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© Professor P. M. Motta et al / Science Photo Library Microbiology: A Clinical Approach © Garland Science Entry – getting in Establishment – staying in Defeat the host defenses Damage the host Exit the host and be transmitted to another host Pathogens use virulence factors as part of the infection process. › They allow pathogens to survive and thrive in the host. › They make harmless organisms dangerous and make dangerous organisms deadly. Any point at which pathogens can enter is called a portal of entry. There are three categories of portals of entry: › Mucous membranes › Skin › Parenteral routes Mucous membranes are in direct contact with the external environment. They allow pathogens to gain access into the body. They are found in the: › Respiratory tract › Gastrointestinal tract › Genitourinary tract This is the most favorable portal of entry to pathogens because we have to breathe continuously. Pathogens can be found on droplets of moisture as well as on dust particles. This is the second most favorable portal of entry for pathogens since we have to eat and drink regularly. It has many barriers to infection but is still the entry point for many pathogens. This is the second most favorable portal of entry for pathogens since we have to eat and drink regularly. It has many barriers to infection but is still the entry point for many pathogens. Pathogens using the GI tract include: › › › › › › Salmonella Shigella Escherichia Hepatitis virus Giardia Entamoeba The GI tract is also an important portal of exit. › Pathogens can be found in fecal material after leaving the body. The fecal-oral route of contamination is very important in the infection process. This portal of entry is more complicated than the ones previously discussed. Urinary tract infections (UTIs) are more common in women than in men. These types of infections cause major problems in hospitals and clinical settings. Diseases of the reproductive tract are usually sexually transmitted and are also part of this portal of entry. Pathogens using the genitourinary tract include: › › › › Mycobacterium Chlamydia Herpesviruses HIV The skin is the largest organ in the body. The large surface area of the skin provides a vast area through which microorganisms may enter the body. Many microorganisms reside on the skin. Skin provides an impermeable barrier to most microbes and must be broken to allow entry. The term parenteral route refers to breaks in the skin which permit entry of microorganisms. The parenteral route depends on injections, cuts, or wounds, and surgical procedures to provide an entry point. Insect bites can also allow entry of microbial organisms. Insect transfer is referred to as vector transmission. © Professors P. Motta & F. Carpino / Univer- Sity "La Sapienza", Rome / Science Photo Library Microbiology: A Clinical Approach © Garland Science © Professor P.M. Motta Et Al / Science Photo Library Microbiology: A Clinical Approach © Garland Science © Professor P.M. Motta Et Al / Science Photo Library Microbiology: A Clinical Approach © Garland Science Pathogens can use adhesins (glycolipids or glycoproteins) to adhere to tissue. An example of this is the plaque found on teeth. › Plaque forms when a pellicle coats the tooth and bacteria subsequently adhere to it. › As many as 300 to 400 different types of bacteria will adhere to each other building a biofilm on the tooth. This is the plaque. Spirochetes like Treponema pallidum (the causative agent of syphilis) corkscrew into tissues. © CDC/ Dr. David Cox Increasing the number of pathogens can establish the infection in the host. Rapid growth and increased numbers of pathogens can happen very quickly. › Some pathogens can double their numbers in as short a period as twenty minutes. › An organism that doubles every twenty minutes will become 1 x 1021organisms in just 24 hours. The body possesses powerful defense mechanisms. Pathogens must avoid, evade, or compromise these defenses in order to survive and thrive. Pathogens can defeat host defenses in 2 ways: › Passive defense – using built-in structures found on the pathogen cell. › Active defense – attacking the host defenses The main passive defense mechanism is the bacterial capsule which inhibits phagocytosis by host cells. Another method of passive defense is through components of the bacterial cell wall. › Mycolic acid is a waxy material found in the cell walls of Mycobacterium species. It can inhibit phagocytosis and the entry of antibiotics. Active bacterial defenses involve the production of extracellular enzymes which can: › Increase protection against host defenses. › Enable the spread of infection by attacking and killing host defensive cells. Pathogens can also hide in order to defend themselves. Getting inside a host cell can protect the pathogen from the host immune defense › Viruses are obligate intracellular parasites and can easily enter host cells. › Bacteria have to use the host cell cytoskeleton (microtubules and microfilaments) to get into and move around a host cell. › Bacteria can also use the molecule cadherin to move into adjacent cells. Damage to the host committed by the pathogen can be direct or indirect › Direct damage Is obvious and includes the destruction of host cells or tissues Is usually controlled by the host immune response. › Indirect damage Involves systemic infection as a result of toxin production by the pathogen. Bacterial toxins are: › Very poisonous › Soluble in aqueous solutions › Easily diffusible into blood and lymph which causes distal pathology. Bacterial toxins can produce fatal outcomes in patients. They produce common symptoms such as fever, shock, diarrhea, cardiac and neurological trauma, and the destruction of blood vessels. There are 2 types of toxins: › Exotoxins › Endotoxins Exotoxins are produced by and exported from certain pathogens and then enter host cells. They are among the most lethal substances known. They are usually an enzymatic protein soluble in the blood and lymphatic system. There are 3 types of exotoxins: › Cytotoxins – kill cells › Neurotoxins – interfere with neurological signaling › Enterotoxins – affect the lining of the digestive system. Anthrax toxin is a cytotoxin. It is produced by Bacillus anthracis (a grampositive rod commonly found in pastures). It is made up of three parts which are: › Produced separately within the pathogen › Assembled outside the anthrax organism cell wall. It increases vascular permeability in host cells. Diphtheria toxin is a cytotoxin. It is produced by Corynebacterium diphtheriae. It is first produced in an inactive form. It inhibits protein synthesis in the host. A single molecule can kill a host cell. Botulinum toxin is a neurotoxin. It is produced by Clostridium botulinum. There are seven forms of this toxin, all of which inhibit the release of the neurotransmitter acetylcholine. › This disrupts neurological signaling of the skeletal muscle. › This disruption causes paralysis. Tetanus toxin is a neurotoxin. It is produced by Clostridium tetani. It causes loss of skeletal muscle control. › Prevents muscle relaxation › Causes uncontrollable convulsive muscle contractions › Lock jaw is an early symptom Vibrio toxin (also known as cholera toxin) is an enterotoxin. It is produced by Vibrio cholerae. It has a 2 chain polypeptide structure › The β chain binds to the target cell › The α chain causes cells to release large amounts of electrolytes. The release of large amounts of electrolytes causes potentially lethal diarrhea and vomiting. Toxic shock syndrome is caused by the enterotoxin from Staphylococcus aureus. This condition causes excessive loss of electrolyte fluids. The loss of the fluids leads to hypotensive shock. Endotoxins cause the following symptoms: › › › › › Chills Fever Aches Muscle weakness Large amounts of endotoxins can cause disseminated intravascular clotting (DIC). Viral host cell damage is referred to as a cytopathogenic effect (CPE). The cytopathogenic effect of viruses occurs in three ways: › From viral overload › From cytocidal effects (killing of host cells) › From noncytocidal effects (damage caused by host defense) Viral host cell damage is referred to as a cytopathogenic effect (CPE). The cytopathogenic effect of viruses occurs in three ways: › From viral overload › From cytocidal effects (killing of host cells) › From noncytocidal effects (damage caused by host defense) © CDC/ Dr. Edwin P. Ewing, Jr. Microbiology: A Clinical Approach © Garland Science Microbiology, A clinical Approach -Danielle Moszyk-Strelkauskas-Garland Science 2010 Lecture PowerPoints Prescott’s Principles of Microbiology-Mc Graw Hill Co. http://en.wikipedia.org/wiki/Scientific_me thod https://files.kennesaw.edu/faculty/jhendri x/bio3340/home.html