the E. coli lac operon are turned off by the lac repressor. every time the host cell's machinery replicates the bacterial chromosome, 4B. it also replicates the prophage DNA. The prophage remains latent within the progeny cells. 5. However, a rare spontaneous event, or the action of UV light or certain chemicals, can lead to the excision (popping-out) of the phage DNA, and to initiotion of the lytic cycle. There are three important results of lysogeny. First, the lysogenic cells are immune to reinfection by the same phage. (however the host cell is not immuyne to infection by other phage types.) The second result of lysogeny is phage conversion: that is, the host cell may exhibit new properties. For example, the bacterium Corynebacterium diphteriae, which causes diphtheria, is a pthogen whose disease-producing properties are related to the synthesis of a toxin. The organism can produce toxin only when it carries a lysogenic phage, because the prophage carries the gene coding for the toxin, As another example, only streptococi carrying a lysogenic phage are capable of causing toxic shock syndrome. The toxin produced by Clostridium botulinum, whish causes botulism , is encoded by a prophage fene, as is the Shiga toxin produced by pathogenic strains of E. coli. The third result of lysogeny is that it makes specialized transduction possible. Bacterial genes can be picked up in a phage coat and transferred to another bacterium in a process called generalized transduction. Any bacterial genes can be transferred by generlized transduction because the host chromosome is broken down into fragments, any of which can be packaged into a phage coat. In specialized transduction , however, only certain bacterial genes can be trans ferred. Specialized transduction is mediated by a lysogenic phage, which packages bacterial DNA along with its own DNA in the same capsid. When a prophage is excised from the host chromosome, adhacent genes from either side may remain attached to the phage DNA. Certain animal viruses that can remain latent in cells for long periods withour multiplying or causing disease may become inserted into a host chromosome or remain seperate from host DNA in a repressed state (as some lysogenic phages). Cancercausing viruses may also be latent.
fungal reprodution types
Budding yeast: following mitosis, a yeast cell that divides unevenly to produce a small cell from the parent cell. Budding yeast, such as Saccharomyces, divide unevenly. In budding, the parent cell forms a protuberance (bud) on its outer surface. As the bud elongates, the parent cell's nucleus divides, and one nucleus migrates into the bud. Cell wall material is then laid down between the bud and parent cell, and the bud eventually breaks away. Pseudohypha: a short chain of fungal cells that results from the lack of separation of daughter cells or budding. One yeast cell can in time produce up to 24 daughter cells by budding. Some yeasts produce buds that fail to detach themselves; these buds form a short chain of cells called a pseudohypha. Candida albicans attaches to human epithelial cells as a yeast but usually requires pseudohypae to invade deeper tissues. Fission yeasts: following mitosis, a yeast cell that divides evenly to produce two new cells. Fission yeasts, such as Schizosaccharomyces, divide evenly to produce two new cells. During fission, the parent cell elongates, its nucleus divides, and two offspring's cells are produced. Increases in the number of yeast cells on a solid medium produce a colony similar to a bacterial colony. Dimorphism: The property of having two forms of growth. Some fungi, most notably the pathogenic species, exhibit dimorphism- two forms of growth. Such fungi can grow either as a mold or as a yeast. The mold like forms produce by budding. Dimorphism in pathogenic fungi is temperature-dependent: at 37 Celsius, the fungus is yeast like, and at 25 Celsius, it is mold like. Spores: A reproductive structure formed by fungi and actinomycetes. Filamentous fungi can reproduce asexually by fragmentation of their hyphae. In addition, both sexual and asexual reproduction in fungi occurs by the formation of spores. In fact, fungi are usually identified by spore type. Asexual spore: A reproductive cell produced by mitosis and cell division (eukaryotes) or binary fission (actinomycetes). Asexual spores are formed by the hyphae of one organism. When these spores germinate, they become organisms that are genetically identical to the parent. Sexual spores: A spore formed by sexual reproduction. Two types of asexual spores are produced by fungi. One type is a conidiophore, or conidium, a unicellular or multicellular spore that is not enclosed in a sac. Conidia are produced in a chain at the end of a conidiophore. Such spores are produced by Aspergillus. Conidia formed by the fragmentation of a separate hypha into single, slightly thickened cells are called arthroconidia. One species that produces such spores is Coccidioides immitis. Another type of conidium, blastoconidia, consists of buds coming off the parent cell. Such spores are found in some yeasts, such as Candida albicans and Cryptococcus. A chlamydoconidium is a thick-walled spore formed by rounding and enlargement within a hyphal segment. A fungus that produces chlamydoconidia is the yeast C. albicans. The other type of asexual spore is a sporangiospore, formed within a sporangium, or sac, at the end of an aerial hypha called sporangiospore. The sporangium can contain hundreds of sporangiospores. Such spores are produced by Rhzopus. Sexual spores result from the fusion of nuclei from two opposite mating strains of the same species of fungus. Fungi produce sexual spores will have species of fungus. A fungal sexual spore results from sexual reproduction, which consists of three phases: 1. Plasmogamy. A haploid nucleus of a donor cell (+) penetrates the cytoplasm of a recipient cell (-). 2. Karyogamy. The (+) and (-) nuclei fuse to form a diploid zygote nucleus. 3. Meiosos. The diploid nucleus gives rise to haploid nuclei, some of which may be genetic recombinants. The sexual spores produced by fungi characterize the phyla. In laboratory settings, most fungi exhibit only asexual spores.
Explain how capsules and cell wall components contribute to pathogenicity.
Capsules: Some bacteria make glycocalyx material that forms capsules around their cell walls; this property increases the virulence of the species. The capsule resests the host's defenses by impairing phagocytosis, the process by which certain cells of the body engulf and destroy microbes. The chemical nature of the capsule appears to prevent the phagocytic cell from adhering to the bacterium. However, the human body can produce antibodies against the capsule. and when these antibodies are present on the capsule surface, the encapsulated bacteria are easily destroyed by phagocytosis. Cell Walls: The cell walls of certain bacteria contain chemical substances that contribute to virulence. For example, Streptococcus pyogenes produces a heat-resistant and acid-resistant protein called M protein. This protein is found on both the cell surface and fimbriae. The M Protein mediates attachment of the bacterium to epithelial cells of the host and helps the bacterium resist phagocytosis by white blood cells. The protein thereby increases the biru.ence of the microorganism. Immunity to S, Pyogenes depends on the body's production of an antibody specific to M protein. Neisseria gonorrhoeae grows inside human epithlial cells and leukocytes. these bacteria use fimbriae and an outer membrane protein called Opa to attach to host cells. Following attachment by both Opa and fimbriae, the host cellstakein the bacteria. (bacteria that produce Opa form opaqye colonies on culture media.) The waxy lipid (mycolic acid) that makes up the cell wall of Mycobacterium tuberculosis also increases virulence by resisting digestion by phagocytes, and can even multiply inside phagocytes.
Explain the function of the CDC.
Centers for Disease Control and Prevention (CDC), a branch of the U.S. Public Health Service located in Atlanta, Georgia, is a central source of epidemiological information in the United States. The CDC issues a publication called the Morbidity and Mortality Weekly Report. The MMWR, as it is called, is read by micrbiologists, physicians, and other hospital and public health professionals.
Explain three methods of disease transmission.
Contact transmission- is the spread of an agent of disease by direct contact, indirect contact, or droplet transmission. Direct contact transmission- a method of spreading infection from onehost to another through some kind of close association between the host. ( also known as person-to-person transmission, is the direct transmission of an agent by physical contact between its source and a susceptible host; no intermediate object is involved. (ie touching, kissing, and sexual intercourse). diseases that can be transmitted via direct contact; viral respritory tract diseases ( the common cold and influenza), staphylococcal infections, hepatitis A, measles, scarlet fever, and sexually transmitted infections (syphilis, gonorrhea, and genital herpes), AIDS and infectious mononuleosis, and also pathogens can be transmitted by directed contact from animals, like rabies and anthrax. Indirect contact transmission The spread of pathogens by formites (nonliving objects). occurs when the agent of disease is transmitted from its resermoir to a susceptible host by means of a nonliving object. the general term for any nonliving object involved in the spread of an infection is a formite. Examples of fomites are tissues, handkerchiefs, towels, bedding, diapers, drinkinf cups, eating utensils, toys, money, and thermometers. Contaminated syringes serve as fomites in transmitting AIDS and hepatitis B. Other formites may transmit diseases such as tetanus. Droplet transmission: the transmission of infectionby small liquid droplets carrying microorganisms. Droplet transmission is a third type of contact transmission in which microbes are spread in droplet nuclei (mucus droplets) that travel only short distances. These droplets are discharged into the air by coughing, sneezing, laughing, or talkinf and travel less than 1 meter from the reservoir to the host. One sneeze may produce 20,000 droplets. diseases that can be spread by droplet transmission are influenza, pneumonia, and pertussis (whooping cough). Vehicle Transmission: the transmission of a pathogen by an inanimate reservoir. Vehicle Transmission is the transmission of disease agents by a medium, such as water, food, or air. Other media include blood and other body fluids, drugs, and intravenous fluids. An outbreak of Salmonella infections caused by vehicle transmission. In waterborne transmission, pathogens are usually spread by water contaminatedwith untreated or poorly treated sewage. Diseases transmitted via this route include cholera, waterborne shigellosis, and leptospirsis. In foodborne transmission, pathogens are generally transmitted in foods that are incompletely cooked, poorly refrigerated, or prepared under unsanitary conditions. Foodborne pathogens cause diseases such as food poisoning and tapeworm infestation. Airborne transmission refers to the spread of agents of infection by droplet nuclei in dust that travel more that 1 meter from the reservoir to the host. These droplets are small enough to remain airborne for prolonged periods. The virus that causes measles and the bacterium that causes tuberculosis can be transmitted via airborne droplets. Dust particles can harbor various pathogens. Staphylococci and streptococci can survive on dust and be transmitted by the airborne route. Spored produced by certain fungi are also transmitted by the airborne route. Spores produced by certain fungi are also transmitted by the airborne route and can cause such diseases as histoplasmosis, coccidioidomycosis, and blastomycosis. Vectors: Arthropods are the most important group of disease vectors- animals that carry pathogens from one host to another. Arthropod vectors transmit disease by two general methods. Mechanical Transmission- is the passive transport of the pathogens on the insect's feet or other body parts. If the insect makes contact with a host's food, pathogens can be transferred to the food and later swallowed by the host. Houseflies, can transfer the pathogens of typhoid fever and bacillary dysentery (shigellosis) from the feces of infected people to food. Biological transmission is an active process and is more complex. The arthropod bites an infected person or animal and ingest some of the infected blood. The pathogens then reproduce in the vector, and the increase in the number of pathogens increases the possibilty that they will be transmitted to another host. Some parasites reproduce in the gut of the arthropod; these can be passed with feces. If the arthropod defecates or vomits while biting a potential host, the parasite can enter the wound. Other parasites reproduce in the vector's gut and migrate to the salivary gland; these are directly injected into a bite. Some protozoan and helminthic parasites use the vector as a host for a developmental stage in their life cycle.
Discuss the relationship between viruses and cancer.
DNA oncogenic viruses Oncogenic viruses are found within several familis of DNA containing viruses. These groups include the Adenoviridae, Herpesviridae, Poxviridae, Papovaviridae, and Hepadnaviridae. Among the papovaviruses, papillomaviruses cause uterine (cervical) cancer. Virtually all cervical and anal cancers are caused by human papillomavirus (HPV). A vaccine against four HPVs, including HPV-16, is recommended for 11-12 year old girls and boy. Epstein-Barr (EB) virus was isolated from Burkitt's lymphoma cells in 1964 by Michael Epstein and Yvonne Barr. The proof that EB virus can cause cancer was accidentally demonstrated in 1985 when a 12-year-old boy known only as David received a bone marrow transplant. Several months after the transplant, he died of cancer. An autopsy revealed that the virus had been unwittingly introduced into the boy with the bone marrow transplant. Another DNA virus that causes cancer is hepatitis B birus (HBV). Many animal studies have been performed that have clearly indicated the causal role of HBV in liver cancer. In one human study, virtually all people with liver cancer had previous HBV infections. RNA Oncogenic Viruses Among the RNA viruses, only the oncoviruses in the family Retroviridae cause cancer. The human T-cell leukemia viruses (HTLV-1 and HTLV-2) are retroviruses that cause adult T-cell leukemia and lymphoma in humans. (T cells are a type of white blood cell involved in the immune response.) Sarcoma viruses of cats, chickens, and rodents, and the mammary tumor viruses of mice, are also retroviruses. Another retrovirus, feline leukemia virus (FeLV), causes leukemia in cats and is transmissible among cats. There is a test to detect the virus in cat serum. The ability of retroviruses to induce tumors is related to their production of a reverse trascriptase by the mechanism described earlier. The provirus, which is the double-stranded DNA molecule synthesized from the viral RNA, becomes intergrated into the host cell's DNA; new genetic material is thereby intoduced into the host's genome, and this is the key reason retroviruses can contribute to cancer. Some retroviruses contain oncogenes; others contain promoters that turn on oncogenes or other cance-causing factors.
Classify diphtheria toxin, erythrogenic toxin, botulinum toxin, tetanus toxin, Vibrio enterotoxin, and staphylococcal enterotoxin
Diphtheria toxin- Corynebacterium diphtheriae produces the diphtheria toxin only when it is infected by a lysogenic phage carrying the tox gene. This cytotoxin inhibits protein synthesis ineukaryotic cells. A-B toxin Erythrogenic toxins- Streptococcus pyogenes has the genetic material to synthesize three types of cytotoxins, designated A, B, and C. These erythrogenic toxins are superantigens that damage the plasma membranes of blood capillaries under the skin and produce a red skin rash. ( scarlet fever) Botulinum Toxin is produced by Clotridium botulinum. Although toxin production is associated with the germination of endospores and the growth of vegetative cells, little of the toxin appears in the medium untilit is released by lysis late in growth. Botulinum toxin is an A-B neurotoxin: it acts at the neuromuscular junction and prevents the transmission of impulses from the nerve cell to the muscle. (Flaccid Paralysis) Tetnus toxin- Clostridium tetani produces tetanus neurotoxin, also known as tetanospsmin. This A-B toxin reaches the central nervous system and bids to nerve cells that control the contraction of various skeletal muscles. These nerve cells normally send inhibiting impulses that prevent random contractions and terminate completed contractions. (spasmodic contractions) Vibrio enterotoxin Vibrio cholerae produces an A-B enterotoxin called cholera toxin. Subunit B binds to epitherlial cells, and subunit A causes cells to secrete large amounts of fluids and electrolytes (ions). Normal muscular contractions are disturbed, leading to severe diarrhea that may be accompanied by vomiting. Staphylococcal enterotoxin Staphylococcus aureus produces a superantigen that affects the intestines inthe same way as v ibrio enterotoxin. A strain of S. aureus also produces a superantigen that results in the symptoms associated with toxic shock syndrome.
Provide an example of direct damage, and compare this to toxin production.
Direct damage once pathogens attach to host cells, they can cause direct damage as the patogens use the host cell for nutrients and produce waste products. As pathogens metabolize and multiply in in cells, the cells usually rupture. Many biruses and some intracellular bacteria and protozoa that grow in host cells are released when the host cell ruptures, Following their release, pathogens that rupture cellscan spread to other tissues in even greater numbers. Some bacteria, Such an E. coli, Shigella, Salmonella, and Neisseria gonorrhoeae, can induce host epithelial cells to engulf them by a process that resembles phagocytosis process, enabling them to enter other host cells. Some bacteria can also penetrate host cells by excreting enzymes and by their own motility; such penetration can itself damage the host cell. Most damage by bacteria, however, is done by toxins.
Identify two beneficial and two harmful effects of fungi.
Economic Effects of Fungi The good: Saccharomyces cerevisiae: Bread, wine, HBV vaccine Trichoderma: Cellulase for clear fruit juice Taxomyces: Taxol Entomophaga: Biocontrol Paecilomyces: Kills termites The bad: Mold spoilage Fungal Diseases - Mycoses Systemic mycosis: infection deep within body, affects many tissues and organs. Histoplasmosis and coccidiomycosis. Subcutaneous mycosis: Saprophytic fungi, e.g.: Sporotrichosis. Cutaneous mycosis = Dermatomycosis: affects keratin-containing tissues (hair, nails, skin). Superficial mycosis: localized on hair shafts and superficial skin cells. Opportunistic mycoses: caused by normal microbiota or fungi that are not usually pathogenic (E.g.: Candidiasis, Pneumocystis pneumonia, et.al.) usually systemic. ********************** The Zygomycota, or conjugation fungi, are saprophytic molds that have coenocytic hyphae. An example is Rhizopus stolonifer, the common black bread mold. The asexual spores of Rhizopus are sporangiospores. The dark sporangiospores inside the spoangium give Rhizopus its descriptive common name. When the sporangium breaks open, the sporangiospores are dispersed. The sexual spores are zygospores. A zygospore is a large spore enclosed in a thick wall. This type of spore results from the fusion of the nuclei of two cells that are morphologically similar to each other. Microsporidia are unusual eukaryotes because they lack mitochondria. Microspoidia do not have microtubules, and they are oligate intracellular parasites. Microsporidia have been reported since 1984 to be the cause of a number of human diseases, including chronic diarrhea and keratoconjunctivitis, most notably in AIDS patients. The Ascomycota, or sac fungi, include molds with septate hyphae and some yeasts. Their asexual spores are usually conidida produced in long chains from the conidiophore. The term Conidia means dust, and these spores freely detach from the chain at the slightest disturbance and float in the air like dust. An ascospore results from the fusion of the nuclei of two cells that can be either morphologically similar of dissimilar. These spores are produced in a saclike structure called an ascus. the members of this phylum are called sac fungi because of the ascus. The Basidiomycota, or club fugi, also possess septate hyphae. This phylum includes fungi that produce mushrooms. Basidiospores are formed externally on a base pedestal called a basidium. There are usually four basidiospores per basidium. Some of the basidiomycota produce asexual conidiospores. The fungi we have looked at thus far are teleomorphs; that is, they produce both sexual and asexual spores. Some ascomycetes have lost the avility to reproduce sexually. These asexual fungi are called anamorphs. Penicillium is an example of an anamorph that arose from a mutation in a teleomorph. ********************** Any fungal infection is called a mycosis. Mycoses are generally chronic (long-lasting) ingections because fungi grow slowly. Mycoses are classified into five groups according to the degree of tissue involment and mode of entry into the host: systemic, subcutaneous, cutaneous, superficial, or opportunistic. Systemic mycoses are fungal ingections deep within the body. They are not restricted to any particular region of the body but can affect a number of tissues and organs. Systemic mycoses are usually caused by fungi that live in the soil. Inhalation of spores is the route of transmission; these infectious typically begin in the lungs and then spread to orher body tissues. Subcutaneous mycoses are fungal infections beneath the skin caused by saprophytic fungi that live in soil and on vegetation. Sporotrichosis is a subcutaneous infection acquired by gardeners and farmers. Infection occurs by direct implantation of spores or mycelial fragments into a pucture wound in the skin. Fungi that infect only the epidermis, hair, and nails, are called dermatoophytes, and thier infections are called dermatophytes, or cutaneous mycoses. Dermathophytes secrete keratinase, an enzyme that degrades keratin, a protien found in hair, skin, and nails. The fungi that cause superficial mycoses are localized along hair shafts and in superficial epidermal cells. These infections are prvalent in tropical climates. Yeast infection, or cadidiasis, is most frequently caused by Candida albicans and may occur as vulvovaginal candidiasis or thrush, a mucocutaneous candidiasis.
List probable reasons for emerging infectious diseases and name an example for each.
Emerging infectious diseases (EIDs) are ones that are new or changing, showing an increase in incidence in the recent past, or a potential ro increase in the near future. An emerging disease can be caused by a virus, a bacterium, a fungus, a protozoan, or a helminth. About 75% of emerging infectious diseases are zoonotic, mainly of viral origin, and are likely to be vectorborne. Avariety of factors contribute to the emergenceof new infectious diseases: *New strains, such as E. coli O 157:H7 and avian influenza (H5N1), may result from genetic recombination between organisms. *A new serovar, such as Vibrio cholerae O139, may result from changes in or the evolution of existing microorganisms. *The widespread, and sometimes unwarranted, use of antibiotics and pesticides encourages the growth of more resistant populations of microbes and the insects ( mosquitoes and lice) and ticks that carry them. *Global warming and changes in weather patterns may increase the distribution and survival of reservoirs and vectors, resultinf in the introduction and dissemination of diseases such as malaria and Hantavirus pulmonary syndrome. * Known diseases, such as cholera and West Nile virus, may spread to new geographic areas bymodern transportation. This was less likely 100 years ago, when travel took so long that infected travelers either died or recoverd during passage. *Previously unrecognized ingections may appear in individuals living or working in regions undergoing ecological changes brought about by natural disaster, construction, wars, and expanding human settlement. In California, the incidence of coccidioidomycosis increased tenfold following the Northridge earthquake of 1994. workers clearing South American forests are now contracting Venezuelan hemorrhagic fever. *Even animal control measures may affect the incidence of a disease. The increase in Lyme disease in recent years could be due to rising deer populations resulting form the killing of deer predators. * Failures in public health measurses may be a contributing factor to the emergence of previously controlled infections. For example, the failure of adults to get a diphtheria booster vaccination led to a diphtheria epidemic in the newly independent republics of the former Soviet Union in the 1990s. The CDC, the National Institutes of Health (NIH), and the World Health Organization (WHO) have developed plans to address issues relating to EIDs. Their priorities include: 1. To detect, promptly investigate, and monitor emerging infectious pathogens, the diseases they cause, and factors that influence their emergence 2. To expand basic and applied research on ecological and environmental factors, microbial changes and adaptations, and host interactions that influence EIDs 3. To enhance the communication of public health information and the prompt implementation of prevention strategies regarding EIDs 4. To establish plans to monitor and control EIDs worldwide
Compare the effects of coagulases, kinases, hyaluronidase, and collagenase.
Enzymes: The virulence of some bacteria is thought to be aided by the production of extracellular enzymes (exoenzymes) and related substances. these chemicals can digest materials between cells and form or digest blood clots, among other functions. Coagulases: Coagulases are bacterial enzymes that coagulate the fibrinogen in blood. Fibrinogen, a plasma protein produced by the liver, is converted by coagulases into fibrin, the threads that form a blood clot. The fibrin clot may protect the bacterium from phagocytosis and isolate it from other defenses of the host. Coagulases are produced by som members of the genus Staphylococcus; they may be inbolbed in the walling-off process in boils produced by staphylococci. However, some staphylococci that do not produce coagulases are still virulent. Kinases: Bacterial kinases are bacterial enzymes that break down fibrin and thus digest clots formed by the body to isolate the infection. One of the better-known kinases is fibrinolysin (streptokinase), which is produced by such streptococci as Streptococcus puogenes. Another kinase, staphylokinase, is produced by Staphylococcus aureus. Hyaluronidase: Hyaluronidase is another enzyme secreted by certain bacteria, such as streptococci. It hydrolyzes hyaluronic acid, a type of polysaccharide that holds together certain cells of the body, particulaly cells in connective tissue. This digesting action is thought to be involved inthe tissue blacvkening og ingected wounds and to help the microorganism spread from its initial site of infection. Hyalutonidase is also produced by some clostridia that cause gas gangrene. For therapeutic use, Hyaluronidase may be mixed with a drug to promote the spread of the drug through a body tissue. Collagenase: Another enzyme, collagenase, produced by several species of Clostridium, facilitates the spread of gas gangrene. collagenase breaks down the protein collagen, which forms the connective tissue of muscles and other body organs and tissues. IgA proteases: As a defense against adherence of pathogens to mucosal surfaces, the body produces a class of antibodies called IgA antibodies. There are some pathogens with the ability to produce enzymes, called IgA proteases, that can destroy these antibodies. N. gonorrhoeae has this ability, as do N. miningitidis, the causative agent of miningocvoccal meningitis, and other microbes that infect the central nervous system.
Define epidemiology and describe three types of epidemiologic investigation.
Epidemilolgy- the science thaat studies when and where a diseases occur and how they are transmitted. epidemiologists use three basic types of inbestigations when analyzing the occurrence of a disease: descriptive, analytical, and experimental. Descriptive epidemiology: Descriptive epidemiology entails collecting all data that describe the occurrence of the disease under study. Relevant information usually includes information about the affected individuals and the place and period in which the disease occurred. Analytical epidemiology: Analytical epidemiology analyzes a particular disease to determine its probable cause. This study can be done in two ways. With the case control method, the epidemiologist looks for factors that might have preceded the disease. A group of people who have the disease is compared with another group of people who are free of the disease. For example, one group with meningitis and one with out the disease might be matched by age, sex, socioeconomic status, and location. These statistics are compared to determine which of all the possible factors-genetic, environmental, nutrional and so forth- might be responsible for the meninfitis. Nightingale's work was an example of analytical epidemiology, in shich she compared disease in soldiers and civilians. With the cohort method, the epidemiologist studies two populations: one that has had contact with the agent causing a disease and another that has not. Experimental epidemiology: Experimental epidemiology begins with a hypothesis about a particular disease; experiments to test the hypothesis are then conducted with a froup of people. One such hypothesis could be the assumed effectivness of a drug. A group of infected individuals is selected and divided randomly so that some receive the drug and others receibe a placebo, a substanc that has no effect. If all other factors are kept constant between the two froups, and if those people who received the drug recovermore rapidly than those who received the placebo, it can be concluded that the drug was the experimental factor (variable) that made the difference.
Review the common disease pattern: incubation period, prodromal period, periods of illness, decline, and convalescence
For an infectious disease to occur, there must be a reservoir of infection as a source of pathogens. Next, the pathogen must be transmitted to a susceptible host by direct contact, by indirect contact or by vectors. Transmission is followed by invasion, in whicch the microorganism injures the host through a process called pathgenesis. The extent of injury depends on the degree to which host cells are damaged, either directly or by toxins. Despite the effects of all these factors, the occurrence of disease ultimately depends on the resistance of the host to the activities of the pathogen. Predisposing factor- anything that makes the body more susceptile to a disease or alters the course of a disease. Incubation period- the time interval between the actual infection and first appearance of any signs or symptoms of disease. Prodromal period- the time following the incubation period when the first symptoms of illness appear. Period of illness- during the period of illness, the disease is most severe. The person exhibits overt signs and symptoms of disease, such as fever, chills, muscle pain (myalgia), sensitivity to light (photophobia), sore throat (pharyngitis), lymph node enlargement (lymphadenopathy), and gastrointestinal disturbances. Period of decline- the signs and symptoms subside. The fever decreases, and the feelinf of malaise diminishes. During this phase, which may take from less than 24 hours to several days, the patient is vulnerable tosecondary infections. Period of convalescence- the recovery period, when the body returns to its predisease state. (the person regains strength and the body returns to its prediseased state.
List the defining characteristics of fungi.
Hyphae: Cell filaments, mostly septate Mycelium: Mass of hyphae Molds: mostly filamentous Yeasts: non-filamentous, unicellular fungi Budding yeasts divide asymmetrically. Dimorphic fungi: yeast-like at 37°C, mold-like at 25°C. Fungal spores are reproductive spores (unlike bacterial spores). Used to differentiate fungi. Growth in acidic, low-moisture, high osmotic pressure environments. The thallus (body) of a mold or fleshy fungus consists of long filaments of cells joined together; these filaments are called hyphae. Hyphae can grow to immense proportions. The hyphae of a single fungus in Oregon extend across 3.5 miles. In most molds, the hyphae contain cross-walls called septa (singular: septum), which divide them into distinct, uninucleate (one-nucleus) cell-like units. These hyphae are called septate hyphae. In a few classes of fungi, the hyphae contain no septa and appear as long, continuous cells with many nuclei. These are called coenocytic hyphae. Even in fungi with septate hyphae, there are usually openings in the septa that make the cytoplasm of adjacent "cells" continuous; these fungi are actually coenocytic organisms, too. Mycelium a mass of long filaments of cells that bring and intertwine, typically found in molds.
Categorize diseases according to frequency of occurrence.
Incidence- The fraction of the population that contracts a disease during a paticular period of time. (It is an indicator of the spread of the disease). Prevalence- The fraction of a population having a specific disease at a given time. (the prevalence of a disease is the number of people in a population who develop a disease at a specified time, regardless of when it first appeared. Prevalence takes into account both old and new cases. It's an indicator of how seriously and how long a disease affects a population). Sporadic disease- a disease that occurs occasionally in a population. (typhoid fever in the US). Endemic disease- Adisease that is constantly present in a certain population. (common cold). Epidemic disease- a disease acquired by many hosts in a given area in a short time. (influenza). Pandemic disease- an epidemic disease that occurs worldwide.
*Differentiate between innate and adaptive immunity.
Innate immunity refers to defenses that are presen at birth. innate immunities first line of defense; skin and mucous membranes and the second line of defense; natural killer cells and phagocytes, inflammation, fever, and antimicrobial substances. It s the immunity's early-warning sustem and are designed to prevent microbes from gaining access into the body and to help eliminate those that do gain access into the bocy and to help eliminate those that do gain access. Adaptive immunity is based on a specific response to a specific microbe once a microbe has breached the innate immunity defenses. It adapts or adjusts to handle a particular microbe. unlike innate immunity is slower to respond, but it does have a memory component. Adaptive immunity involves lymphocytes called Tcells (T lymphocytes) and B cells (B lymphocytes).
Explain latent viral infections and give an example.
Latent Viral Infections A virus can remain in equilibrium with the host and not actually produced disease for a long period, often many years. The oncogenic viruses just dicussed are examples of such latent infections. all of the human herpesviruses are reactivated by immunosuppression (for example, AIDS), the resulting infection may be fatal. The classic example of such a latent infection is the infection of the skin by Simplexvirus, which produces cold sores. This virus inhabits the host's nerve cells but causes no damage until it is activated by a stimulus such as fever of sunburn hence the term fever blister. In some individuals, viruses are produced, but symptoms never appear. Even though a large percentafe of the human population carries Simplexvirus, only 10-15% of people carrying the virus exhibit the disease. The virus of some latent infections can exist in a lysogenic state withen host cells. The chickenpox virus (Varicellovirus) can also exist in a latent state. Chicken (varicella) is a skin disease that is usually acquired in childhood. The virus gains access to the skin via the blood. From the blood, some viruses, causing shingles (zoster). The shingles rash appears on the skin along the nerve in which the virus was latent. Shingles occurs in 10-20% of people who have had chickenpox.
Define the following terms: morbidity, mortality, and notifiable disease.
Morbidity- 1) the incidence of a specific disease, 2) the condition of being diseased. Mortality- the number of deaths from a specific notifiable disease. Notifiable infectious diseases- a disease that physicians must report to the U.S. Public Health Service; also called reportable disease. Morbidity rate- the number of people affected by a disease in a given period of time in relation to the total population. Mortality rate- the number of deaths from a disease in a given period of timein relation to the total population.
Explain the difference between normal, transient, and opportunistic microbes
Normal Microbiota The new born's first contact with microorganisms is uxually with lactobacilli (produced by a woman's vagina just before she gives birth), and they become the predominant organisms in the newborns intestine. More mictoorganisms are introduced to the newborns body from the environment when breathing begins and feedinf starts. After birth, E. coli and other bacteria acquired from foods begin to inhabit the large intestine. These microorganisms remain there throughout life and, may increase or decrease in number and contribute to disease. The microorganisms that establish more or less permanent residence (colonize) but that do not produce disease under normal conditions are members of the body's normal micrbiota, or normal flora. Others, called transient micrbiota may be present for several days, weeks, or months then disappear. Microorganisms are not found throughout the entire human body but are localized in certain regions. Many factors determine the distrbutionand compostion of the normal microbiota. Among these are nutrients, physical and chemical factors, defenses of the host, and mechanical factors. Accordingly, microbes can colonize only those body sites that can supply the apporpriate nutrients. These nutrients may be derived from secretory and excretory products of cells, substances in body fluids, dead cells, and foods in the gastrointestinal tract. A number of physical and chemical factors affect the growth of microbe, (ie temperature, pH, available oxygen and carbon dioxide, salinity, and sunlight. Opportunistic Microorganisms Although categorizing symbiotic relationships by type is convenient, keep in mind that under certain conditions the relationships can change. For example, given the proper circumstanes, a mutualistic organism, such as E.coli, can become harmful. E.coli is generally harmless as long as it remains in the large intestine; but if it gains access to other body sites, such as the urinary bladder, lungs, spinal cord, or wounds, it may cause urinary tract infecrions, pulmonary infections, menigitis, or absscesses, respectivly. Microbes such as E. coli are called opportunistic pathogens. They ordinarily do not cause disease in their normal habitat in a healthy person but may do so in a different environment. Microbes that gain access through broken skin or mucous membranes can cause opportunistic infections. Or, if the host is already weakened or compromised by infections, microbes that are usually harmless can cause disease, AIDS is often accompanied by a common oppotuistic infection, Pneumocystis pneumonia, caused by the opportunistic organism Pneumocystis jirovecii. This secondary infection can develop in AIDS patients because their immune systems are suppressed. Before the AIDS epidemic, this typs of pneumonia was rare. Opportunistic pathogens possess other features that contribute to their ability to caus disease. For exampe, they are present in or on the body or in the external environment in relatively large numbers, Some opportunistic patogens may be found in locations in or on the body that are somewhat protected from the body's defenses, and some are resistant to antibiotics. Pathogens that are frequently carried in healthy individuals are echoviruses (echo comes from enteric sytopthogenic human orphan), which can cause intestinal diseases, and adenoviruses, which can cause repiratory diseases, Neissera meningitidis, which often resides benignly in the repiratory tract, can cause meningitis, a disease that inflames the coberings of the brain and spinal cord. Streptococcus pneumoniae, a normal resident of the nose and throat, can cause a type of pneumonia.
Define nosocomial infections and explain their importance and prevention.
Nosocomial infection does not show any evidence of being present or incubating at the time of admission to a hopital; it is acquired as a result of a hospital stay. Health care-associated infection (HAI) has been introduced to include infections acquired in settings other than just hospitals. These include same-day surgical centers, ambulatory outpatient health care clinics, nursing homes, rehabilitation facilities, and in-home health care environments. The CDC estimates 5-15% of all hospital patients acquire some type of nosocomial infection. Nosocomial infections result from the interaction of several factors: 1. microorganisms in the hospital environment 2. the compromised (or weakened) status of the host 3. the chain of transmission in the hospital. Nosocomial pathogens are oppertunistic and thrive in hospital because peoples immune system is down. many of them have become resistant to antimicrobial drugs. ie P. aeruginosa and other such gram negative bacteria tend to be difficult to control with antibiotics because of their R factors (Resistance factors a bacterial plasmid carrying genes that determine resistance to antibiotics), which carry genes that determine resistance to antibiotics.
Compare commensalism, mutualism, and parasitism, and give an example of each.
Once established, the normal microbiota can benefit the host by preventing the overgrowth of harmful microorganisms. This phenomenon is called microbial antagonism, or competitive exclusion. The relationship between the normal microbiota and the host is called symbiosis, a relationship between two organisms in which at least one organism dependent on the other. In the symbiotic relationships called commensalism, one of the organisms benefits, and the other is unaffected. Many of the microorganisms that make up our normal microbiota are cemmensals; these include staphylococcus epidermidis that inhabit the surface of the eye, and certain saprophytic mycobacteria that inhabit the eat and external genitals. These bacteria live on secretions and sloughed-off cells. and they bring no apparent benefit or harm to the host. Mutualism is a type of symbiosis that benefits both organisms. For example, the large intestine contains bacteria, such as E. coli, that synthesize vitamin K and some B vitamins. These vitamins are absorbsed into the blood stream and distributed for use by body cells. In exchange, the large intestine provides nutrients used by the bacteria, resulting in their survival.
*Identify the principal portals of entry and exit.
Pathogens can gain entrance to the human body and other hosts through several avenues, which are call portals of entry. The portals of entry for pathogens are mucous membranes, skin, and direct deposition beneath the skin or membranes (the parenteral route). Mucous Membranes: Many bacteria and viruses gain access to the body by penetrating mucous membranes lining the respiratory tract, gastrointestinal tract, genitourinary tract, and conjunctiva, a delicate membrane that cover the eyeballs and lines the eyelids. Most pathogens enter through the mucous membranes of the gastrointestinal and respiratory tracts. Skin: The skin is the largest organ of the body in terms of surface area and weight and is an important defense against disease. Unbroken skin is impenetrable by most microorganisms. Some microbes gain access to the body through openings in the skin, such as hair follicles and sweat gland ducts. Larvae of the hookworm actually bore through the skin, and some fungi grow on the keratin in skin or infect the skin itself. The conjunctiva is a delicate mucous membrane that lines the eyelids and covers the white of the eyeballs. Parenteral route: a portal of entry for pathogens by depositions directly into tissues beneath the skin and mucous membranes. Punctures, injections, bites, cuts, wounds, surgery, and splitting of the skin or mucous membrane due to swelling of drying can all establish parenteral routes. HIV, the hepatitis viruses, and bacteria that caus tetanus and gangrene canbe transmitted parenterally. Even after microorganisms have entered the body, they do not necessarily cause disease. The occurrence of disease depends on several factors, only one of ehich is the portal of entry. Many pathogens have a preferred portal of entry that is a prerequisite to their being able to cause diseas might not occur. For example, the bacteria of typhoid fever, Salmonella typi, produce all the signs and sypmtoms of the disease when swallowed (preferred route), but if the same bacteria are rubbed on the skin, no reaction (or only a slight inflammation) occurs. Streptococci that are inhaled (preferred route) can cause pneumonia; those that are swallowed generally do not produce signs or symptoms. Some pathogens, such as Yersinia pestis, the microorganism that causes plague, and Bacillus anthracis, the causative agent of anthrax, can initiate disease from mote than one portal of entry. The virulence of a microbe is often expressed as the ID50 (infectious dose for 50% of a sample population). The 50 is not an absolute value; rather, it is used to compare relative virulence under experimental conditions. The potency of a toxin is often expressed as the LD50 (lethal dose for 50% of a smaple population).
*Define pathology, etiology, pathology, pathogen, infection, and disease
Patholgy is the sientific study of disease (pathos=suffering; logos=science). Etiology- the study of the cause of a disease. Pathogenesis- the manner in which a disease develops. Pathogen - a disease-causing organism Infection is the invasion or coloization of the body by pathogenic microorganisms Disease occurs when an infection results in any change from a state of health.
Discuss how a proteins can be infectious.
Prions A few infectious diseases are caused by prions. In 1982, American neurobiolofist Stanley Prusiner proposed that infectious proteins caused a neurological disesase in sheep called scrapie. The infectivity of scrapie- infected brain tissue is reduced by treatment with proteases byt not by treatment with radiation, suggesting that the infectious agent is pure protein. prusiner coined the name prion for proteinaceous infectious particle. Nine animal diseases now fall into this category, including the "mad cow disease" that emerged in cattle in Great Brirain in 1987. all nin are neurological diseases called spongiform encephalopathies because large vacuoles develop in the brain. The human diseases are kuru, Creutzfeldt-jakob disease (CJD), Gerstmann-Straussler-Scheinker syndrome, and fatal familial insomnia. These diseases rusn in families, which indicates a possible genetic cause. However, they cannot be purley inherited, because mad cow disease arose from feeding scrapie-infected sheep meat to cattle, and the new (bovine) variant was transmitted to humans who ate undercooked beef from infected cattle. Additionally, CJD has been transmitted with transplanted nerve tissue and contaminated surgical instruments. These diseases are caused by the conbersion of a normal host glycoprotein called prpC ( forcellular prion protein) into an infectioues form called prp SC ( for scrapie protein). The gene for prpC is located on chromosome 20 in humans. Recent evidence suggests that prpC is inbolbed in regulating cell death. One hypothesis for an infectious agent that lacks any nucleic acid can reproduce. The actual cause of cell damage is not known. Fragments of prpSC molecules acccumulate in the brain, forming plaques; these plaques are used for postmortem diagnosis, but they do not appear to be the cause of cell damage.
Define reservoir of infection and distinguish between human, animal, and nonliving reservoirs. Give an example of each.
Reservoirs of Infection: For a disease to perpetuate itself, there must be a continual source of the disease organisms. This source can be either a living organism or an inanimate object that provides a pathogen with adeqyate conditions for survival and multiplication and an opportunity for transmission. These reservoirs may be human, animal, or nonliving. Human Resevoirs: People harbor pathogens that are showing signs and symptoms of disease may transmit them directly or indirectly to others. Then there are those who transmit pathogens even though they are not showing signs of illness. They are known as carriers, they are an important living reservoirs of infection. Animal Reservoirs: Both wild and domestic animals are living reservoirs of microorganisms can cause human disease. These diseases transmitted from baoth types of animals to humans is called zoonoses. ie rabies and lyme disease. Can be transmitted direct contact with pet feces and urine, contamination of food and water, air contaminated via the hides, fur, or feathers, by consumming infected animal products, or insect vectors. Nonliving Reservoirs: The two major nonliving reservoirs of infectious disease are soil and water. Soil harbors such pathogens as fungi, which cause mycoses such as ringworm and systemic infections; Clostridium botulinum, the bacterium that causes botulism; and C. tetani, the bacterium that causes tetanus. both species of clostridia are part of the normal intestinal microbiota of horses and cattle, the bacteria are found especially in soil where animal feces are used as fertilizer. Water that has been contaminated by the feces of humans and other animals is a reservoir for several pathogens, notably those responsible for gastrointestinal diseases. These include Vibrio cholerae, which causes cholera, and Salmonella typhi, which causes typhoid fever. Other nonliving reservoirs include foods that are improperly prepared or stored. They may be sources of diseases such as trichinellosis and salmonellosis.
Differentiate between a tick and a mosquito, and name a disease transmitted by each.
Some parasites multiply in their vectors. When this happens, the parasites can accumulate in the vector's feces or saliva. Large numbers of parasites can then be deposited on or in the host while the vector is feeding there. The spirochete that causes Lyme disease is transmitted by ticks in this manner, and West Nile virus is transmitted in the way by mosquitoes. Plasmodium is an example of a parasite that requires that its vector also e the definitive host. Plasmodium can sexually reproduce only in the gut of an Anopheles mosquito's saliva, which acts as an anticoagulant that keeps blood flowing.
Differentiate a communicable from a noncommunicable disease.
Symptom- A change in body function that is felt by a paitent as a result of a disease. (such as pain and malaise, a vague feeling of body discomfort). Sign- A change due to disease that a person can observe and measure. (which are objective changes the physician can observe and measure). Syndrome- A specific group of signs or symptoms that accompany a disease. Communicable disease- Any disease that can be spread from one host to another. (Chickenpox, measles, genital herpes, typhoid fever, and tuberculosis). Contagious diseases- A disease that is easily spread from one person to another. (chickenpox and measles). Noncommunicable disease- A disease that is not transmitted from one person to another. (These diseases are caused by microorganisms that normally inhabit the body and produce disease only when introduced into the body. An example is tetanus: Clostridium tetani produces disease only when it is introduced into the body via abrasions or wounds.)
Differentiate an intermediate host from a definitive host.
The Apicomplexa are not motile in their mature forms and are obligate intracellular parasites. Apicomplexans are characterized by the presence of a complex of special organelles at the apexes (tips) of their cells. An example of an apicomplexan is Plasmodium, the causative agent of malaria. Plasmodium grows by sexual reproduction in the Anopheles mosquito. When an Anopheles carrying the infective stage of Plasmodium, called a sporozoite, bites a human, sporozoites can be injected into the human. The sporozoites undergo schizogomy in liver cells and produce thousands of progeny called merozoites, which infect red blood cells. The young trophozoite looks like a ring in which the nucleus and cytoplasm are visible. This is called the ring stage. The red blood cells eventually rupture and release more merozoites. Upon release of the merozoites, their waste products, which cause fever and chills, are also released. The mosquito is the definitive host because it harbors the sexually reproducing stage of Plasmodium. The host in which the parasite undergoes asexual reproduction (in this case, the human) is the intermediate host. Definitive host: An organism that harbors the adult, sexually mature form of a parasite. Intermediate host: An organism that harbors the larval or asexual of a helminth or protozoan.
Provide a rationale for the elaborate life cycles of parasitic worms.
The life cycle of parasitic helminths can be extremely complex, involving a succession of intermediate hosts for completion of each larval stage of the parasite and a definitive host for the adult parasite. Adult helminths may be direction; male reproductive organs are in one individual, and female reproductive organs are in another. In those species, reproduction occurs only when two adults of the opposite sex are in the same host. Adult helminths may also be monoecious, or hermaphroditic one animal has both male and female reproductive organs. Two hermaphrodites may copulate and simultaneously fertilize each other. A few types of hermaphrodites fertilize themselves. Humans as Definitive Hosts: The adults of Taenia saginata, the beef tapeworm, live in humans and can reach a length of 6m. The scolex is about 2mm long and is followed by a thousand or more proglottids. The feces of an infected human contain mature proglottids, each of which contain thousands of eggs. As the proglottids wriggle away from the fecal material, they increase their chances of being ingested by an animal that is grazing. Upon ingestion by cattle, the larvae hatch from the eggs and bore through the intestinal wall. The larvae migrate to muscle (meat), in which they encyst as cysticerci. When the cysticerci are ingested by humans, all but the scolex is digested. The scoles anchors itself in the small intestine and begins producing proglottids. Humans are the only know definitive host of the pork tapeworm, Taenia solium. Adult worms living in the human intestine produce eggs, which are passed out in feces. When eggs are eaten by pigs, the larval helminth encysts in the pig's muscle; humans become infected when they eat undercooked pork. The human-pig-human cycle of T. solium is common in Latin America, Asia, and Africa. In the US, however, T. solium is virtually nonexistent in pigs; the parasite is transmitted from human to human. Eggs shed by one person and ingested by another person hatch, and the larvae encyst in the brain and other parts of the body, causing cysticercosis. The human hosting T. solium's larvae is serving as an intermediate host. Humans as Intermediate Host: Humans are the intermediate hosts for Echinococcus granulosus. Dogs and coyotes are the definitive host for this minute 2-8mm tapeworm. 1. Eggs are excreted with feces. 2. Eggs are ingested by deer, sheep, or humans. Humans can also become infected by contaminating their hands with dog feces or saliva from a dog that has licked itself. 3. The eggs hatch in the human's small intestine, and the larvae migrate to the liver or lungs. 4. The larva develops into a hydatid cyst. The cyst contains "brood capsules," from which thousands of scoleces might be produced. 5. Humans are a dead-end for the parasite, but in the wild, the cysts might be in deer that is eaten by a wolf. 6. The scoleces would be able to attach themselves in the wolf's intestine and produce proglottids. Eggs Infective for humans: Ascaris lumbricoides is a large nematode (30 cm long). It is dioecious with sexual dimorphism; that is, the male and female worm look distinctly different, the male being smaller with a curled tail. The adult ascaris lives in small intestines of human exclusively; it feeds primarily on semi-digested food. Eggs, excreted with feces, can survive in the soil for long periods of time until accidental ingested by another host. The eggs hatch in the small intestines of the host. The larvae then borough outside of the intestine and enter the blood. They are carried to the lungs, where they grow. The larvae will then be coughed up, swallow, and return to the small intestines, where they mature into adults. The pinworm: The pinworm Enterobius vermicularis spends his entire life in a human host. Adult pinworms are found in the large intestine. From there, the female pinworm migrates to the anus to deposit her eggs on the perianal skin. The eggs can be ingested by the host or buy another person exposed contaminated clothing or bleeding. Larvae infective for humans: adult hookworms, Necator Americanism and ancylostoma duodenale, live in the small intestine of humans; the eggs are excreted in feces. The Larvae hatch in the soil, where they feed on bacteria. A larva enters its host by penetrating the host's skin. It then enters a blood or lymph vessel, which carries it to the lungs. It is coughed up in sputum, swallowed and finally carried to the small intestine.
Explain the difference between enveloped and nonenveloped viruses.
The nucleic acid of a virus is protected by a protein coat called the capsid. The structure of the capsid is ultimately determined by the viral nucleic acid and accounts for most of the mass of a virus, especially of small ones. Each capsid is composed of protein subunits called capsomeres. In some viruses, the proteins composing the capsomeres are of a single type; in other viruses, several types of protein may be present. Individual capsomeres are often visible in electron micrographs. The arrangement of capsomeres is characteristic of a particular type of virus. In some viruses, the capid is covered by an envelope, which usually consist of some combination of lipids, proteins, and carbohydrates. Some animal viruses are released from the host cell by an extrusion process that coats the virus with a layer of the host cell's plasma membrane; that layer becomes the viral envelop. In many cases, the envelope contains proteins determined by the viral nucleic acid and materials derived from normal host cell components. Depending on the virus, envelopes may or may not be covered by spikes, which are carbohydrate-protein complexes that project from the surface of the envelope. Some viruses attach to host cells via spikes. Spikes can clump rbc's together, causing hemagglutination. Viruses whose capsids are not covered by an envelope are know as nonenveloped viruses. The capsid of a nonenveloped virus protects the nucleic acid from nuclease enzymes in biological fluids and promotes the virus's attachment to susceptible host cells.
List the defining characteristics of protozoa.
The term protozoan means "first animal," which generally describes its animal-like nutrition. In addition to getting food, a protozoan must reproduce, and parasitic species must be able to get from on host to another. Unicellular, eukaryotic chemoheterotrophs. Large and diverse group. Few are pathogenic. Found in soil and water and as normal microbiota in animals. Trophozoite: Vegetative form (feeding and growing)(feeds upon bacteria and small particulate nutrients). Asexual reproduction via fission, budding, or schizogony (multiple fission). Sexual reproduction via conjugation. Some protazoa produce gametes (gametocytes), haploid sex cells. Suring reproduction, two gametes fuse to form a diploid zygote. Some protozoa can produce a cyst that provides protection during adverse environmental conditions (when food, moisture, or oxygen are lacking, when temperatures are not suitable, or when toxic chemicals are present). Protoaoa are mostly aerobic heterotrophs, although many intestinal protozoa are capable of anaerobic growth. Two chlorophyll-containing groups, dinoflagellates and euflenoids, are often studied with algae. Some Medically Important Protozoa Giardia lamblia (G. intestinalis or G. duodenalis) a parasite without mitochondria. In small intestines of humans and other mammals. Diagnosis via cysts in feces Trichomonal vaginalis has an undulating membrane, which consists of a membrane bordered by flagellum. T. vaginalil does not have a cyst stage and must be transferred from host to host quickly before desiccation occurs. T. vaginalis is found in the vagina and in the male urinary tract. Apicomplexa: not mobile, intracellular Plasmodium , Babesia, Toxoplasma, Cryptosporidium Euglenozoa: Hemoflagellates Trypanosoma Move by flagella Hemoflagellates Sleeping sickness Chagas' disease Amoebae Move by pseudopods Entamoeba histolytica in human GI tract. ~ 10% carriers. Amoebic disentery. Acanthamoeba in water. Can infect cornea.
Define toll-like receptors.
Toll-like receptors (TLRs) play a crucial role in the recognition of invading pathogens and the activation of subsequent immune responses against them. Individual TLRs recognize distinct pathogen-associated molecular patterns (PAMPs). Toll-like receptors (TLRs) are a class of proteins that play a key role in the innate immune system. They are single membrane-spanning non-catalytic receptors that recognize structurally conserved molecules derived from microbes. Once these microbes have breached physical barriers such as the skin or intestinal tract mucosa, they are recognized by TLRs which activates immune cell responses. They receive their name from their similarity to the protein coded by the Toll gene identified in Drosophila in 1985 by Christiane Nüsslein-Volhard.[1]
Contrast the nature and effects of exotoxins and endotoxins.
Toxins- any poisonous substance produced by a microorganism. They are often the primary factor contributing to the pathogenic properties of those microbes. Toxigenicity- the capacity of a microorganism to produce a toxin. Toxins transported by the blood or lumph can cause serious, and sometimes fatal, effects. Some toxins produce fever, cardiobascular disturbances, diarrhea, and shock. Toxins can also inhibit protein synthesis, destroy blood cells and blood vessels, and disrupt the nervous sustem by causing spasms. Exotoxins: Exotoxin- a protein toxin released from living, mostly gram-positve bacterial cells. Exotoxins are produced inside some bacteria as part of their growth and metabolism and are sectered by the bacterium into the surrounding medium or released following lysis. Exotoxins are proteinsm, and many are enzymes that catalyze only certain biochemical reactions. Because of the enzymatic mature of most exotoxins, even small amounts are quite harmful because theu can act over and over again. Bacteria that produce exotoxins may be gram-positive or gram-negative. the genes for most (perhaps all) exotoxins ate carried on bacterial plasmids or phages. because exotoxins are carried on bacterial plasmids or phages, because exotoxins are soluble in body fluids, they can easily diffuse into the blood and are rapidly transported throughout the body. Exotoxins work by destrying particular parts of the host's cells or by inhibiting certain metabolic functions. They are highly specific in their effects on body tissues. Exotoxins are among the most lerhal substances known. Only 1 mg of the botulinum exotoxin is enough to kill 1 million guinea pigs. Fortunately, only a few bacterial species produce such potent exotoxins. Diseases caused by bacteria that produce exotoxins are often caused by minute amounts of exotoxins, not by the bacteria themselves. It is the exotoxins that produce the specific signs and symptoms of the disease. Thus, exotoxins are disease specific. For example, botulism is usually due to ingestion of the exotoxin, not to bacterial infection. Likewise, staphylococcal food poisoning is an intoxication, not an infection. Antitoxin- a specific antibody produced by the body in response to a bacterial exotoxin or its toxoid. (The body produces antibodies called antitoxins that provid immunity to exotoxins). Toxoid- an inactivated toxin. When toxoids are injected into the body as a vaccine, they stimulate antitoxin production so that immunity is produced. neurotoxin- an exotoxin that interferes with normal nerve impule conduction. Cytotoxin- a bacterial toxin that kills host cells or alters their functions. Endotoxins: Endotoxin- part of the outer portion of the cell wall (lipid A) of most gram-negative bacteria; released on destruction of the cell. Endotoxins differ from exotoxins in several ways. Endotoxins are part of the outer portion of the cell wall of gram-negative bacteria. (gram-negative bacteria have an outer membrane surrounding the peptidoglycan layer of the cell wall. This outer membrane consists of lipoproteins, phospholipids, and lipopolysccharides (LPSs). The lipid portion of LPS, called lipid A, is the endotoxin. Thus, endotoxins are lipopolysaccharides, whereas exotoxins are proteins. Endotoxins are released when gram-negative bacteria die and their cell walls undergo lysis, thus liberating the endotoxin.( Endotoxins are also released during bacterial multiplication.) Antibiotics used to treat diseases caused by gram-negative bacteria can lyse the bacteial cells; this reaction releases endotoxin and may lead to an immediate worsening of the symptoms, byt the condition usually improbes as the endotoxin breaks down. Endotoxins exert their effects by stimulating macrophages to release cytokines in bery high concentrations. At these levels, cytokines are toxic. All endotoxins produce the same signs and symptoms, regardless of the species of microorganism, although not to the same degree. These include chill, fever, weakness, generalized aches, and ,in some cases, shock and even death. Endotoxins can also induce miscarriage. Another consequence of endotoxins is the activation of blood cltting proteins, causing blood clots to form and block capillaries. which causes decreased blood supply causes death of tissues. Fever caused via endotoxins.; 1. gram-negative bacteria are ingested by phagocytes. 2. as the bacteria are degraded in vacuoles, the LPSs of the bacterial cell wall are released. These endotoxins cause macrophges to produce cytokines calle interleukin-1 (IL-1), formerly called endogenous pyrogen, and tumor nectosis factor alpha (TNF-a). 3. The cytokines are carried via the blood to the hypothalamus, a temperature control center in the brain. 4. The cytokines induce the hypothalamus to release lipids called prostaglandins, which reset the thermostat in the hypothalamus at a higher temperature. The result is a fever. Shock refers to any life-threatening decrease in blood pressure, shock caused by bacteria is called septic shock. Gram-negative bacteria cause endotoxic shock. Limulus amebocyte lysate (LAL) assay- a test to detect the presence of bacterial endotoxins.
*Differentiate a virus from a bacterium.
Viruses were originally distingished from other infectious agents because they are especially small (filterable) and because they are obligatory intracellular parasites-that is, they absolutely require living host cells in order to multiply. However, both these properties are shared by certain small bacteria, such as rickettsias. The truly distinctive features of viruses are now known to relate to their simple structural organization and their mechanism of multiplication. Accordingly, viruses are entities that * Contain a single type of nucleic acid, either DNA or RNA. * Contain a protein coat ( sometimes itself enclosed by an envelope of lipids, proteins and carbohydrates) that surrounds the nucleic acid. *Multiply inside living cells by using the synthesizing machinery of the cell. * Cause the synthesis of specialized structures that can transfer the viral nucleic acid to other cells. Viruses have few or no enzymes of their own for metabolism; for example, they lack enzymes for protein synthesis and ATP generation. To multiply, viruses must take over the metabolic machineryof the host cell. This fact has considerable medical significance for the development of antiviral drugs, because most drugs that would interfere with viral multiplication would also interfere with the fucnctioning of the host cell and therefore are too toxic for clinical use.
Describe the function of siderophores.
When a microorganism invades a body tissue, it initially encounters phogocytes of the host. If the phgocytes are successful in destroying the invader, no further damage is done to the host. But if the pathogen overcomes the host's defense, then the microorganism can damage host cells in four basic ways: 1. by using the host nutrients 2. by causing direct damage inthe immediate vicinity of the invasion 3. by producing toxins, transported by blood and lymph, that damage sites far removed from the original site of invasion 4. by inducing hypersinsitivity reactions. Siderophores: Iron is required for the growth of most pathogenic bacteria. However, the concentration of free iron in the human body is fairly low because most of the iron is tightly bound to iron-transport proteins, such as lactoferrin, transferrin, and ferritin, as well as hemoglobin. To obtain free iron, some pathogens secrete proteins called siderophores. When a pathogen needs iron, siderphores are releasedinto the medium, where they take the iron away from irontransport proteins by binding the iron even more tightly. Once the iron-siderophore complex is formed, it is taken yp by siderophore receptors on the bacterial surface. Then the iron is brought into the bacterium. In some cases, the iron is released from the complex to enter the bacterium; in other cases, the iron enters as part of the complex.