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55 Cards in this Set

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Ziehl Neelsen, aka acid fast stain
Stains acid fast bacteria red. Drives stain into bacteria using acid and heat, the only way bacteria with a thick waxy cell wall, such as Mycobacterium tuberculosis, can be penetrated with stain.
India Ink
Used for negative staining, everything else but the organism is stained black. used to detect/see cryptococcus because India ink is not taken up by the Crytococcus capsule, so the capusle appears as a halo.
Giemsa
General stain for blood smears. consists of eosin (pink) and blue dye, and so gives differential stain.
Periodic Acid Schiff
Tests for polysacchardies, such as glycogen and muco[polysaccharides.
Prussian blue
blue dye test used to detect iron
Congo red
Stains amyloid red and causes amyloid to take on an apple-green birefringemce when viewed under polarizing light microscope.
Osmic acid
fixative and stain for electron microscopy
Gram stain
Gram + for bacteria with thick peptidoglycan walls stain blue-violet. Gram negative bacteria with thin peptidoglycan walls stain pink-red. Gram negative bacteria have a plasma membrane and an outer membrane.
Steps of gram staining.
1. Crystal Violet
2. Gram iodine - creates bonds
3. Alcohol - sweeps away anything not bonded
4. Safranin
Cell Wall
All bacteria, except for mycoplasma have a cell wall. All bacteria except mycoplasma and chlamydia have peptidoglycan in their cell wall.
gram positive bacteria
thick peptidoglycan wall and techoic acid
grame negative bacteria
thing peptidoglycan wall encased by outer membrane; outer membrane contains lipopolysaccharide (LPS). A component of LPS is lipid A. The outer membrane also has porins.
mycobacteria
have waxy cell walls containing mycolic acid
Mycoplasma
have no cell wall - just a membrane (and that membrane has cholesterol in it like our cell membranes)
Spores
Contain dipicolinic acid; can survive for thousands of years
Capsules
a layer of meshed molecules around the bacterium - external to its cell wall. Only some bacteria have capsules. Another type of outer covering is known as a slime layer.
Bacterial toxins
Endotoxin, also known as lipid A of LPS. Poor antigen because not protein. Heat stable because not a protein.
exotoxin
polypeptide is made of proteins. Produced and released by the bacterium. Very specific in its effect - different effects with different eotoxins. Very antigenic because is a protein. The body has the most vigorous immune responses, complete with antibody production, to substance comprised of proteins. Therefore, a deactivated version of exotoxin, known sa a toxoid, is used as a vaccine for some of diseases associated with exotoxin production. Usually heat labile.
Exotoxin
Polypeptide toxin, produced and released by the bacterium. Very specific in its effect - different effects with different exotoxins (as opposed to endotoxins that all have the same effects). Very antigenic because it is a protein, the body has the most vigorous immune responses, complete with antibody production, to substances comprised of proteins --> therefore, a deactivated version of exotoxin, known as a toxoid, is used as a vaccine for some diseases associated with exotoxin production, ie for protection against --> corynebacterium diphtheriae, clostridium tetani, and bordetella pertussis. Usually heat labile because it is a protein.
Tetanus toxin
Produced by clostridium tetani. Blocks glycine and GABA release in interneurons of the spinal cord. Muscle spasms result. Features tetany with lockjaw, risus sardonicus, opisthotonos, tetanic paralysis of respiratory muscles.
Botulinum toxin
Most potent exotoxin. Produced by clostridum botulinum. Blocks release of ACh at the neuromuscular junctions. Muscle paralysis (flaccid) results. Features constipation, the descending flaccid paralysis, flaccid paralysis of respiratory muscles.
Diphtheria toxin
Inhibitis protein synthesis in human cells. Produced by corynecbacterium diphtheria. Affects throat, then toxin gets into the blood and travels to the heart nad nueral tissues. Inhibitis protein syntheiss in these areas by modifying elongation factor -2. Features: pharyngeal pseduomemrane development and myocarditis with arrhythmias, lifethreatening circulatory collapse and muscle weakness or paralysis, paralysis of pharyngeal muscles leading to regurgitation of fluids through nose and peripheral neuritis/neuropathy.
Alpha toxin, two types produced
clostridium perfringens and staphylococcus aureus.
Staph Aureus' alpha toxin: creates holes in cell membranes, allowing easy transit of substances into and out of the cell to yield eventual cell death. Causes marked necrosis of skin and hemolysis.
C perfringens' alpha toxin = lecithinase: digests lecithin, a phospholipid in cell membrane: this results in massive cell membrane damage and eventual cell death. Causes marked necrosis of deep tissues, especially muscles, and hemolysis.
Toxic shock syndrome toxin
Binds to clas II MHC proteins (HLA) directly without intracellular processing and is a super antigen. Produced by staph. aureus. Inducted cytokines. Features: fever, rash desquamation, diarrhea, then hypotension then shock.
Cholera toxin
Produced by vibrio cholerae. Binds to gangliosides in intestinal cell membranes.
The toxin stimulates Gs protein, which stimulates adeylate cyclase, causing an overproduction of cAMP and secretion of chloride ions and water causing a massive watery diarrhea (without inflammmatory cells in the stool).
Pertussis toxin
Produced by bordetella pertussis, which causes pertussis (also known as whooping cough). the toxin binds to ciliated respiratory tract epithelial cells and to lymphocytes.
Te toxin inhibits Gi protein...ultimately causing lymphocytosis and copious respiratory mucus.
Enterotoxin
Any toxin that causes direct GI pathology with concomitant symptoms. Two major types are produced by E. coli: heat labile and heat stable.
Heat labile stimulates adenylate cyclase via binding to enterocyte gangliosides and Gs protein.
Heat stabile stimulates guanylate cyclase, resulting in increased cGMP, causing a blockade of ion movement from intestinal lumen into enterocytes. Water is drawn into the lumen by the attraction to the excess ions in the lumen.
Obligate aerobes
Must have plentiful oxygen supply to survive. Utilize glycolysis, kerbs cycle, then the electron transport chain. Possess many enzymes for removal of damaging oxygen radicals.
Microaerophilics
Have no oxygen requiremnt, rely on fermentation for metabolism. Are able to tolerate low concentrations of oxygen because they possess superoxide dismutase.
Obligate anaerobes
Have no oxygen requirement. Rely on on non-oxygen dependent mechanisms for metabolism, including fermentation and/or respiration that utilizes molecules other than oxygen. Cannot tolerate any oxygen exposure because they possess no enzymes for removal of oxygen radicals. Wil due upon oxygen exposure.
Facultative anaerobes
Will use oxygen when it is available, but will utilize other metabolic mechanisms when it is not available. When oxygen is available, they function like obligate aerobes metabolically. They possess many enzymes for the removal of damaging radicals. When oxygen is not available, they rely on fermentation. Very versatile organisms that can live in oxygen-rich or oxygen-free nevironments. Includes the largest number of bacterial species.
ETEC - enterotoxigenic E. coli
Enterotoxigenic E. Coli. Secretes LT and ST, therefore, high chloride and water loss from the enterocytes and blockade of ion movement into enterocytes (with water accumulation on the lumen. This leads to severe, watery diarrhea (rice water). Te cause of traveler's diarrhea. Acquired via fecal oral contamination. The toxin is produced in the bowel after ingestion.
EIEC - enteroinvasive E. Coli
organism is ingested an grows in bowel. Invades and enters enterocytes, initiating an immune-mediated reaction leading to fever, WBCs inthe stool, bloody diarrhea, leukocytosis. Acquired via fecal-oral contamination.
EAEC - enteroaggregative E. coli
Acquired via fecal-oral contamination. Causes watery diarrhea. Produces a 'stacked brick' adherence pattern in cultures.
EHEC - enterohemorrhagic E. Coli
Secretes Shiga-like toxin. Causes death of enterocytes that line the bowel. Via the toxin, inhibitis enterocyte protein synthesis, resulting in those cells' death --> bloody diarrhea, abdominal cramps (all together yielding hemorrhagic olitis). The toxin is produced after ingestion in the bowel. Acquired from feces of cattle, sheep, goats, and deer; also via ground beef contaminated with bovine stool. Infection can slo be acquired by contact with those with current infection.
Escherichia coli 0157:H7 - a type of EHEC
has all the abilities as a standard EHEC, plus causes non-immune hemolytic anemia, thrombocytopenia, and acute renal failure --> hemolytic uremic syndrome. HUS is more common in the affected pediatric population.
EPEC
An enteropathogenic e. coli. Acquired via fecal-oral contamination. Organism adheres to bowel wall, but does not invade. Causes severe watery diarrhea that occurs almost exclusively in children < 2 years old.
Enterotoxin A-F
Preformed toxin. The toxin itself is ingested tp roduce the first symptoms in 30 minutes to 6 hours. Responsible for staph aureus food poisoning. Stimulates emetic centers, causing nausea and vomiting. Stimulates peristalsis, causing diarrhea and abdominal pain.
Toxic Shock Syndrome toxin
Fever, hypotension, nausea, vomiting, watery diarrhea, may damage the liver, kidneys, CNS, muscle, or blood cells. A few days after symptoms begin, then a red mascular rash occurs that subsequently undergoes desquamation
Exfoliatin toxin
the toxin responsible for scalded skin syndrome, a disease of young children infected with certain strains of staph. aureus. Causes fever, bullae, and a red macular rash. The middle epidermis of the skin is cleaved, cuasing large areas of skin to slough off along with loss of a lot of fluid and electrolytes; hair and nails may also slough off (recovery usually occurs within 7 to 10 days).
Alpha toxin
forms pores in cell membranes, causing cellular death and tissue necrosis --> skin necrosis and hemolytic anemia.
Group A beta hemolytic strep
Causes 3 possible disease: 1. pyogenic disease with purulent lesions, 2. toxigenic disease with multiple possibilities: high fever with hypotension, necrotizing fasciitis, scarlet fever, tissue necrosis - all due to toxins the bacterium can elaborate. 3. Immunoligc idsease: 2 different possibilities: rheumatic fever with later rheumatic heart disease or post-stretococcal glomerulonephritis.
M protein is a virulence factor that determines the type of Group A beta-hemolytic strep. Interferes with phagocyte ingestion, making Group A strep less subject to our immune defenses. Also determines whether, immunologically, the bacterium will be rheumatoogenic or nephritogenic.
Exotoxins of Group A beta-hemolytic strep
Streptokinase - activates plasminogen to dissolve clots
Streptodornase - DNAse. Produced commercially for use in cystic fibrosis and bronchiectasis patients to decrease thickness of sputum and respiratory secretions by degrading DNA released by dying neutrophils
Hyalurondiase - spreading factor. Digests a major component of connective tissue --> cellulites.
Erythrogenic toxin - causes the rash of scarlet fever. Get fever, rough, erythematous diffuse rash, strawberry tongue, focal streptococcal infection
Streptolysin O - inactivated by oxygen. Is antigenic, stimulating the production of Abs ASO which will also be positive in rheumatic fever. ASO is used in the diagnosis of post-sreptococall glomerulonephritis and acute rheumatic fever since it proves there was a recent infection with streptococcus pyogenes.
Neisseria
Must be cultured on chocolate medium. Oxidase positive.
Neisseria meningitidis
meningococcus
+IgA protease. Encapsulated --> confers antiphagocytic qualities and induces protective Abs (so organism is able to resist immune mechanisms of phagocytosis, allowing for rapid invasion; but, one will eventually develop immunity via antiody production if vaccinated (vaccine is made of capsule components) or previously infected with the meningococcus. The meningococcus has a prticularly rich supply of LPS (endotoxin). Initially causes meningococcmia (by gaining entry to the bloodstream) and then can migrate to meninges to cause rapidly life threatening meningitis. LPS causes fever and shock and launches DIC mechanisms. Waterhouse-Friderichsen syndrome can occur (fever, cyanosis, petechiae, with bilateral adrenal hemorrhage)
Gonococcus - neisseria gonorrheae
IgA+ protease. Not encapsulated, therefore, more easily phagocytosed but no protective antibody developed. So the immune system is usually able to keep it as a focal infection, but no protective antibody is developed, meaning that a person can get gonorrhea as many times as they wish. Purulent urethral dischage or vaginal discharge or rectal discharge or pharyngeal exudates; may also infect eye to cause a purulent conjenctivitis. Untreated gonorrhea in females may lead to PID. Untreated PID ma lead to fitz-hugh-curtis syndrome, RUQ abdominal pain, fever, and violin string adhersions from the liver to either the adnexa or abdominal wall. Transmitted sexually or vertically during delivery. Often the focal infection is asymptomatic in women. Causes ophthalmia neonatorum in infants whose eyes were infect while passing through mother's infected bith canal. Systemic gonorrheal infection rarely results (since it is not encapsulated, and our immune system easily keep it focal via phagocytosis). Outcomes are gonococcal arthritis or tenosynovitis (inflammation of tendon sheath with pain, redness, or warmth).
Bacillus anthracis
zoonotic, it's spores persist for many years in soil. Spores often transmitted on herbivore products since the spores are liberated from soil as the herbivore razes. Produces anthrax toxin with 1. edema factor, 2. protective antigen, 3. lethal factor.
Cutaneous anthrax
most common form; at site of entry, painless ulcer with a black crust (eschar) with massive local edema. The entire lesion is 'malignant pustule'. Most resolve spontaneously, but some do progress to bacteremia then death.
Pulmonary anthrax
Woolsorter's disease, after spores are inhaled, they germinate. Get a dry cough, swevere dyspnea, fever, malaise, rapidly progresses to hemorrhagic mediastinitis, mediastinal widening on x-ray, bloody pleural effusion, septic shock and death.
Gastrointestinal anthrax
spores are ingested and germinate. Leads to vomiting, abdominal pain, blood diarrhea, shock, and death. Get from consuming contaiminated meat. Spore is heat resistant so can't prevent by cooking.
DOC for anthrax
Penicillin if the organism is penicillin sensitive. Vaccine available to military
Corynebacterium diphtheriae
produces diphtheria toxin if infected with a bacteriophage. Causes diphtheria if it elaborates the toxin during infection. Signs and symptoms: pseudomembrane in throat, fever, myocarditis, paralysis. Must culture on loeffler's telluride. When viewed microscopically, appear club-shaped and appear arranged in chinese character formation.
Listeria monocytogenes
affects primarily neonates, immunosuppressed, and pregnant women. Chinese character formation with tumbling movement. Causes sepsis and meningitis in newborns, abortion or premature delivery in pregnant women, or gastroenteritis in anyone without optimal immuen system function. Most common sources: unpasteurized dairy products.
clostridium species
obligate anaerobes: different species cause different diseases: tetanus - clostridium tetani
botulism clostridum botulinum
gas gangrene - clostridium perfringens
food poisoning - clostridium perfringens
pseudomembranous colitis - clostridium difficile
lactobacillus
causes dental caries via polymicrobial infection. Produces lactic acid, protecting the GI tract and vagina by maintaining an acidic environment that is inhospitable to many pathogens. Maintains acidic pH.