Chapter 15 Microbiology
Endotoxins
Lipopolysaccharides differ from exotoxins, part of outer region of cell wall of gram negative bacteria (outer membrane surrounding the peptidogylcan layer of the cell wall, outer layer has lipoproteins, phospholipids, and LPS; lipid portion is called Lipid A, the endotoxin released when gram - bacteria die and their cell wall undergoes lysis, liberating hte endotoxin stimulate macrophages to release cytokines in high concentrations , produce same signs and symptoms also activate blood clotting proteins, obstruct capillaries and result in decreased blood supply and death of tissues
Fungi disease effects
don't have well-defined set of virulence factors; have metabolic products that are toxic to human hosts; indirect cause of the disease; can create an allergic response in the host
virulence
extent of disease
exoenzymes
extracellular enzymes
AB toxins
first toxins to be studied; and consist of two parts, A is the active enzyme part adn B is the binding component (polypeptides) often A alters the function of the host cell by inhibiting protein synthesis
Toxins
poisonous substances that are produced by certain microbes; often primary factor contributing to the pathogenic properties of those microbes
LD50
potency of a toxin lethal dosage for 50% of sample population;
Protozoa
prescence of them and waste products ; some can evade host defenses adn cause disease for a very long time
toxemia
presence of toxins in the bloods 2 kinds: endotoxin and exotoxins
Helminths
presence produces disease symptoms in a host; use host tissues for their own growth, cellular damage causes symptoms
Algae
produce neurotoxins like saxitoxin , shellfish poisoning
collagenase
produced by several clostridium, facilitates teh spread of gas gangrene; breaks down collagen (connective tissue)
Exotoxins
produced inside some bacteria as part of their growth and metabolism and are secreted by the bacterium into the surrounding medium or released by lysis Proteins, and many are enzymes that catalyze only certain biochemical reactions , even small amount are harmful because they can act over and over again can be gram + or gram - genes are carried on bacterial plasmids or phages, soluble in body fluids, easily diffuse work by destroying particular parts of the host's cells or by inhibiting certain metabolic functions; highly specific in heir effects diseases caused by bacteria that produce exotoxins are often caused by minute amounts of exotoxins, not by bacteria ; disease-specific
Shock
refers to any life-threatening decrease in blood pressure low blood pressure affects kidney's, lungs, and gastrointestinal tract, and can cause a weakening of the blood brain barrier
Antiendotoxins?
No, do not promote formation of effective antitoxins
mycotoxins
toxins produced by fungi
What factors contribute to a pathogens ability to invade a host?
Capsul, cell wall components, enzymes, membrane ruffling, antigenic variation
pathogenicity
ability to cause disease
how oes death occur by virus?
accumulation of large numbers of multiplying viruses, by effects of viral proteins, or by inhibition of host DNA, RNA, or protein synthesis
Adherence
adhesion, necessary step in pathogenicity almost all pathogens have some means of attaching themselves to host tissues at their portal of entry
tumor necrosis factor alpha
also endotoxins
toxoids
altered exotoxins to stimulate antibody production ex. tetanus
fimbriae
and opa are used to attach to host cells, host cell takes in the bacteria
Superantigens
antigens that provide a very intense immune response; bacterial proteins, nonspecifically stimulate the proliferation of immune cells called T cells, WC that act against foreign organisms and tissue transplants and regulate activation and proliferation of other cells of the immune system, in response to superantigens, T cells release cytokines lots of cytokines lead to a number of symptoms like fever, nausea, vomitting, diarrhea, shock, death
cardiotoxins
attack heart cells
leukotoxins
attack leukocytes
entertoxins
attack lining of gastrointestinal tract
hepatotoxins
attack liver cells
cytotoxins
attack wide variety of cells
coagulases
bacteria enzymes that coagulate (clot) the fibrongen in blood; Fibrogen (plasma protein)is converted into fibrin the threads that form a blood clot Fibrin clot may protect bacterium from phagocytosis and isolate it from other defenses of the host Staphylococcus
antitoxins
body produces antibodies called antitoxins; that provide immunity to exotoxins; even when exotoxins are inactivated by heat, formaldehyde or iodine they don't cause disease, but they stimulate body to make antitoxins
IgA proteases
can destroy IgA antibodies
toxigenicity
capacity of microbe to produce toxins toxins carried by blood or lymph can cause serious and sometimes fatal effects (fever, shock, diarrhea, inhibit protein synthesis, destroy RBCs, disrupt nervous system),
membrane disrupting toxins
cause lysis of the host cells by disrupting their plasma membrane; some do this by forming protein channels in the plasma membrane or by disrupting the phospholipid portion of the membrane
noncytocidal effects
cell damage, but not death
Eukaryotic cytoplasm
complex internal structure, consiting of protein microfilaments, intermiediate filaments, and microtubules; and a major component is protein actin, which is used by microbes to penetrate host cells by others to move through and between host cells
Cell Wall Components
contain chemical substances that help virulence; ex. streptococcus pyrogenes produces heat resistant and acid-resistant protein called M protein; protein is found on both the cell surface and fimbriae; mediates attachment of bacterium to epithelial cells of host and helps bacterium resist phagocytosis
CPE
cytopathic effects, or visible effects of viral infection;
interluekin 1
endogenous pyrogen, cytokines; carried via blood to hypothalamus, which controls temp; induce prostaglandins which reset thermostat in hypothalamus to higher temperature
Hyaluronidase
enzyme secreted by certain bacteria like streptococci; hydrolyzes hyaluronic acid (polysaccharide that holds together certain cells, like connective tissues) this digesting action is involved in the tissue blackening of infected wounds that help the microbes spread from its initial site of infection
Kinases
enzymes that break down fibrin and thus digest clots formed by the body to isolate the infection; ex. fibrinoylsin
membrane ruffling
ex. salmonella leads to dramatic changes in the membrane at point of contact disruption of the cytoskeleton of the host cell; microbe sinks into ruffle and is engulfed by cell Some bacteria can use the actin to propel themselves through the host cytoplasm and from one host cell to another
Parenteral route
gain access when they are directly deposited into the tissues beneath the skin or into mucous membranes when these barriers are penetrated or injured Punctures, injections, bits, cuts, wounds, surgery, splitting of the ski due to swelling or drying can establish these routes HIV, Hepatitis, tetanus
Capsuls
glycocaylx material that forms capsuls around their cell walls; increases virulence; resists the host's defenses by impairing phagocytosis Chemical nature of capsul prevents the phagocytic cell from adhering to the bacterium; but human body can produce antibodies against capsuls that can easily destroy these bacteria ex. stretpococcus pnuemonia has a capsul that causes pneumonia ex. Bacillus anthracis
adhensions on microbes
glycoproteins and lipoproteins
How can viruses gain access to cells?
have attachment sites for receptors on their target cells; such an attachment site is brought together with a receptor , the birus can bind to and penetrate the cell; others gain access because their attachment sites mimic substances useful to those cells, ex. rabies virus enters the host cell along with neurotransmitter ex. AIDS: hiding attachment sites form immune response by attacking componenets of immune system directly; cell-specific (CD4 protein)
M protein
heat and acid resistant protein; helps prevent phagocytosis
Enzymes
help contribue to virulence by producing exoenzymes that have functions like digesting blood clots, or forming them
streptolysins
hemolysins produced by streptococci; inactivated by O2, SLS is stable in O2 enviornment
sclerotia
highly resistant portions of mycelia of the fungus that can detach
Portal of entry
how pathogens gain entrance to the human body and other hosts Mucous membranes, skin, direct deposition beneath skin or membranes
Numbers of invading microbes
if only a few microbes enter the body, they will probably be overcome by host's defenses; if large numbers enter, the stage is probably set for disease
LAL
limulus amoebocyte lysate assay, detecs evne a small amount of endotoxins
Mucous membranes
many bacteria gain entrance through respiratory tract, intenstinal tract, conjuctiva etc; respiratory tract is the easiest and most frequently traveled; inhaled in teh nose and mouth in drops of moisture and dust particules ex. common cold, pnuemonia, tb Genitourinary tract is a portal of entry that are contracted sexually, STD;s: some penetrate an unbroken mucous membrane, others require a cut or abrasion Gastrointestinal tract: via contaminated fingers touching food and water; most are destroyed by HCl and enzymes in the stomach or by bile and enzymes in small intestines; those that survive cause disease; hep. A, typhoid fever, cholera, and are eliminated by feces which can contaminate more water etc
leukocidins
membrane disrupting toxins that kill phagocytic leukocytes WBCs (act by forming protein channels), active against macrophages as well
hemolysins
membrane-disrupting toxins that destroy RBCs do some by forming protien channels
bioflims
microbes that come together in asses, cling to surfaces, and take in and share nutrients; masses o microbes and their extracellular products that can attach to living on nonliving surfaces ex. dental plaque involved in 65% of human bacterial infections
Skin
most preferred mode of entry Skin is the largest organ, unbroken skin is impenetrable by most microbes (some go through sweat glands/hair follices)
How do microbes cause disease?
must gain access to host, adhere to host tissues, and penetrate or evade host defenses, and cause damage Most don't do it directly, but their waste causes disease Some don't enter body, like acne
waxy lipid
mycolic acid in cell wall (MTB), resisting digestion and can multiply inside phagocytes
preferred portal of entry
organisms that enter do not necessarily cause disease; occurrence of disease depends on several factors including portal of entry; ex. s. typhi only causes problems when its swallowed, not when rubbed on skin
opa
outer membrane protein
siderophores
released into the medium where they take the iron away form iron transport proteins by binding the iron even more tightly; once iron-sidephore complex is formed, it is taken up by siderophore receptors on bacterial surface; iron brought to bacterium
lysogeny
remain latent, host bacterial cell and its progeny may exhibit new properties encdoed by bacteriophage DNA; such a change in characteristic is called lysogenic conversion bacterial cell is immuned to infection by same type of phage
Who produces endotoxins?
salmonella typhi, proteus, etc
Portal of exit
secretions, excretiongs, discharges, tissue that is shed; related to the part of the body that has been infected, depending on portal of exit, pathogens can spread to susceptible hosts coughing, sneezing, droplet form feces secretions from penis/vagina, etc skin, blood
septic shock
shock caused by bacteria
cytokines
small protein molecules that regulate immune responses to mediate cell to cell communication
Antigenic variation
some pathogens can alter their surface antigens thus rendering adaptive immunity useless Can activate alternative genes ex. N. gonorrhaeae, HIV
receptors on host cell
sugars, like mannose, different strains of the same species can vary in structure ; if adhesion, receptors etc can be interfered with, infection can be prevented
aflatoxin
toxin with carcinogenic properties in peanut butter
invasins
surface proteins produced by microbes that rearrange nearby actin filaments of cytoskeleton
adhensions/ligands
the attachment between pathogen and host is accompanied by these surface molecules that bind to specifically complementary surface receptors on the cells of certain host tissues
ID 50
the virulence of a microbe expressed as this; infection dose for 50% of a sample population; smaller ID 50, better portal of entry ex. Anthrax (inhalation is 10,000 +, where skin is 10 to 50), skin is desired portal of entry
cytocidal effects
those that result in cell death
Types of exotoxins
three groups: A-B toxins, membrane-disrupting toxins, and superantigens
ergot
toxin is an alkloid that can cause hallucinations resembling those produced by LSD; constricts capillaries and cause gangreene in limbs
Naming exotoxins
type of host attacked; ex. neurotoxins (attack nerve cells); or by the disease they cause, ex. diptheria toxin causes diptheria others are named by the specific bacteria that causes them (botulinum toxin)
Direct damage
use host cell for nutrients and produce waste products, as pathogens metabolize and multiply in cells, the cells usually rupture, and can spread to other tissues in even greater numbers ex. E. coli, Salmonella
How bacterial pathogens damage host cells
using host's nutrients, produce toxins, direct damage
ex.s
vibrio entertoxin: produces AB enterotoxin called cholera toxin, severe diarrhea tetanus toxin: teteanospasmin; reaches nervous system an binds to nerve cells to control contraction of various muscles
Viral mechanisms for evading destruction by host's immune response;
viruses can penetrate and grow inside host cells, where components of immune system can't reach them