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233 Cards in this Set
- Front
- Back
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How does the bacterial (prokaryotic) cell differ from that of humans (eukaryotes)?
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-dsDNA, single circular chromosome
- Not contained within nucleus, general region= nucleoid - plasmid may be present - only contains ribosomes for protein synthesis - has cell wall & capsule |
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What is a "plasmid"? Are they present in all bacteria?
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An extrachromosomal, usually circular, DNA molecule. It can confer genes of resistance to bacteria by integrating with the bacterial chromosome.
Not present in all bacteria! |
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Why are antimicrobials (such as aminoglycosides), able to particularly target and kill bacteria?
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They target the unique Ribosome of Bacteria (a 70S Ribosome), thus preventing protein synthesis and growth of the organism.
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What are the functions of the bacterial plasma membrane?
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1. Electron transport-Energy (contains enzymes for cell respiration)
2. Regulates movement of material into & out of cell 3. Involved in synthesis of cell wall & coordination of DNA replication |
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What is a capsule and what is it's function?
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A loose polysaccharide or protein layer that surrounds bacteria (lies outside the cell wall).
1. mediates adherence of bacteria to cell surface 2. protects bacteria from phagocytes or detergents |
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What are the two major components of the bacterial cell envelope?
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Plasma membrane + cell wall
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What is the function of fimbriae (pili)?
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Short hair-like structures that are involved in attachment of bacteria to specific host.
Also can enhance virulence of bacteria. |
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What is a "slime layer"?
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Capsule that is loosely adherent and less dense. It is a secreted polysaccharide capsule.
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What is the role of flagella?
What are different types of flagella? |
Motility (also can be antigenic)
- Polar (single), Lophotrichous (multiple), Peritrichous (hariy all over) |
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What process of replication do most bacteria use?
What critical structure must form between bacteria that allows for formation of identical daughter bacteria? |
Asexual reproduction- binary fission
Septum must form from invagination of cell membrane. |
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What is the function of the cell wall?
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To protect the cell from mechanical damage (such as lysis and osmotic rupture)
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What is the structural component of bacterial cell walls?
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Peptidoglycan= murein
= a polymer of sugars that is cross linked by short chains of amino acids or peptides. |
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What are the two alternating molecules that make up peptidoglycans called?
What type of molecule are they (polysaccharide, protein, etc.)? |
N-acetylglucosamine (G)
N- acetylmuramic acid (M) These are polysaccharides (glycan backbone). |
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Why do the staining characteristics of gram+ vs. gram- bacteria differ?
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Gram+: has a thick outer wall due to pentaglycine bridge so crystal violet and iodine dye will not diffuse out. Stains dark purple.
Gram-: has a thin outer wall (no pentaglycine), so dye diffuses out. With Sarafin red counter stain, it shows up pink. |
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T or F
All bacteria are either gram + or gram- |
False
There are atypical bacteria that are neither gram+ or gram - There is also mycobacterium that has a waxy material to cell wall and stains by "acid fast". They can retain carbolfuchsin after washed by alcohol which doesn't affect their cell wall. |
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What are some different shapes of bacteria?
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Spheres (coccus)
Rods (bacillus) Vibrio (sort of boomerang shape) Spiral-shape (spirochete) |
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What are siderophores?
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Small molecules secreted by bacteria that bind iron. These bacteria can compete with the host for iron.
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Most pathogenic bacteria grow in what type of temperature and pH condition?
What are they called? |
Mesophiles
grow at intermediate temperature and neutral pH range (compatible with host body). |
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What is the difference between Aerobic and Anaerobic bacteria?
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Aerobic- final electron acceptor is oxygen (they get energy from respiration!)
Anaerobic- final electron acceptor is some other organic/inorganic compound, not oxygen. They get energy by fermenting. |
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What makes a bacteria an obligate anaerobe?
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Obligate anaerobe- cannot grow in presence of oxygen.
They lack enzymes that will detoxify oxygen radicals (superoxide dismutase, catalase or perioxidase) |
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What is an aerotolerant anaerobe?
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An anaerobe that is indifferent to the presence of oxygen. It contains the enzymes that detoxify oxygen free radicals.
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What kind of energy requirements do most pathogenic bacteria have?
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Most are facultative organisms (meaning that they will use oxygen when available but they can also ferment in it's absence).
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How do superoxide dismutase, catalase, and peroxidase fit together in terms of preventing free radical damage?
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Free radicals are turned into H2O2 by superoxide dismutase.
Catalase and Peroxidase break down H2O2 to water and oxygen (thus they detoxify the free radicals). |
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What are "sterile spaces" of the human body in which bacteria or micro-organisms should never be found?
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CSF, blood, lung, deep tissue, brain, and muscle
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What parts of the body are heavily colonized by bacteria?
How do they differ from parts that are only "colonized"? |
Heavily colonized- direct contact with extracellular environment (ex: mouth, skin, vagina, colon)
Colonized= small intestine, trachea, stomach (not in direct contact with outside) |
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Why do some women who are prescribed antibiotics get Candida or yeast infections in their vagina?
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Normal lactobacillus like to live in the vagina (acclimated to more acidic pH).
If they are killed by antibiotics they can no longer protect against opportunistic yeast like candida. |
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What are three possible outcomes that occur when an individual is exposed to an organism, including normal flora?
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1. TRANSIENTLY colonize the person (ex: washes away from skin)
2. PERMANENTLY colonize person (ex: normal flora in GI tract) 3. PRODUCE DISEASE (directly damage host cell or use toxins) |
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What are the three major roles of normal flora?
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1. Provide nutrients (synthesize and excrete vitamin K and B12). Also aid in digestion and absorption of nutrients.
2. Stimulate immune system (particularly humoral, IgA response in infants. They have antigens that can cross react with related pathogens and stimulate immune response). 3. Antagonize other bacteria (produce toxins to kill other bacteria or compete for essential attachment sites and receptors). |
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What is the definition of "pathogenicity"?
What is "virulence"? |
The ability for an organism to produce a disease in a host.
Virulence= degree of pathogenicity |
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What is required for a bacteria to attach to a eukaryotic cell surface?
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1. receptor on host cell to bind
2. Adhesin on the invading pathogen that will bind recpetor |
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What are examples of Adhesins?
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- Pili
- Outer membrane protein (ex: - M protein of Streptococci) Polysaccharide capsule |
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T or F
A small inoculum is enough for a pathogen to cause disease? |
False!
Rarely does a pathogen cause disease without first multiplying (exception= intoxication, ex: botulism) |
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What are superantigens?
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Toxins that activate T cells directly without requiring antigens. They can cause release of lots of cytokines and interleukins resulting in toxic shock syndrome.
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What are examples of exotoxins?
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Exotoxins= secreted outside cell wall
-cytolytic or membrane disrupting enzymes - superantigens - A-B subunit toxins |
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What are examples of endotoxins or cell wall toxins (in the case of gram + organisms)?
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Toxins that make up part of the bacterial cell wall:
Gram +: Techoic acid, Lipotechoic acid Gram -: LPS |
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What are two main mechanisms a bacteria uses to escape host defenses?
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1. Evasion of phagocytosis and complement (ex: anti-phagocytic capsule)
2. Intracellular growth (by growing in a cell, they can escape host defenses) |
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What is an A-B toxin?
Give an example of a single and complex A-B toxin. |
Dimeric protein with A and B subunit in which-
B= Binding subunit (recognized specific receptor) A= enzymatically active subunit released into cell - Single: botulism, tetanus, diphtheria - Complex: A:5B cholera |
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T or F
It takes a high concentration of bacterial toxins to kill a person. |
False!
Bacterial toxins work at low concentrations (1g can kill 10 million people in the case of Botulism!) |
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What are the most common or important gram+ rods (break them down into spore-forming and non-sporeforming)?
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Spore-forming:
- Aerobes: Bacillus cereus, B. anthracis -Anaerobes: Clostridium perfringens, C. difficile, C tetani, C. botulinum Non-sporeforming rods -Corynebacterium |
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What type of bacteria is Clostridia (Gram, oxygen requirement, spore or non spore, shape)?
Where can it be found? |
Gram +
obligate anaerobe spore forming rods Found in environment (soil, water, sewage, animal intestine) |
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What is an endospore?
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Dormant form of an organism, typically generated during periods of stress.
Under favorable conditions, spores will germinate. |
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What is the difference in the appearance of C. tetani, C. perfingens and B. anthracis (all there are spore-forming, gram + rods)?
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C tetani- looks like tennis racket
C.perfingens- centered spore B. anthracis- rods are elongated and more connected looking |
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What is the structure of a bacterial endospore?
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1. Core contains bacterial chromosome, ribosome, and enyzmes for protein synthesis.
2. surrounding wall of peptidoglycans (Core wall) 3. Cortex and spore coat |
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What type of bacteria is C. botulinum (Gram, oxygen requirement, spore or non spore, shape)?
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Gram+
obligate anaerobe Spore forming rod |
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A patient presents with floppy legs and difficulty breathing is brought to the emergency room by her roommate. Several hours before, her roommate indicates she cooked peas on the stove which she obtained from a can. What condition might she have?
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Botulism (anaerobic, so comes from canned food which is kept air tight).
Likely that contaminated food wasn't heated properly and toxins survived. |
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T or F
In order for bacterial infection to occur through intoxication, the bacteria must always replicate within the host. |
False!
Intoxication is NOT a true infection. These bacteria don't have to replicate and can cause symptoms simply by the production of toxin. |
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What are two ways the the C. botulinum bacteria can establish an infectious niche?
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1. Intoxication (preformed toxins themselves mediate symtpoms)
2. Infection (bacteria absorbed through gut, lung, or open wound and will germinate and form toxins) |
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What is the pathogenesis of flaccid paralysis, the classic symptom of botulism?
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B subunit binds to pre-synaptic motor neurons (at neuromuscular junction)
A subunit is released within neuron and acts as protease, interfering with synaptic vesicle release of Ach. This prevents muscle contractions and results in paralysis. |
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An anxious mother bring in her 9 mo. old child. About an hour ago, she noticed that her child, who had been constipated, began drooling and seemed "floppier" when she tried to hold her. Now, in the ER, she is weakly crying and her eyes are drooping. A history reveals that the child is beginning to teeth and mom gave her a teaspoon of raw honey to sooth her gums.
What might the child have and what is the treatment? |
Infant Botulism cause by spores of C. Botulinum that live in honey.
Treatment= BIG-IV or botulinum immunoglobulin given parenterally |
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What is the principal clinical symptom of the disease caused by C. Tetani?
How does the bacteria enter the host? |
Spastic Paralysis (Tetanus)
Typically enters host through penetration of foreign object (dirty wound, rust nail scrapes skin). |
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How is it that stepping on a rust nail can cause CNS symptoms like spastic paralysis?
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Organism is localized but toxin travels to distant target.
Targets the Presynaptic motor neurons and inhibits release of Glycine and GABA (inhibitory NTs).This results in a constant contracted state. |
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A 45 year old homeless male is brought in to the ER and is experiencing spasms in his neck, back, and jaw. Unfortunately he undergoes respiratory failure and subsequently expires. Your team does a thorough examination of the tent he has been sleeping in and find open needles and recreational drugs.
What did he die from and how could it have been prevented? |
Classic case of Tetanus. Homeless tend to have open wounds and sores, in combination with use of dirty needles increase risk of tetanus.
He presented with spastic paralysis and died of respiratory failure (spasm of diaphragm). Could have been prevented with a tetanus vaccination (DPT). |
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In tetanus, do you expect to see face/jaw involvement or limb involvement first?
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Face/jaw- can present with lock-jaw or trismus in which the masseter muscle is contracted.
In more progressed cased you will find arching of back and legs (flexor>extensor) |
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What is the most common species of Clostridium seen clinically (note, it is also the major pathogen of wound infection)?
What does it look like? |
Clostridium perfringens
Roads, gram+, look like "boxcar" or rectangular |
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T or F
Identification of C. perfingens in a patient's vaginal tract is reason for immediate treatment. |
False!
It is part of the normal flora in vagina and GI tract. |
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What diagnostic measure can identify the C. perfringens pathogen?
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Culture on a blood agar medium will reveal a "double-zone of hemolysis"
alpha= partial hemolysis surrounding beta= complete lysis |
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T or F
C. perfingens (like C. tetani and C. botulinum) produces a single, deadly toxin that is responsible for gas gangrenes or myonecrosis. |
False!
It produces multiple exotoxins (at least 12). |
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Which cytotoxin, produced by C. prefringens is responsible for production of myonecrosis (gas gangrene)?
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a-toxin (Lecithinase)
It lyses endothelial cells, RBC, WBC, and platelets by hydrolyzing the cell membrane components. Produces gas, H2 and CO2 via fermentation process which accumulates in subcutaneous space and deep tissue. |
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Besides alpha-toxin, what is produced by the C. perfringens bacteria and what effects do they have on the body?
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Degradative enzymes: proteases, DNAses, etc. liquify the tissue and promote spreading of bacteria.
Cause necrosis and dissemination of infection. |
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A patient is brought to the ER in severe pain. Exam reveals a necrotic, gangrenous lesion along his foot which he claims was fractured during a car accident. The patient has sustained multiple other compound fractures on his body. You palpate the skin around the lesion and feel crepetations.
What organism might be causing his clinical presentation? |
Clostridia perfringens- can introduce into deep tissue sites during severe trauma/compound fracture/ open wounds.
The crepetation is from gas bubble forming subcutaneously. |
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What is myonecrosis?
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A gas gangrene formed by toxins from C. perfringens that cause tissue destruction and build up of gasses.
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A patient is hospitalized for a bacterial infection and is put on antibiotics. Several days later, she has watery stool and complains of stomach cramping.
What agent is causing the problem (be as specific as possible)? |
C. difficile (leading cause of antibiotic-associated diarrhea in hospitalized pts). Also causes pseudomembranous colitis.
Specifically Toxin A (which is an enterotoxin) |
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What are the two toxins produced by PATHOGENIC strains of C. difficile?
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Toxin A: enterotoxin (causes diarrhea, excessive fluid secretion)
Toxin B: cytotoxin; causes inflammation and pseudomembrane formation |
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A gross section of an ulcerated lumen of a colon shows white, fibrinoid plaques, mucus, and polys/inflammatory cells. Testing on the sample comes back positive for C. difficile.
What is this gross finding called and what toxin of C. difficile do you suspect caused it? |
This is a "pseudomembrane" formed by cytotoxin (or Toxin B).
This is characterized by mucus, cell debris and inflammatory cells. |
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What is unique about Corynebacterium diphtheriae that distinguishes it from the other toxin-producing, gram+ rods?
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It does NOT produce spores
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What part of the body is preferentially infected by Corynebacterium diphtheriae?
What does it form? |
The throat
Forms a pseudomembrane (thick, grayish exudate that adheres to throat and is made up of mucous and inflammatory cells). |
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What is the pathogensis of Diphtheria toxin (i.e. how does it work)?
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B binds receptor and A+B enter via endocytosis.
A is released (via cleavage) and interferes with cell protein synthesis by ADP ribosylation of EF2 (elongation factor 2) |
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What does the DPT vaccine stand for?
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Diphtheria, Pertussis (whooping cough), and Tetanus
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A 10 year old boy from rural Kansas is brought to the ER. He has been complaining of a sore throat. His respiratory rate is 32 and he is febrile. Examination shows a grey-black, thick, fiber film on the back of his airways. Social Hx reveals that his parents are part of the Christian Scientists movement and as such, refuse antibiotics or immunization.
Throat culture comes back positive for a bacterium. What is it? |
Corynebacterium diphtheriae (note pseudomembrane on throat)
Most children in US are vaccinated for DPT. |
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What is a strict pathogen?
Give some examples. |
A pathogen that is not part of the normal flora and only causes damage.
Ex: Nisseria gonorrhea and Mycobacterium Tuberculosi |
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What is the hallmark of pathogenic bacteria?
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The ability to induce damage from:
- host response (cytokines, inflammation) - bacterial production of toxins |
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T or F
Only gram+ bacteria secrete exotoxins? |
False
BOTH Gram+ and Gram- bacteria can form exotoxins. |
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What are three classes of exotoxins?
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1. Cytolytic or membrane disrupting enzymes
2. Superantigens 3. A-B Subunit toxins |
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What are the three most medically important types of Staphylococcus organisms?
Which make exotoxins? |
Staph aureus (grapes of wrath)- most virulent
S. epidermidis* (can be opportunistic, stick to catheter because of slimy capsule) S. saprophyticus* (can cause UTI in sexually active women) * do not make exotoxins |
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What does staph look like when gram stained?
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Gram +, looks like dark bundles of grapes
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Where is staph found in the body?
Why is it particularly dangerous in a hospital setting? |
Everywhere (ubiquitous)
Dangerous because it colonized nasopharynx and many hospital workers carry it. It can cause nosocomial or hospital-acquired infections in compromised pts. |
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What is the role of coagulase in bacteria?
What is the "Coagulase" test used for? |
Coagulase is enzyme that clots blood plasma (converts fibrinogen to fibrin). In bacteria it forms a protective fibrin barrier around bacteria.
Coagulase test used to distinguish Staph Aureus from Strep and Enterococci. Staph Aureus is coagulase + |
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What is the role of catalase in bacteria?
What is the "Catalase" test used for? |
Catalase turns H2O2 into H2O + Oxygen. This neutralizes the oxygen free radicals that phagocytes use to kill bacteria.
Catalase test distinguishes Staph from Strep. Staph contains the enzyme so it forms O2 bubbles. Strep does not. |
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What is an abscess?
Why is it a 'civil war zone'? |
Enclosed Collection of Pus
Pus= dead bacteria, neutrophils, enzymes (from polys), and tissue that's been damaged The bacteria are protected from the immune system because they are in an enclosed space but the immune system is walling them off to keep them from causing damage. Need to use antibiotics or drain the abscess. |
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What is MRSA?
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Methicilin Resistant Staph Aureus
It is a strain of Staph the is becoming a superbug. It has incorporated a gene that encodes a penicllin-binding protein which confers resistance to methicilin. Now starting to be present in the community and not just in hospitals. |
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What three things must a bacteria be capable of in order for it to be pathogenic?
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1. Evade phagocytosis
2. Produce surface proteins to mediate attachment 3. Produce specific toxins |
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What structural components of Staph allow it to adhere to the host cell?
What does it bind to on the host? |
Teichoic acid and surface adhesion proteins
Bind to host matrix proteins (fibronectin, fibrinogen, elastin, collagen) |
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What are two very important strutural components that provide defense for Staph?
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Protein A (bind the Fc portion of antibody and prevents clearance)
Capsule (block antigenic determinants and block opsonization or phagocytosis) |
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What are the cytolytic or membrane-damaging exotoxins made by S.aureus?
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They damage the cell membrane-
1. Alpha toxin (punch hole in blood cells) 2. Panton-Valentine Leukocidin (lyse polys and macrophage, found in MRSA) 3. Beta toxin (sphingomyelinase C- lyse membrane phospholipid) |
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What are exfoliative toxins A and B?
What devastating syndrome can they cause in neonates and young kids? |
Serine proteases secreted by S. aureus. Separates layers of epidermis at desmosomes.
Causes peeling of skin and SSSS (Staphylococcal scalded skin syndrome) |
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What is a Superantigen?
How do Superantigen Toxins work? |
Superantigen = antigen that hyperactivates Th cell
Binds outside of groove, Variable B (VBeta) molecule of TCR. Superantigen Toxins cause the hyperactivation of Th cells and release of cytokines leading to major systemic effects. |
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What is Toxic Shock Syndrome?
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Superantigen TSST-1 (Toxic Shock Syndrome Toxin-1) stimulates release of cytokines. Can cause vascular permeability and toxin enters blood stream.
* found in women who leave tampons in for a long time. Staph aureus can colonize vaginal tract and produce these toxins that spread. |
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What type of toxin is Staph aureus's "Enterotoxin"?
What strain is most commonly associated with food poisoning? |
Superantigen
Enterotoxin A is most commonly associated with food poisoning. Resistant to heat and hydrolysis by gastric enzymes * VERY IMPORTANT, NOTE: caused by intoxication (toxin spreading) instead of infection (bacteria spreading) |
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What are the major enzymes produced by Staph aureus?
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1. Immune evasion (coagulase, catalase)
2. Invasins (Hyaluronidase, collagenase, kinase) 3. Penicillinase (Beta-lactamase)- contribute to resistance |
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What is the role of "Hyaluronidase" produced by S. Aureus?
What is the role of "Kinase" produced by S. aureus? |
Hyaluronidase (hydrolyzes hyaluronic acids present in connective tissue, so bacteria can get through CT layer)
Kinase (When bacteria wants to be released from protective coagulase clot, kinase will break open clot). |
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What does Streptococcus look like on a gram stain?
Is it Catalase positive or negative? |
Gram +
Seen in pairs or in chains (GAS= pear like, round. GBS= strep agalactiae more elongated) Catalase Negative |
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What is the most virulent strain of Strep?
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Strep A = Streptococcus pyogens (GAS). Individual cells look more circular.
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Describe how Strep is classified based on Hemolysis.
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Use a blood agar colony, look for hemolytic patterns:
1. Alpha hemolytic- partial clearing with greenish discoloration (Viridans- strep pneumoniae) 2. Beta hemolytic- complete clearing, group A and B 3. Gamma hemolytic- non hemolytic, no color change |
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What are the lancefield groupings?
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Classification of Strep based on cell-wall antigenic structure of bacteria.
"Lancefield antigens" = typically identify pyogenic or Beta hemolytic strep (GAS and GBS) |
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What type of hemolytic pattern do Viridans Streptococci have?
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Alpha-hemolytic, produce a green pigment on blood agar medium (no Lancefield group)
*NOTE: important in dental caries, endocarditis, etc. |
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How does the bacterial Capsule promote Virulence?
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1. Interferes with complement and opsonization
2. Inhibits the effects of phagocytic cells (hydrophilic capsule resists hydrophobic phagocyte) *capsule is hydrophilic vs. hydrophobic phagocytic cells |
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What are the most common and clinically important species of Enterococcus?
What is a particularly severe complication of these bacteria? |
E. faecalis and E. faecium
*commonly recovered from human and animal feces. They can cause ENDOCARDITIS |
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There are two classes of Haemophilus influenzae. What are they?
Which serological type is considered the most potent and associated with meningitis, epiglottitis, and cellulitis? |
1. Nonencapsulated- normal flora, no invasive disease
2. Encapsulated- 6 serological types (a-f), Hib (or type b) is associated with invasive disease |
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What family of Strep does Streptococcus pneumoniae belong to?
What does it look like? |
Viridian Streptococci (alpha hemolytic and generates green pigment)
Gram +, encapsulated lancet-shaped, diplococci |
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Does the encapsulated or the non-encapsulated strain of H. influenza have a higher carrier rate?
Where does H influenza tend to colonize in the body? |
Non-encapsulated (because it is part of the normal flora and also the encapsulated is more virulent)
Nasopharynx. |
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Were does H. flu tend to colonize?
What medical conditions is it most frequently associated with? |
Nasopharyx
Lower RTI (pneumonia) Upper RTI (otitis media, bronchitis, sinusitis, laryngitis) Also causes bacteremia (b/c of capsule) and meningitis |
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What two things does H. flu produce that will help it destory epithelial cells and invade the local mucosa?
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IgA protease (allows it to evade mucosal antibody)
LPS (an endotoxin on gram- bacteria, impairs ciliary function) |
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How come a person who has had pneumonia, can get pneumonia again?
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There are a large number of serotypes of pneumonia (>80)
(serotypes based on diversity of polysaccharide capsule) |
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What is the Capsule of H. flu made of (something special)?
Why is it that young children < 3 years need to be given a special Hib vaccine that is conjugated to a protein? |
PRP (polyribosephosphate- ribatol + ribose + phosphate)
Young kids do not generate efficient antibody response to carbohydrate antigen. Protein (toxoid) conjugation allows immature immune system to respond |
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Is S. Pneumoniae a catalase + or catalase - bacteria?
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It is catalase - (it does not have the specific enzymes to break down Hydrogen Peroxide). Rather, it uses H2O2 to it's advantage to damage other microflora and take over the environment.
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How is S. Pneumoniae transmitted?
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Droplets of respiratory secretions. Hand contaminated with secretions.
*Asymptomatic carriers should be aware when living in a house with children/ susceptible individuals |
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S. Pneumoniae has many important virulence factors.
Which factors help promote survival early in infection? |
- Capsule (antiphagocytic)
- Secretory IgA protease (break down IgA so it can survive in the epithelium) |
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Does S. Pneumoniae produce endotoxins/exotoxins?
What virulence factors of S. pneumoniae help in tissue destruction? |
No- elicits acute inflammatory response
Pneumolysin- Pore forming toxin that damages epithelial cells (impairs mucocilliary clearance, intracellular- not secreted) Degradation and release of cell wall components (lipoteichoic acid)- cytokine release |
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What does Haemophilus influenzae look like?
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Small, gram-, rod. looks pleomorphic
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How is H. Ducreyi transmitted?
What clinical symptoms does it result in? |
Sexually transmitted (skin/mucous membrane contact)
Causes chancroid *vesicles, ulcers. Also painful inguinal lymphadenopathy (bubos) |
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What condition is H. Aegyptius most commonly associated with?
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Conjunctivitis
& Purpuric fever |
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Why is it difficult to get rid of intracellular parasites?
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They are protected against antibodies because they live within our cellls.
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What is the shape of mycobacterium tuberculosis?
What special stain can they be visualized on? |
Slim, rod-shaped.
Can be dx on Ziehl-Neelson or Acid fast stain. 1. stain with Z-N 2. decolorize with HCl 3. mycobacteria retain Z-N stain because of high lipid content in envelope |
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Are mycobacteria tuberculosis slow growing or fast growing? Why does this make sense?
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Slow growing
They have a complex cell wall (contains mycolic acid- lipids), takes a while to make |
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Are they aerobes or anaerobes?
Are mycobacteria catalase positive or negative? |
They are obligate aerobes (must live in the areas with lots of oxygen, that's why they tend to colonize lung)
Catalase + (must be able to make enzymes that break down O2 free radicals) |
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Describe the complex structure of the Mycobacterium cell wall.
|
Tip
glycolipid ^ LAM= lipoarabinomannan (induces cytokines) ^^ Mycolic Acid (lipid) ^^^ Arabinogalactan ^^^^ Peptidoglycan and cell membrane *note, these cell wall particles make up the PPD test |
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What special medium do M. tuberculosis colonies grow on?
Why do they need this special medium? |
Lowenstein-Jensen agar
They are extremely fastidious organisms, require a lot of things to grow. The agar is rich in carbohydrates. They look creamy/ tan color on plate. |
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What special stain identifies mycobacterium tuberculosis?
How does it work? |
Acid fast stain or Ziehl-Neelson
1. Stain with Z-N 2. Decolorize with HCl 3. Retain Z-N stain (because of high lipid content)- looks like pink colored rods |
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What is the difference in coloration and growth rate between M. Tuberculosis and Nontuberculous Mycobacteria?
|
M tuberculosis is slow growing and non-pigmented
Nontuberculous mycobacteria are all strongly pigmented (bright yellow) and slow growing |
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What cell does M. Tuberculosis preferential inhabit?
What is a major requirement for these bacteria to grow? |
Macrophages
Oxygen! They are obligate aerobes |
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T or F
A person who is colonized by tb will preset with the signs and symptoms of the illness. |
False
Tb can remain latent for years before reactivating and live inside macrophages. |
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Describe the process by which a granuloma is formed during infection with mycobacterium tuberculosi?
What is another word for a hard, node like granuloma? |
1.Mycobacterium ingested by alveolar macrophage
2. Macrophage tries to kill but can't, activates CD4+ t cells 3. They secrete INF-g to rev up macrophages 4. More inflammatory cells are recruited. Eventually Epitheloid macrophages wall off organism and are surround by collar of leukocytes Tubercle |
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What type of necrosis is classically associated with TB?
|
Caseous or caseating necrosis
Necrosis and debris at center of granuloma looks cheesy |
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What happens in people whose tb lesions heal?
What happens in the case of Miliary TB? |
Lesions that heal become fibrotic and calcified. They can be seen as cavitations on a chest xray.
In Miliary TB the organism is not contained and can disseminate through blood affecting other organisms. Multiple tubercles and cavities are seen on a chest X-ray. |
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What is a Gohn complex?
|
Seen on chest xray, the granulomatous lesion or cavity in the lungs that can have central caseating necrosis.
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When you read a ppd or Mantoux test 48-72 hours after planting, what are you looking for and does it indicate disease?
|
Looking for induration (hardening)
Does NOT indicate disease, only hypersensitivity meaning exposure to TB in the past or something that launches Th1 repsonse |
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What patient population do we tend to see MAC or M. Avium Intracelluare complex in?
What does the name indicate about the bacteria and where can you find it? |
Most common opportunistic bacteria in late AIDS patients. Produces disease in the immunocompromised.
Can cause TB in birds, found in soil and water |
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What is an organism for which the armadillo is a natural host?
|
Mycobacteria leprae
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What areas of the body does M. Leprae like to grow on?
|
Skin and superficial nerves (lives in macrophages and Schwann cells, remember it's an intracellular pathogen)
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How is leprosy transmitted?
|
Prolonged exposure and contact with exudates of skin lesion
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What are the two clinical extremes of leprosy?
How are they different and why? |
Tuberculoid: granulomas form but few organisms are present in lesion because the individual has strong cell mediated immune response.
Lepromatous: large number of organisms present, overtake macrophages. Cell mediated immunity is depressed; more severe clinical presentation. |
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What type of bacteria is Legionella pneumophila?
Where does it tend to be found? |
Gram negative rod, with single flagella
It lives in Protozoa that are in aquatic environments. It can be inhaled from contaminated water. |
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T or F
Legionella can be spread from person to person and is thus an important community-acquired cause of pneumonia. |
False
It is an important community acquired cause but it doesn't spread from person to person. It establishes niches and thus might infect a community. |
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What host cell does legionella live within?
What is the pathogenesis of this organism (I.e. How can it escape attack by immune system?) |
Alveolar macrophages
Lives inside macrophages and blocks fusion of phagosome and lysosome. Thus happily replicates. |
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What individuals are most susceptible to infection and colonization of the lung by Legionella?
|
Elderly
Males Smoker Immunosuppressed (HIV, cancer, alcoholism, diabetes, etc.) |
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What histopathologic finding do you see in lung tissue from a person infected with legionella?
|
You will see organism within alveolar macrophage forming a "coiling phagocytosis" - i.e. Wrapping itself up in the ribosomes, ER, mitochondria, etc, and creating replicative vacuole
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What are some pro-inflammatory cytokines?
What are some anti-inflammatory cytokines? In sepsis, which type of cytokine is more plentiful? |
Pro: IL-1, IL-8, INF-g, TNF-a
Anti: IL-10, TGF-B pro-inflammatory >> anti inflammatory |
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T or F
A localized inflammatory response is beneficial whereas a system response is dangerous. |
True
Local = protective, systemic= bacteremia, organ failure, disseminated intravascular coagulation, septic shock |
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What is the catalytic domain of the gram- endotoxin?
|
Lipid A = toxic component of LPS
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Can gram + organisms (staph, strep) also produce septic shock?
Why is it that mycobacteria and other atypical bacteria don't produce septic shock? |
Yes (using techoic and lipoteichoic acid)
Fungi also implicated Atypical bacteria don't produce LPS or any other the components that can elicit shock |
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What is the "O" antigen on LPS responsible for?
|
It is an oligosaccharide antigen; can be species specific
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Describe in step-wise fashion how a lysed gram-negative bacteria can cause sepsis.
|
1. Release LPS into blood
2. LPS binds to a binding protein 3. This complex binds to TLR on macrophage 4. This activates NFkB and induces transcription of IL-1 and TNF 5. multiple inflammatory cytokines are produced and disseminate causing damage to - blood vessels - multi organ failure - adult resp. distress syndrome (ARDS) - DIC |
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LPS can trigger complement activation and the release of specific anaphylatoxins.
What are they? |
C3a, C5a
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What is the shape and pigmentation of Neisseriae?
What are the two pathogenic strains? |
Gram - diplococci, pink in color
1. N. gonorrhea (strict pathogen) 2. can colonize the nasal pharynx but also cause meningits |
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Does Nisseria Gonorrhea have a capsule?
|
No (N. meningitidis does)
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How is N. Gonorrhea spread?
|
Via intimate sexual contact. It cannot survive easily and so must pass through protected mucous membranes.
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Does N. Gonorrhea, like other gram- bacteria, possess the same LPS structure?
|
No. It does not have the "O-antigen", and rather has a highly-branched oligo structure called Lipooligosaccharide (LOS)
LOS= main toxic agent of bacteria! no exotoxins produced |
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What type of agar must you grow N. gonorrhea on?
|
Chocolate colored (aka heated blood, brown colored) agar
aka. Thayer Martin agar. Selective in the sense that antimicrobials inhibit growth of organisms |
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Is gonorrhea a strict human parasite?
How does it attach to the mucosal epithelium? |
Yes (obligate, only survives in humans)
1. pili 2. opa proteins (more firmly attach organism to mucosal cell) |
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What are the steps by which gonorrhea establishes infection?
|
1. Attaches (pili and opa protein)
2. Penetrate and multiply (within endocytosed vesicle) 3. Pass through cell via Transcytosis |
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Gonorrhea's variable structure makes it an ineffective target for vaccines. In what way's is it's structure "variable"?
|
1. Phase Variation: shift in translational reading frame is shifted when gene is moved. Pilin and Opa proteins can be turned On or Off.
2. Gene Conversion: in pilin genes. Can express or silence genes by shuffling chromosome and placing them near promoter. |
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The spread and multiplication of N. Gonorrhea is facilitated by what features of the organism?
Hint: what element might it need being an OBLIGATE intracellular parasite? How does it evade the immune system |
1. IgA protease
2. Iron acquisition (has special, iron stealing receptors) 3. Antiphagocytic properties (pili and opa) 4. LOS sialylation |
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N. Gonorrhea doesn't have a true capsule but it is able to protect itself.
What does it have instead? |
LOS sialylation. Sialic acid is common substrate in host so it protects itself from antibody-complement system.
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What clinical symptoms are associated with N. gonorrhea?
|
- dysuria
- purulent urethral discharge (thick, yellow, painful) - painful intercourse, vaginal discharge, abdominal pain |
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26 year old female medical student comes in to you in pain. You notice swollen looking, joints that are edematous and pus filled. She also has several necrotic skin lesions (grey in center with erythematous base). Of note she had symptoms of abdominal cramping and painful urination for the past two weeks. She is sexually active with one other person and they use condoms 50% of the time.
What do you suspect given her history and symptoms? |
N. Gonorrhea
Most common cause of septic arthritis in young people. Test partner. Other sxs: Dysuria and abdominal pain plus dissemination to other tissues and systemic illness |
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What particularly devastating clinical finding can occur in children infected during birth with N. gonorrhea?
|
Contact with mucous membrane and conjunctiva can cause OPHTHALMIA NEONATORUM.
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Is N. meningitidis an encapsulated or non encapsulated organism?
Can it be found in healthy individuals, immunocompromised people, or both? |
Encapsulated (helps it disseminate)
It can be found in both. It can colonize nasopharynx in some people. |
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|
Patients with spleen injuries might be more closely monitored for meningits and sepsis. Why?
|
Spleen helps digest capsular organisms and antibodies. If spleen is damaged you are not as efficient at getting rid of encapsulated organisms (such as the kind that cause meningitis).
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What is the best method for prevention of N. meningitidis?
Is there any serotype not protected for by this mechanism? |
Vaccination (w/ capsular polysaccharides)
Yes. Antigenically diverse LOS, >14 serogroups. Amongst disease causing groups (A, B, C)- group B strain cannot be protected for. |
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|
What is purpura fulminans?
|
Cutaneous hemorrahgic syndrome with sepsis, typically in neonates with meningococcal infection.
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|
What does the pathogen Pseudomonas aeruginosa look like?
|
Gram - rod, has flagella and ALGINATE (mucoid) capsule
*opportunistic pathogen! |
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|
Where can you find pseudomonas?
|
Widely distributed (environment, hospitals, catheters, etc.)
*Major cause of NOSOCOMIAL infections and pneumonia |
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|
What are the functions of the unique alginate/mucoid polysaccharide capsule of P. aeruginosa?
|
Like any other envelope structure:
- mediates attachment to epithelial cells - inhibits phagocytosis * associated with CF |
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|
There are a variety of toxins produced by P. aeruginosa. Briefly describe the role of the following:
Exotoxin A Exotoxin S |
Exotoxin A: inhibits protein synthesis of host by ADP-ribosylating elongation factor 2
Exotoxin S: also inhibits protein synthesis |
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What is the role of Phospholipase C and Elastase which are virulence factors of P. aeruginosa?
|
Phospholipase C: breaks down lipids, facilitate tissue destruction, stimulate inflammation
Elastase: degrade elastin, cause tissue damage to things like lung tissue |
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|
How do you identify P. aeruginosa in the lab setting?
|
Pyocyanin- blue green pigment. (F) forms tissue damaging free radicals like superoxide dismutase and H2O2
Pyoverdin- yellow green that fluoresces under UV light (F) stimulates inflammation |
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|
What two bacteria are considered obligate intracellular parasites?
|
Chlamydia
Rickettsia |
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|
What is the mechanism by which chlamydia sustains itself within a cell?
What cells does it preferentially invade? |
It prevents phagolysosomal fusion.
Invades mucosal epithelial cells ( nonciliated cuboidal, columnar, or transitional epithelium) |
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|
In what ways is chlamydia considered an "energy parasite"?
|
Grows in cytoplasmic vacuoles b/c unable to make ATP or regenerate NAD.
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|
What are the two morphological forms of chlamydia and in what ways do they differ?
|
EB= elementary bodies (metabolically inactive, INFECTIOUS form. mediates attachment and infection. rigid outer membrane- protection
RB= reticulate bodies (metabolically active, NON-infectious, intracellular, REPLICATIVE form. Fragile membrane) Has flower-like look within a cell |
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|
Does chalmydia stain gram + or gram -?
|
trick question-
It's an ATYPICAL bacteria. Has LPS but doesn't have thin peptidoglycan layer of gram - bacteria. |
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|
What are the 3 major species of Chlamydia and what disease are they associated with?
|
C. trachomatis: trachoma (eye infection), GU tract disease, STI
C. pneumoniae: 'walking pneumonia'- community acquired C. psittaci: acute pneumoia |
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|
Describe the process by which Chlamydia infects cells and disseminated.
|
1. EB attaches to cell surface and is endocytosed
2. EB in endosome DOES NOT FUSE with lysosome 3. EB reorganize into RB which replicates via binary fission 4. RB's then reorganize into EBs 5. EBs are released via reverse endocytosis (pneumonia and trachomatis) or lysis (psittaci) |
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|
What is the leading cause of preventable blindness worldwide?
|
C. trachomatis
- infects epithelial cells of eyes (and genital tract) |
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|
T or F
Chlamydia infects ciliated epithelial cells. |
False!
Non-ciliated epithelial cells (typically columnar) |
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|
What is the most common sexually transmitted disease in the U.S.?
|
Chlamydia
(2nd is Gonorrhea) |
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|
What are the clinical symptoms associated with C. trachomatis?
|
Recurrent genital infections with scarring and mucopurulent cervicitis
(cell mediate immunity leads to necrosis and scar tissue formation) |
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|
What sertoypes cause the urogenital symptoms that occur with chlamydia infection?
What serotypes are responsible for trachoma formation? |
D-K= urogenital
A-C= trachoma |
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|
What is a trachoma?
|
Inflammation. Thickening. Scarring. of tarsal conjunctiva aka. the one that lines the eyelid.
Prevents tear flow (inefficient first line of defense). Eyelids turn inward and eyelash abrade the cornea causing scarring/opacity |
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|
A young man comes in to the ER with acute onset of tender, enlarged lymph nodes in both groins. He is sexually active, has no current girlfriend, and denies IV drug use.
What is the name of this condition, what organism is responsible and which serotypes are involved? |
Lymphogranuloma venerum (LGV)- the lymph nodes are called "buboes"
C. trachomatis involves L1-L3 serotypes |
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|
Psittacosis is a disease transmitted by what?
What is the most typical clinical presentation associated with the syndrome? |
Birds, typically parrots. (inhalation of infected excreta)
Lungs are affected (acute pneumonia), can cause bacteremia and seeding in liver, spleen, etc. Inflammatory response occasionally leads to necrosis and hemorrhage. |
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|
How is C. pneumoniae transmitted?
|
Person-to-person via respiratory droplets
Bronchitis, sinusitis, or walking/atypical pneumonia can result |
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|
What does Listeria monocytogenes look like under the microscope?
What cell does it infect? |
Gram + Rod
does not form spores Macrophages ("monocytogenes") |
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A pregnant woman comes into the office and has what appears to be flu-like symtpoms. She is starting to develop stiffness in the neck and fever. She can't think of anything that might have triggered this except that she ate an old ham sandwich that was in the fridge for over a week.
What is the causative agent? What are you worried about in terms of her baby? |
Listeria monocytogenes
Worried about precipitated labor and premature birth weight. Concerned about exposure to baby if it colonized vagina- can lead to sepsis and meningitis. |
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|
Does Listeria live in cells?
What is the pathogenic mechanism by which listeria infects cells? |
Yes and no. It infects cells but can escape and replicate in cytoplasm.
1. enters gut epithelium/ macrophage 2. "Listeriolysin O" facilitates lysis of phagolysosome 3. Listeria multiplies and assembles actin filament tail 4. Propells to surface of host cell and transfers to other cell via pseudopod extensions. |
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|
What are the three major Gastrointestinal rods that we learned about?
Note: one is a family of enteric rods... |
- Enterobacteriaceae (ex: Escherichia, Klebsiella, Shigella, Salmonella)
- Campylobacter - Helicobacter |
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|
What does campylobacter jejuni look like under a microscope?
What growth conditions does it like? |
- Curved, slender "seagull" or S-shape
- gram negative rod - single, long, polar flagellum - Microaerophilic aka low oxygen conditions (fastidious and slow-growing) |
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|
What is the most common source of infection by campylobacter jejuni?
|
Undercooked chicken (you cannot get it from humans!). Mostly animals who eat infected poop.
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|
What is the leading cause of acute diarrhea (watery or dysenteric) worldwide?
|
C. jejuni
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|
What does Helicobacter pylori look like under a microscope?
What type of growth conditions does it favor? |
- gram neg. rod
- curved and slender - polar flagella (almost like C. jejuni but not s shaped) - microaerophilic (low O2) conditions. |
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|
What cells/tissue does H. pylori tend to colonize?
What is the course of an infection with H. pylori (ie. chronic, fulminating, etc.)? |
Likes to colonize gastric mucosa.
Slow growing, persistent infection. Mostly acquired during childhood and can take years to become symptomatic. |
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|
How does H. pylori survive the acidic environment of the stomach?
|
Produces urease enzyme (produces ammonia which neutralizes HCl)
|
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|
When they do occur, what clinical symptoms can be seen in colonization with H. pylori?
|
- ulcers (peptic or duodenal ulcer, epigastric pain)
- atrophic gastritis (inflammation --> loss of epithelial glands) - gastric cancer (in combination with nitrates, enhance DNA damage) (MALT Lymphomas) |
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|
What do Enterobacteriaceae aka Enterics look like?
Do they produce spores? |
Gram negative rods, short, rounded edge. Most have peritrichous flagella (aka hairy)
NO SPORES. |
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|
What type of growth conditions do the Enterics favor?
|
They are facultative organisms (ferment or respire).
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|
Which of the Enteric species are non-motile (aka no flagella)?
|
Shigella and Klebsiella
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|
Which Enterics are primary pathogens (aka. cause disease in everyone)
Which are strictly opportunists (otherwise part of normal flora)? Are there any that are both? |
Primary pathogen= strict pathogen: Shigella, Salmonella (S for Strict!), Yersinia
Opportunistic pathogen= Proteus Both= E.coli, Klebsiella pneumoniae |
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|
Describe the Lactose fermentation test and what it is used for.
|
Used to identify GI pathogens amongst normal flora
-Eosin methylene blue (EMB) or MacConkey agar -If they are are able to ferment lactose, plate will change color due to lactic acid buildup. Shigella, salmonella (GI pathogens) unable to ferment lactose! |
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|
What do the K, H, and O antigen on the capsule of Enterobacteriaceae code for?
|
K (Vi)= polysaccharide capsule; antiphagocytic and helps adhesion
H: Flagella (not in Shig and Klebs) O: side chain of LPS, promote adherence to GI/GU epithelium |
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|
Does shigella have a flagella?
Is it encapsulated? How is it transmitted? |
No flagella or capsule. It is a small GNB
Transmitted via fecal-oral contact (person-to-person, or from contaminated food/water). * MOST contagious bacterial diarrhea!!!! |
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|
What disease does Shigella cause?
Which strain of Shigella produces high levels of the Shiga toxin? |
Shigellosis (bacillary dysentery)= Bloody, mucous feces w/ intestinal pain
S. dysenteriae |
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|
How does Shigella survive passage through the stomach?
What cells does it invade? |
It is acid-resistant.
Invades intestinal epithelial cells which triggers potent inflammatory response. |
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|
How do Shigella reach the basal surface of intestinal cells?
|
1. Enter M cells (APCs in the peyers patches) with help of Ipa proteins
2. Lyse phagocytic vacuole and replicate in cytoplasm 3. Use actin filaments to propel to adjacent cell. Also can enter lamina propia. 4. cell death causes focal ulcer and inflammatory cells + RBC pour into lumen |
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|
What are Ipa proteins?
What is a Type III secretion system? |
Invasion plasmid antigens (proteins that help facilitate attachment)
Type III secretion system= molecular syringe. Bacteria injects Ipa proteins into cells causing membrane ruffling of M cell and engulfment. |
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|
How does shigella get through the epithelial tight junctions?
|
When it lyses M cell it is able to release pro-inflammatory cytokines that increase vascular permeability. It takes advantage and migrates through to adjacent cell.
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|
What type of toxin is Shiga Toxin?
How does it cause dysentery and diarrhea? |
It is a cytotoxin (kills intestinal epithelial and endothelial cells).
A-B toxin (1A:5B)- cleaves host ribosomal RNA, thus blocks protein synthesis. * decreased Na+ absorption leads to H2O buildup and diarrhea |
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|
What species of Salmonella is known to cause gastroenteritis?
What species causes Typhoid fever? |
S. enteriditis (cause gastroenteritis)
S. typhi and S. paratyphi A and B (cause Typhoid fever) |
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|
Is Salmonella normally found in the gut flora?
How is it transmitted? |
No. It is a strict pathogen.
Transmitted via fecal-oral route. Found in eggs, poultry. Also pet turtles can carry it. |
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|
How does the entry of Salmonella differ from that of Shigella?
|
They both invade M cells and use type III secretion system and can cross the cytoplasm. However, Slamonella does NOT cross adjacently (doesn't use actin polymerization).
It can travel within the macrophage and disseminate (unlike shigella which is more localized) |
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|
What types of symptoms may occur with S. enteriditis infection?
How should you treat it? |
Gastroenteritis (N/ V/ fever)
- non-bloody diarrhea No need to treat- typically self limiting |
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|
What organ can S. typhi or paratyphi chronically colonize?
What clinical symptoms does a person with typhoid present with? |
Gall bladder
Systemic infection, fever, abdominal sxs. Usually acquired from foreign travel. Faint maculopapular rash (rose spots) might develop. Can cause intestinal hemorrhage and perforation. |
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|
What is the most abundant facultative anaerobe in the gut?
It is the important primary pathogen in what three kinds of infections? |
Escherichia coli
Intestinal (diarrhea/colitis) UTI Neonatal meningitis |
|
|
What accounts for the diversity of E. coli?
|
The polysaccharides that make up O antigen (part of LPS)
ex: O157:H7= most commonly identified serotype in U.S. It was a strain that lead to an outbreak in the 1980s. |
|
|
What are the 4 major classes of E. coli?
|
1. Enterohemorrhagic E. coli (EHEC)
2. Enteropathogenic (EPEC) 3. Enterotoxigenic (ETEC) 4. Enteroinvasive (EIEC) |
|
|
What symptoms are associated with EHEC and how does one obtain it?
What is Hemolytic uremic syndrome (HUS)? |
bloody diarrhea, hemorrhagic colitis, HUS
Transmission from animal to human, contaminated meat. HUS= toxin binds to renal tissue and can cause triad of hemolytic anemia, thrombocytopenia, and renal failure. |
|
|
How does EPEC invade?
|
Attaches to microvilli and initiates a process that forms pedestal (involves release of Intimin that makes receptor and then through polymerization of actin, it pushes itself up).
|
|
|
What strain of E. coli is the most common cause of "Traveler's diarrhea"?
|
Enterotoxigenic or ETEC. Can be transmitted through fecal/oral route. Resolves in a few days. Unfortunately, it's an important cause of infant mortality in developing nations.
|
|
|
How does ETEC colonize the intestinal epithelium and cause damage?
|
Uses specialized Pili called CFA (colonization factor antigen) to mediate attachment.
Has enterotoxins (Heat labile and heat stable) that prolong secretion of Cl ions and water enters lumen. |
|
|
Which type of E. coli can be endocytosed into cell and is an uncommon cause of bloody diarrhea?
|
EIEC (enteroinvasive)
* note: Humans are the only reservoir! It does not involve toxins and is a self-limiting disease |
|
|
What is the most virulent member of the Strep viridans group?
What is the most virulent of streptococcal group? |
S. pneumoniae
In general: GAS or Group A strep = Streptococcus pyogenes |
|
|
Where is GAS found?
|
Lives on human skin, mucous, can colonize upper respiratory tract (pharyngitis)
|
|
|
What syndromes does Strep Pyogenes cause?
|
Can lead to toxic-shock
Pharyngitis ("strep throat") Meningitis Osteomyelitis Post-strep glomerulonephritis acute rheumatic fever (mimic's heart muscle) |
|
|
Why can someone get multiple strep throat infections throughout life?
|
There are 80+ M protein serotypes.
M protein= two polypeptide chains arranged as alpha helix. It is antiphagocytic (blocks binding of complement to underlying peptidoglycan). |
|
|
In the context of GAS, what is:
Protein F Capsule |
Protein F: fibronectin binding protein
Capsule: non-antigenic, prevents opsonization/phagocytosis (made of hyaluronic acid which promotes immune evasion). |
|
|
Various toxins and enzymes contribute to the virulence of Strep A. Provide the function of the following:
Streptococcal pyrogenic exotoxins (Spe) Streptolysin S Streptolysin O |
Spe= acts as superantigen, enhance proinflammatory cytokines. Responsible for clinical manifestations of strep *toxic shock, rash, etc.*
Streptolysin S= serum-soluble, O2 stable hemolysin. Lyses blood cells, causes Beta hemolysis. Streptolysin O= O2 labile (unstable) hemolysin, Lyses blood cells. ASO= antibodies against streptolysin O. |
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|
What is the role of Streptokinase A and B? What about C5a peptidase?
|
A and B- enzymes lyse blood clots, fibrin, to help S. pyogenes move through infected tissues.
C5a peptidase- disrupts complement pathway's C5a (pro-inflammatory) |
|
|
During the rapid strep test, what is measured?
What is measured by the Anti-ASO blood test? |
Rapid Strep: Antigen (lancefield grouping antigen)
Anti-ASO: looks for antibodies against Streptolysin O, indicated a previous infection (could indicate Rheumatic fever in the patient) |
|
|
What is impetigo and what bacteria can cause it?
|
Purulent infection of the skin (introduced into tissue via break in skin).
|
|
|
What organism causes cellulitis and is often known as the "flesh eating bacteria"?
|
Cellulitis (local inflammation of skin and subcutaneous tissues)
Necrotizing fascitis (strep gangrene)- caused by GAS |
|
|
What are "erysipelas"?
|
Erythros= red, pella= skin
acute infection of skin- erythematous, localized pain and inflammation |
|
|
What is impetigo and what bacteria can cause it?
|
Purulent infection of the skin (introduced into tissue via break in skin).
|
|
|
What organism causes cellulitis and is often known as the "flesh eating bacteria"?
|
Cellulitis (local inflammation of skin and subcutaneous tissues)
Necrotizing fascitis (strep gangrene)- caused by GAS |
|
|
What are "erysipelas"?
|
Erythros= red, pella= skin
acute infection of skin- erythematous, localized pain and inflammation |
