Cell Mediated Immune Response Flashcards, test questions and answers
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How is Tuberculosis transmitted? |
Droplet Nuclei via coughing, highly communicable |
How is the tuberculosis primary infection acquired? |
the person inhales the organisms and they multiply in the alveolar macrophages unaffected by the immune system Hypersensitivity and cell-mediated immunity develop in 2-6 weeks |
What are the typical symptoms of tuberculosis? |
development of a tuberule (microscopic granuloma) in the lung |
What is reactive tuberculosis? |
occurs in the lung apex via formation of pulmonary cavities |
What is the pathogenesis of tuberculosis |
chronic fever, weight loss, night sweats, blood cough along with an extra-pulmonary disease (dissemination to bones and CNS) |
How is tuberculosis diagnosed? |
skin test (PPD) which measured delayed-type hypersensitivity to tuberculoprotein. Tuberculosis can also be diagnosed by serodiagnosis in which the cell-mediated immune response is measured in whole blood samples inoculated with mycobacterial antigens |
What is the treatment for tuberculosis? |
combined prolonged drug therapy to prevent resistance (Isoniazid, Rifampin, Ethamtubol and Pyrazinamide), treatment must be directly observed therapy (watch the patient take his drugs) |
What is the clinical significance of NTM? |
bacteria can cause non-communicable chronic pulmonary diseases, disseminated diseases and cutaneous infections. |
What are the unique characteristics of mycobacteria |
growth rate and recovery time and pigment production in relation to light |
What are the 7 safety precautions to be followed while working in a mycobacteria laboratory? |
(1) negative pressure room (2) biological safety cabinet (3) face mask (4) safety cups for centrifugation (5) splash-proof discard containers (6) disposable loops/needles and (7) proper disposal of waste |
What is used to digest mycobacteria for processing? |
NALC- N-acetyl-L-cysteine |
What is used to decontaminate mycobacteria for processing? |
Sodium hydroxide or benzalkonium chloride and oxalic acid |
What is used to concentrate mycobacteria for processing? |
centrifuge |
What is used to stop the decontaminate process? |
phosphate buffer |
Why do you need to digest, decontaminate and concentrate mycobacteria specimens? |
specimen when plated with be overgrown with normal flora. |
What is the procedure of the auramine-rhodamine fluorochrome stain? |
heat fix the slides then flood with auramine-rhodamine fir 15-20 minutes, rinse with DI water, decolorized with 0.5% acid-alcohol for 2-3 minutes, rinse with DI water, flood with potassium permanganate for 2-4 minutes, rinse and allow to dry |
What are the advantages to the auramine-rhodamine stain? |
Detection is enhanced against a dark background and the slide can be viewed at a lower magnification allowing for visualization of more fields at one time. Another advantage is that you can re-stain with ziehl-nelson to confirm right on the same slide, you do not need a fresh slide |
What are the disadvantages to the auramine-rhodamine stain? |
rapid growers do not always appear fluorescent and you need to confirm with a ziehl- nelson stain. The stained bacteria can also float into the oil and off the slide yielding a false negative |
What is the procedure for the Ziehl-neelsen stain? |
heat fix the smear to the slide, flood the slide with carbol fuchsin stain and steam the slides for 1 minute, keep stain on slides for 4-5 minutes, rinse, decolorize with 3% acid-alcohol, rinse, flood with methylene blue for 1 minute, rinse, and let dry. Red is positive for ziehl-neelsen |
What is the procedure for the kinyoun stain? |
The procedure is heat fix the slide, flood with carbol fuchsin for 5 minutes, rinse, decolorize with 3% acid- alcohol, rinse, and flood with methylene blue for 1-3 minutes, rinse, let dry. |
What is the Runyon classification? |
based on growth and pigment production and is used for NTM |
What are schotochromogens? |
develop pigment in the dark or the light |
Examples of schotochromogens |
M. scrofulaceum and M. gordonae |
What are photochromogens? |
form pigment following exposure to light after being grown in the dark |
examples of photochromogens? |
M. kansasii, and M. marinum |
What are nonphotochromogens? |
nonpigmented whether grown in light or dark |
examples of nonphotochromogens? |
M. avium-intracellulare (MAC, MAI) |
Egg-based solid medias |
Lowenstein-Jensen (inhibits normal flora), Lowenstein-Jensen Gruft modification (added antibiotics) or mycobactosel (antibiotics) |
Serum/agar based solid medias |
middlebrook 7H10/7H11 |
liquid media |
Middlebrook |
The arylsulfatase test principle |
used to identify potentially pathogenic rapid growers, The enzyme arylsulfatase is present in some mycobacteria and the test is used to determine how fast the bacteria can break down phenolphthaliein disulfate into phenolphthalein which forms a pink color in the presence of sodium bicarbonate. |
Which bacteria are arylsulfatase positive? |
M. fortuitum and M. chelonae and slow-growing M. marinum and M. szulgai (14 days) |
The catalase test principle |
Most mycobacteria produce catalase which can split hydrogen peroxide into water and oxygen. The test can be used semi-quantitatively in that if the bacteria can produce 45 mm of bubbles in a test tube is in one group of mycobacteria and if it cannot it is another group. The ability of the catalase enzyme to remain active after heating also separates mycobacteria |
Which bacteria are catalase negative? |
M. tuberculosis, M. bovis, M. gastri and M. haemophilum |
The iron uptake test principle |
utilized to identify rapidly growing mycobacteria capable of converting ferric ammonium citrate to an iron oxide. An LJ slant is inoculated with the organism incubated until visible growth develops, aqueous ferric ammonium citrate added, and the slant incubated for up to 21 days at 37°C. Positive is reddish brown color in the colonies indicates production of iron oxide and Negative shows no color change. |
The niacin accumulation test |
bacterium lacks the enzyme necessary to convert niacin to another metabolite in the coenzyme pathway. A positive test is yellow, a negative is clear liquid. |
Which bacteria is niacin accumulation positive? |
M. tuberculosis |
The nitrate reduction test principle |
The presence of nitrate is detected by production of a red colored product on the addition of several reagents. Development of a pink-red color indicates the presence of nitrite, demonstrating the ability of the organism to reduce nitrate to nitrite. If there is no color then the organism cannot reduce nitrite |
Which bacteria is nitrate reduction positive? |
M. tuberculosis, M. kansasii, M. szulgai and M. fortuitum |
Tween 80 hydrolysis test principle |
detect lipase that is able to hydrolyze Tween 80 into oleic acid and polyoxyethyated sorbitol |
Which bacteria are tween 80 hydrolysis positive? |
Mycobacteria that are positive for Tween 80 hydrolysis are non-pathogenic, slow-growing scotochromogens and nonphotochromogens |
Tellurite reduction test principle |
detect species that can reduce potassium tellurite at variable rates. If the bacteria can reduce potassium tellurite in 3-4 days, it is M. avium complex. All rapid-growers reduce tellurite in 3 days. |
Inhibition of TCH test principle |
used to distinguish M. bovis from M. tuberculosis because M. bovis cannot grow in the presence of TCH. |
The molecular methods used to identify mycobacteria |
DNA hybridization, amplification with reserve hybridization, amplification and restriction enzyme analysis or DNA sequencing and DNA microarrays. |
Susceptibility testing methods for M. tuberculosis |
The proportion method uses standardized inoculums (100-300 colonies) to inoculate the agar-based media which contains antibiotics. It is incubated for 3 weeks and if more than 1% of the inoculums survive it indicated resistance. There is broth based susceptibility testing which take 5 days and probes for resistance genes |
Susceptibility testing methods for NTM |
MIC methods with aminoglycosides and sulfonamides. |
How do you process a sterile specimen? |
centrifuge and use sediment, screen by AFB smear and inoculate one liquid media and one solid media. |
How do you process a non-sterile specimen? |
Liquefaction (NALC), decontamination (NaOH), neutralization (buffer or water), centrifugation, screen by AFB smear and inoculate one liquid media and one solid media. |
What is the tuberculin skin test? |
used to measure delayed-type hypersensitivity to tuberculoprotein (PPD). A positive test indicates that the person was once infected at some time with M. tuberculosis or cross-reacting strain. The value of the test depends on the incidence of primary infections. |

What is pneumococcal meningitis caused by? |
Streptococcus pneumoniae |
Where is Streptococcus found normally? |
In the throat. Part of the normal microbiota. |
This is a Gram+ lancet-shaped coccus. Often seen in pairs. |
Streptococcus Pneumoniae |
Many strains of this bacteria are protected from phagocytosis by a polysaccharide capsule. |
Streptococcus Pneumoniae |
What does Streptococcus pneumoniae commonly cause? |
Otitis media, sinusitus, and pneumonia...any of which can precede pneumoncoccal meningitis. |
What is damage in Meningitis largely due to? |
The sever inflammatory response. Causes brain swelling and clots form in capillaries and block blood supply. |
What is the most deathly form of meningitis? |
Streptococcus pneumoniae |
What is used to treat pneumoncoccal meningitis usually? |
Penicillin |
This bacteria is frequently responsible for epidemics of meningitis. |
Neisseria meningitidis |
Where is Neisseria meningitidis usually found? |
commonly part of the normal respiratory microbiota. |
Symptoms of this are similar to that of pneumococcal meningits, but also may include petechia. (purplish spots on the skin.) |
Neisseria meningitidis |
this can lead to septic (endotoxic) shock |
Neisseria meningitidis |
A gram - encapsulated diploccus. Like Niesseria gonorrhoeae, it can vary in its anitgens and acquire DNA through gene transfer easliy. |
Neisseria meningitidis |
These bacteria attach by pili to mucous membranes and multiply. Proteins in their outer membranes all the bacterial cells to pass through the epithelial lining in the resp tract and into the blood to the meninges. (rare) |
Neisseria meningitidis |
This bacteria releases blebs of the outer membrane and the endotoxin causes vasodilation and capillary leakage leading to drop in blood pressure and septic shock. |
Neisseria meningitidis |
Avoid phagocytosis with capsule |
Neisseria meningitidis |
Person to person transmission via respiratory droplets. Easy transmission in crowded, stressed populations |
Neisseria meningitidis |
Meningitis is the most common result of the food-borne disease of this bacteria |
Listeria monocytogenes |
Infections by this are usually mild in most healthy people. Fever and muscle aches and sometimes nausea or diarrhea. |
Listeria monocytogenes |
Pregnant women who become infected usually miscarry or deliver terminally ill babies. |
Listeria monocytogenes |
A motile, non-spore forming, facultative anaerobis, gram + rod that can grow at 4 degrees celcius. (Can grow on vaccum packed refrigerated foods) |
Listeria monocytogenes |
Mode of entry of Listeria monocytogenes is usually what? |
The GI tract |
These bacteria penetrate the intestinal mucosa through the M cells and into the Peyers patches and into the blood. |
Listeria monocytogenes |
Can be killed with penicillin, but you must catch it quickly, especially in pregnant women. |
Listeria monocytogenes |
This food borne disease can be killed by thouroughly cooking meat. Soft cheeses may carry as well as raw veggies. |
Listeria monocytogenes |
Disfigurement, loss of limbs, and blindness can result from this bacteria. |
Mycobacterium leprae |
Aerobic, rod-shaped, acid fast bacteria. Grows very slowly with a generation time of about 12 days. |
Mycobacterium leprae |
Preferentially infects peripheral nerves. From there the course depends on the persons immune system. |
Mycobacterium leprae |
When the cell-mediated immunity succeffully stops the proliferating bacteria Mycobacterium leprae, the disease is called what? |
tuberculoid leprosy |
When cell-mediated immunity fails to develop or is suppressed. |
lepromatous leprosy |
This bacteria causes a severe form of intoxication that can eventually lead to paralysis. |
Clostridium botulinum |
What does the exotoxin produced by C.botulinum do? What type of toxin is it? |
It is an A-B toxin. The A portion enters the nerve cell and inactivates proteins that regulate the release of neurotransmitter. The B portion binds to specific receptors on the motor nerve endings. |
This is a strictly anaerobic Gram +, spore-forming, rod-shaped bacterium that can cause paralysis if you ingest it. (via its' exotoxin) |
Clostridium botulinum. |
There are several types of neurotoxin that Clostridium botulinum produces. What are three that are key to human cases? |
The A, B, and E type strains |
How does Clostridium botulinum produce paralysis? |
the toxin attaches to the motor neurons blocking transmission of signals to the muscles. |
Where does intestinal botulism usually occur? |
in infants. (Honey!) |
In what way does Clostridium botulinum usually cause death? |
it causes respiratory paralysis. |
Epidemic viral encephalitis is usually caused by what? |
Arboviruses (arthropod borne viruses) |
THis is a group of enveloped, single stranded RNA viruses transmitted by insects, mites or ticks |
Arboviruses |
What are some examples of arboviruses? |
Lacrosse encephalitis West Nile encephalitis eastern and western equinine viruses. |
What type of bacteria is Staphylococcus aureus? |
It is a gram+ cocci in clusters. Coagulase positive. Facultative anaerobes. pyogenic (pus producing) |
Where does Staphylococcus aureus normally reside? |
It is part of the normal microbiota. Up to 20% of healthy people carry it in their nose. |
What can Staphylococcus aureus cause in the body? |
It plays a role in hair follicle infections(boils and carbuncles), Food-borne intoxication, Toxic shock syndrome, and is the leading cause of wound infections. |
What is the medical significance of Escherichia coli? (E. coli) |
Normal microbiota of intestinal tract. Some strains cause 1. urinary tract infections 2. types of intestinal disease 3. some cause meningitis in newborns |
What type of bacteria is E. coli? |
A gram - rod |
What is an exotoxin? |
A protein that a pathogen produces that has very specific damaging effects |
What does STEC stand for? What is the most common one? What does it cause? |
1. Shiga-toxin producing E.coli 2. The most common strain is 0517:H7 3. It causes colonization in the large intestine and leads to Fever, cramps, bloody diarrhea, and some hemolytic uremic syndrome. |
What are ETEC? What do they cause? |
Enterotoxigenic E.coli. THey make pili that allow them to colonize the small intestine. secrete enerotoxins. |
WHat are EIEC? What do they cause? |
Enteroinvasive e coli. They invade the intestinal epithelium and cause disease similar to shigellosis. |
What are EPEC? What do they cause? |
Enteropathogenic E.coli. They produce pili that allow them to colonize the small intestine where they inject effector proteins that cause A/E lesions. |
What are EAEC? What do they cause? |
Enteroaggregative E.coli. THey have pili and adhere to intestinal epith. They grow in characteristic aggregations in a thick mucous associatec biofilm. They produce enterotoxins and cytotoxins that damage cells and cause an inflammatory response. |
DAEC? What do they cause? |
Diffusely adhering Ecoli. like EAEC, but they grow as a diffuse layer. |
What does Streptococcus pyogenes cause? |
Strep throat, scarlet fever, wound infections(Flesh-eating disease). |
What type of bacteria is Streptococcus pyogenes? |
a gram + coccus that grows in chains. Characterized by the A carb in the cell wall. |
What are some of the mechanisms S.pyogenes uses to evade host response? |
a special adhesin to attach, M protein which also interferes with phagocytosis, |
What do Psuedomonas aeruginosa infections cause? |
Opportunistic pathogen. Widespread in environment. health-care assoc infections, and outside hospital. Produces two pigments that color wounds green. |
What type of bacteria is Pseudomonas aeruginosa? |
an aerobic, gram- rod with a single polar flagellum. |
This type of bacteria is a non-invasive, anaerobic gram+ rod that produces am extoxin that prevents inhibitory neurons from releasing their neurotransmitter. (musles contract without control) |
Clostridium tetani |
This is the exotoxin produced by C. tetani |
tetanospasm |
This bacteria causes pain and swelling in wound infections, followed by discharge of a thin brown bubbly fluid and dark discoloration of overlying skin. THe toxin causes tissue necrosis. |
Clostridium perfringens |
This is an alpha toxin producing anaerobe |
C. perfringens |
What does C. perfringens produce? |
Clostridial Myonecrosis (Gas Gangrene) |
How do you avoid/ fix gangrene? |
Clean wounds and remove dead tissue asap so that it doesn't have space to produce toxins |
What are the most common ways wound infections occur? |
they happen easily in hospitals where the skin is broken. THey usually happen from normal microbiota of the environment. |
What are the two bacteria that cause the most wound infections? |
S.aureus and S. epidermidis |
what property of S. epidermidis help it to colonize plastic materials used in medical procedures? |
It binds to fibronectin the blood protein that quickly coats surgical implants in the body. |
This is a Beta- hemolytic gram + chain forming, aerotolerant bacteria |
S. pyogenes |
This protein also binds fibronectin like S.epidermidis. (An F protein) |
S. pyogenes |
Strains of this produce exotoxin A, A superantigen that causes toxic shock and exotoxin B which is a protease that destroys tissue |
Strains of S. pyogenes |
What is the bacteria that causes severe infection in burns that has a greenish tint? |
P. aeruginosa |
This is a gram- facultatively anearobic coccobacillus. Most isolates have capsules. It usually causes infections due to animal bites. |
Pasteurella multocida |
If untreated, bite wounds infected by this bacteria can cause bacteremia leading to endocarditis or meningitis. |
Pasteurella multocida |
Cat scratch disease is caused by this curved, gram- rod. |
Bartonella henslae |
THis is a short, curved, gram-, macroaerophilic bacterium that can cause peptic ulcers. It has multiple polar flagella covred by sheaths. |
Helibacter pylori |
Infection by this bacterium can persist for year or even life. they produce urease(an enzyme that converts urea to ammonia) and burrow within mucous |
Helibacter pylori |
What bacteria causes dental caries? |
Streptococcus mutants |
these are gram+ cocci that live only on teeth. |
streptococcus mutants |
an association of these three bacteria contribute to periodontal disease. |
1.porphyromonas gingivalis,2. Treponema denticola and 3.Tannerella forysthia |
This is a ds enveloped virus that contains linear DNA. There are two types of the virus. One causes oral infections (cold sores) and the other causes genital infections(herpes) |
HSV-1 and HSV-2 Herpes Simplex Virus |
WHy does HSV-1 cause reccurent cold sores? |
Because its non infectious DNA persists in sensory nerves and the DNA becomes the source of infectious virions that are carried to the skin or mucous membranes causing sores. |
this type of toxin involved in intestinal infections causes water and electrolytes to flow from intestinal cells. |
enterotoxins |
This type of toxin in intestinal infections causes cell death. some types can be absorbed into the blood stream resulting in systemic effects. |
cytotoxins |
Characteristic damage caused when bacteria inject proteins that rearrange actin filaments resulting in the replacement of microvilli on the intestinal surface with a thick structure or "pedestal" under the bacterium. |
Attaching and effacing (A/E lesions) |
What is the third way bacterium attack intestinal cells? |
through cell invasion. They go into and take over the cell. |
This bacterium causes potentially fatal diarrhea. (watery diarrhea) Person can lose up to 20 liters a day! Rice water stool. Loss of fluids and electrolytes can cause death without oral rehydration therapy. |
Cholera caused by Vibrio Cholerae |
This bacterium in killed by stomach acid, but if enough are ingested it can get in a produce an enterotoxin that activates ion transport channels causing chloride and other electrolytes to exit the cells. |
Vibrio cholerae |
THis toxin in an A-B toxin. The b portion attaches irreversibly to receptors on the microvilli of epithelial cells ,the a (active) portion enters the cell and activates G prtoeins that usually regulate the in and outs of the cell. |
Vibrio cholerae |
How are most intestinal infections spread? |
Via the fecal-oral route |
These are gram- rods that classically cause dysentery. |
Shigella (S. dysenteriae) |
THis species invades intestinal epithelial cells causing a strong inflammatory response. |
Shigella |
Some strains of this produce a potent cytotoxin known as a shiga toxin(A-B toxin) It is responsible for HUS (hemolytic uremis syndrome) |
Shigella dysenteraie |
This causes red blood cells to break up in tiny blood vessels resulting in anemia and kidney failure |
HUS (hemolytic uermic syndrome) |
What two things can cause HUS? |
Shigella dysenterae and some E coli strains |
This bacterium is not motile by itself but over takes the actin of the cells it invades and causes the cells to run into other cells and spread infection |
shigella syseteriae |
This is a gram- rod that induces uptake by epithelial cells in the region btwn th esmall and large intestine. Bacteria multiply in the phagosome and then discharge at the base of the cell. inflammatory response increases fluid secretion. |
Salmonella enterica (S. enterica) |
Ingestion of food contaminated by animal feces, especially poultry |
samlmonella enterica |
What are typhoid and paratyphoid fever caused by? |
Typhoid fever is caused by Salmonella serotype Typhi. Paratyphoid fever by Salmonella serotype paratyphi |
These are gram- members of the Enterobacteriaeceae family. They are serotypes of Salmonella |
typhi and paratyphi |
This bacterium is a curved gram- microaerophilic rod |
Campylobacter jejuni (C. jejuni) |
This bacterium has a low infected dose the bacteria multiplies within and beneath the epithelial cells causing inflammatory response. |
C. jejuni (Campylobacter jejuni) |
This is a gram+, rod that is endospore forming and an obligate anaerobe. The endospores are highly resistant to common disinfectants. |
C. difficile (Clostridium difficile) |
This bacteria has toxins that disrupt host cell actin, causing lethal effects to the intestinal epithelium. |
C. difficile |
This disease primarily occurs in hospitalized patients on antibiotic therapy |
C. difficile (CDAC-Clostridium difficile associated disease.) |
These type of virus account for nearly 500,000 deaths of children worldwide due to lack of fluid replacemtn |
rotavirus |
These are naked viruses with double walled capsid and double stranded segmented RNA |
rotavirus |
THese are naked, SS RNA viruses that are the most common cause of viral gastroenteris in the US. |
norovirus |
This virus causes abdominal cramping vomiting and diarrhea lasting 12 to 60 hrs |
Norovirus |
This is a naked, ss RNA virus of the picornavirus family. It usually has mild symptoms, but often prolonged full recovery. Vaccine is available |
Hep A |
This is an enveloped DS DNA hepadnavirus that is transmitted through blood and semen. It often has acute symptoms and if chronic can lead to cirrhosis and cancer |
Hep B |
This is an enveloped, SS RNA flavavirus . It has no vaccine. It usually has few symptoms, but liver damage can lead to cirrohsis and cancer |
Hec C |
WHen an infection becomes ______, it means that it has been carried to all parts of the body, producing disease in one or more vital organs. |
Systemic |
Illness that results from a circulating agent or its toxins |
sepsis (blood poisoning) |
When a substance is circulating in the blood stream, the condition is given that specifies the nature of the substance. Ex? |
bacteremia, viremia, fungemia (Does not necessarily mean disease) |
WHen sepsis causes blood pressure to fall to such low levels that blood flow to vital organs is insufficient. |
septic shock |
This term is used to describe infections of the heart valves or the inner surfaces of the heart. |
endocarditis |
This starts suddenly with a fever and is usually caused by virulent species such as S. aureus and S. pneumoniae. Can infect normal and abnormal heart valves. |
Acute bacterial endocarditis |
This is an infection of the heart valves and inner surfaces of the heart that is slower and not usually caused by virulent species. (less likely to be fatal) |
subacute bacterial endocarditis (SBE) |
Where do bacteria in SBE come from usually? |
from dental procedures, tooth brushing, trauma. |
What usually causes SBE? |
Staphylococcus epidermidis and other normal microbiota of the skin or mouth |
Why do the microbes live in the heart valves? |
They get caught in thin blood clots formed around deformes heart valves or other areas with disturbed bloodflow. They multiply and create a biofilm. |
How does a biofilm evade host immune response? |
They are protected from phagocytosis and antimicrobial medications. |
How does SBE lead to sickness? |
The bacteria continually wash off into the bloodstream and pieces of the infected clot can break off and block important blood vessels which can lead to death of tissue. |
This is a component of the outer membrane of the gram- cells that can cause symptoms such as fever and shock. Lipid A is responsible for the effects of this |
endotoxin |
The most fatal cases of sepsis usually involve gram ____ bacteria like E.coli P. aeruginosa and other Enterobacteriacea species . |
gram negative bacteria |
What is sepsis initially caused by? |
It usually begins with an infection somewhere in the body other than the bloodstream. It is initially due to and overstimulation of the inflammatory response. |
Widespread clotting often associated with Sepsis and often accompanied by hemorrhage. |
Disseminated intravascular coagulation. (DIC) |
What are the steps of sepsis? |
1. TLRs on macrophages and neutrophils detect endotoxin or other PAMPs, and phagocytess release pro-inflammatory cytokines. WHen this occurs systemically, a cytokine storm results and further activation of the complemnet system. |
Bacteriocidcal antibiotics often lyse bacterial cells and release more endotoxin, resulting in worsening of this blood infection. |
Sepsis |
What are some of the effects of sepsis? |
fever, impaired oxygen exchange, increased leakage of plasma from blood vessels, tissue damage from clotting, etc... |
This disease is widespread in the US and found in rabbits, muskrats, and bobcats. |
Tularemia |
This organism causes Tularemia |
Francisella tularensis |
This is a non-motile, aerobic, Gram- rod that enters through breaks in the skin or mucous membranes and is carried to the regional lymoh nodes making them large and tender. |
Francisella tularensis |
THis organism is ingested by phagocytic cells and grow within them, then spread throughout the body |
Francisella tularensis |
This organism is considered a category A risk for bioterrorism. |
Francisella tularensis |
This |
This is a part of the family Enterobacteriaceae, is a gram- rod, and is facultatively anaerobic. It is non motile and is spread widely through fleas. |
Yersinia pestis (Plague) |
If transmitted through fleas, Y. pestis results in ______ ______. If spread through inhalation, Y.pestis results in _______ ________. |
1.bubonic plague 2. pneumonic plague |
If Y.pestis spread via the bloodstream, the person may develop ____ ______. Which could lead to DIC (disseminated intravascular coagulation) |
septicemic plague |
This organism forms biofilms in the diegestive tract of infected fleas so that when they try to feed, they actually regurgitate the bacteria into the bite wound |
Yersinia pestis (plague) |
This is a ds DNA virus of the herpesvirus family. |
EBV Epstein-Barr virus |
What disease does EBV cause? |
Mono |
This virus infects the mouth and throat and then becomes latent in another cell type. After that, it is carried to the lymph nodes where is infects B lymphocytes where it can produce a productive or latent infection. |
Epstein-Barr Virus |
This is a mosquito born viral disease similar to, but milder than yellow fever. It is caused by a ss RNA virus that has 4 closely related serotypes. |
DENV1, DENV2, DENV3, DENV4. (dengue fever) |
This is transmitted primarily by the Aedes family of mosquitos |
Dengue fever |
THis is generally self-limiting and rarely fatal, but a severe form of the disease can occur in patients who experience a second infection of the dengue virus. |
1.Dengue fever 2. Dengue hemororrhagic fever |
In this model, preexisting (dengue) antibodies from a primary dengue infection recognize the virus and bind to them forming immune complexes. However, because they are for a different serotype, they instead facilitate viral entry into cells that express Fc receptors and more freely replicate in macrophages. |
Antibody-dependent enhancement (ADE) |
This is an emerging disease and the fastest spreading mosquito-born viral disease in the world currently. |
Dengue fever |
This is a sickness caused by a virus that is transmitted by mosquitoes of the Aedes family, similar to dengue fever. It is an alphavirus in the family of Togaviridea. |
CHIK |

What portion of the Immune System is important in adaptive immunity and is where T-cells are formed & mature? |
Thymus |
What portion of the immune system houses most of the immune cells that deal with blood born infections? |
Spleen |
What portion of the Immune system consists of small collections of lymphoid tissue that help clear local infection? |
Lymph Nodes |
What types of cells are important for adaptive immunity? |
T & B cells |
What types of cells are important in Innate Immunity? |
Macrophages, neutrophils, dendritic cells |
Name the Antigen presenting immune cells. |
Dendritic Cells, B cells, and Macrophages |
What types of cells are important in allergic responses? |
Mast Cells |
Describe the Innate immune response. |
first line of defense, works with adaptive (may be able to clear infection w/o adaptive), almost immediate response, less divers |
Describe the Adaptive immune response. |
takes time b/c specific T & B cells must be found & replicated, more specific, more likely to cause auto-immune problems |
Name the organs of the body that work via Innate Immunity to protect the host. |
Skin, Mouth & upper alimentary canal, Stomach, Small Intestine, Large Intestine, Airway & Lungs |
Describe the process of Phagocytosis. |
Bacteria attaches to membrane, ingested formong a phagosome, phagosome fuses to lysosome, enzymes digest material, digestion products released |
Describe the process of Inflammation. |
Tissue damage triggers vasoactive & chemotactic factors that cause increase blood flow & capillary permeability, fluid & cells exudate from capillaires, phagocytes migrate to site via chemotaxis, phagocytes & exudates destroy bacteria |
What structures help the innate immune system recognize infection? |
Pathogen Associated Molecular Patterns (PAMPs) |
What are the receptors for microbial components such as LPS, lipoproteins, peptidoglycan & ssRNA? |
Pattern Recognitation Receptors (PRRs), ie. Collectins, CRP, & Toll-like |
What type of receptors use an extracellular receptor to interact w/intracellular component to trigger cytokines? How does its recognition work? |
Toll-like Receptors (TLRs); it recognizes classes of bacteria not individual bacteria |
What is described as encountering pathogen getting sick then being immune or getting vaccine to get immunity? |
Active Immunity |
What is being immune w/o encountering pathogen ie. given Abs? |
Passive Immunity |
What has B cells that have been triggered to become Plasma cells? |
Humoral Immunity |
What's the most important cell in Cell-mediated Immunity? |
T-cells |
What type of immune cells prodcue cytokines that direct the immune response? |
T helper Cells |
What type of immune cells are turned on by Th1 cells and directly kill body cells that have been invaded by virus or bacteria inducing apoptosis? |
T cytotoxic Cells |
What is described as T regulatory cells ; cytokines helping turn T cell response back off after infection? |
Self-Limiting Response |
What helps combat self-reactive T cells? |
Tolerance |
What are the two most important functions of cytokines? |
regulate immune system and therapeutic reagents |
What is the term for cytokines made by monocytes? What about those made by activated T cells? |
Monokines; Lymphokines |
What cytokines are made by leukocytes ; act on leukocytes? |
Interleukins; now know lots of cells can make these |
What cytokines are important in controlling viral infections ; augmenting immune responses? |
Interferons |
What cytokines are important in the maturation of leukocytes? |
Colony-Stimulating Factors |
What cytokines are important in directed migration of leukocytes during immune responses? |
Chemokines |
What cytokines are involved in stem cell differentiation ; other functions? |
Growth Factors |
What are the four main functions of Cytokines? |
1. Pleiotropic (mediate different fxns) 2. Redundant (can do the same thing) 3. Synergistic (when acting together their fxn is more than additive) 4. Antagonistic (help turn immune system off) |
Name 5 properties of cytokines. |
1. low MW proteins or glycoproteins 2. Synthesized in active ; inactive forms 3. Secretion brief ; self-limiting 4. Active at very low concentrations 5. Signal cells by binding specific receptors on target cells |
What are the 4 main properties of cytokine receptors? |
1. each cytokine has a receptor 2. grouped into 5 families 3. often mutli-chain complexes 4. signaling through receptors requires multiple events |
What are the 5 cytokine receptor families? |
Immunoglobulin: IL-1 Class I: IL-2 (hematopoietin) Chemokine: IL-8 ; Chemokines Class II: IFN-;,;,; (interferon) TNF: TNF-;,; |
What portion of the cytokine receptor actually binds to the cytokine?; Which portion send signals to direct cell activity? |
Cognate receptor subunit; Signaling receptor subunit ; |
How can cytokine receptors send signals to effect transcription? |
JAK's phosphorylate STATs which dimerize & can cross the nuclear membrane in order to effect transcription |
What effect occurs when a cytokine acts on the cell that produced it? Give an example. |
Autocrine; IL-2 → Tcells |
What effect is described as a cytokine acting on adjacent/nearby cells? Give an example. |
Paracrine; Interferons |
What effect is described as a cytokine acting on distant parts of the body like a hormone? Give an example. |
Endocrine; TNF & IL-1 |
What cytokine is an important signal for B cells to continue maturation? |
IL-7 |
What cytokine are T cells dependent on for activation after Ag binding? |
IL-2 |
What is aided by cytokines produced by Th1 cells? Give examples of these cytokines. |
Cell-mediated Immunity; IFN-γ and IL-2 |
What is aided by cytokines produced by Th2 cells? Give examples of these cytokines. |
Antibody production; IL-4,5,6 |
What cytokine is a major growth factor for B cells? What cytokines are involved in isotype switching? |
Growth factor=IL-6; Isotype switching= TGF-β for IgA and IL-4 for IgE |
What recognized viral genetic material as foreign? What does their binding lead to? |
TLRs; production of Interferons |
What are the two types of interferons and where are they produced? What are their innate & adaptive functions? |
Type I: produced by all cells (IFN-α/β) Type II: prodcued by active Tcells (IFN-γ) Innate: viral clearance Adaptive: lymphocyte activation/maturation, induces MHC expression |
What portion of the bacteria do TLRs bind? Give examples. |
PAMPS; TLR-4=LPS and TLR-5=flagellin |
What three events occur in Acute Phase Response? Which cytokines direct this response? |
1. Eliminate invading pathogen 2. Prevent on-going tissue damage 3. Activte repair processes "Pro-inflammatory" cytokines: TNF-α, IL-1, IL-6, IL-8, and IFN-γ |
What are 6 characteristics of Tumor Necrosis Factor-Alpha? |
induced by LPS and made by fibroblasts & MO; activates myeloid cells; induce production of cytokines, initiates acute phase response (fever); induces adhesion molecule expression; toxic at high levels (septicemia) |
What are the three groups of Acute Phase Proteins? Give examples. |
1. Host Defense Proteins: CRP, complement, fibrinogen 2. Proteinase Inhibitors: C1 inhibitor, α1-proteinase inhibitor 3. Anti-oxidants: Haptoglobin, ceruloplasmin |
What are chemokines classified by, what are they involved in, and where are they expressed? |
by Cysteine Motifs; inflammation, cell recruitment, lymphocyte trafficking, lymphoid organ development, & wound healing; in primary & secondary lymphoid organs |
What are the current cytokine therapies? |
IFN-α: chronic myeloid leukemia, Bechet's disease, aggressive oral giant cell tumors TNF-;: root resorption, refractory posterior uveitis, rheumatoid arthritis, (anti) orofacial granulomatosis IFN-;: multiple sclerosis |
What is defined as a groupd of sequentially reacting protein, which upon activation, mediate a number of biological reactions important to host defense? |
Complement |
Tell whether the proteins of Activation, Regulation, and Receptors are Serum Soluble or Membrane Bound. |
Activation=Serum Soluble;; Regulation=Both;; Receptors=Membrane Bound |
What Domain do the following Complement Proteins belong to: Enzymes, Collectins, Cytolytic, Regulatory and Receptor, and True? |
Enzymes: Serine Protease Domain Collectins: Collagen Stalk, Globular Domain, MACPF/CDC superfamily Regulatory and Receptor: SCR Domain "True" Complement Proteins: C3,4,5 |
T/F; The same fragments are generated through both the classical ; alternative pathways. |
True |
What are the functions of both cleavage products of C3 and C5? |
C3a: Chemotaxis and Inflammation C3b: Opsonization, Neutralization, and Bcell activation C5a: Chemotaxis and Inflammation C5b: Lytic complex formation |
Describe the opsonization of C3b. |
covalently binds to surface of invading pathogen via amide (NH2) or ester |
What activates complement in each of the three pathways? |
Classical: Ag-Ab complexes (uses one IgM or two IgG molecules) Mannan-Binding Protein: Mannose, N-acetylglucosamine Alternative: LPS, zymosan |
Describe the action of C1q. |
C1q auto-activates C1s ; C1r which activates the classical pathway |
Describe the make-up and function of C3 convertase. |
C2a + C4b (C2a=enzymatic portion); cleaves C3, when C3b is added to complex it becomes C5 convertase |
Describe the way in which the complement system causes a cell to lyse. |
C5b bind C6,7,8 which triggers C9 to form a pore to lyse the cell |
What initiates the alternative pathway?; Describe it's action. |
C3 tickover; C3 interacts with water which binds Factor B, Factor D cleaved Factor B leaving Factor Bb+C3H20 = Alternative Pathway Initiator Convertase (cleaves C3 & joins classical pathway) |
Describe the functions of C3a & C5a. |
Anaphylatoxic & Chemotactic molecules; Degranulation; Increased vascular permeability; Induce cytokine release, adhesion molecules, and acute phase protein expression; Induces respiratory burst |
What are the functions of C5b? |
Initiation of the Membrane Attack Complex leading to formation of membranolytic pore-forming complex and signals transduction for cellular events |
What are the functions of C3b? |
Opsonization of Ag-Ab complexes for clearance, Solubilization of immune complexes, and neutralization of invading pathogens |
What five things regulate complement? |
1. Regulation proportional to amount of activator 2. Limited half-life of convertases 3. Inhibitory protein control early activation 4. Carboxypeptidases inactivate anaphylatoxins 5. Inhibitory proteins modulate MAC formation |
What is the effect of DAF on Complement? |
DAF binds C3b & prevents Factor B from binding to form C3 Convertase (Alt Path); if convertase is already formed, DAF can increase its decay |
What is the effect of CD59 on complement? |
binds C5b,6,7,8 complex & blocks C9 addition = can't form pore complex; if one C9 has already attached CD59 can prevent more from attaching ; the pore from growing |
Which complement deficiencies cause recurrent bacterial infections? |
Activation Component Deficiencies ; Terminal Component Deficiencies (common in Japan ; predisposed to Meningitis) |
What are the Complement Deficiencies that have to do with Regulatory Components?; What about those with Receptor deficiences? |
Reg=HANE(spontaneous inflammation, low C1 inhibitor levels), PNH (spontaneous RBC lysis), ; aHUS;; Receptor=SLE (also Activation - Lupus) |
At what level of the vasculature does leukocyte rolling take place? |
Post-Capillary Venules (b/c the vessels are smaller ; blood flow is slower) |
What are the four families of adhesion molecules? |
1. Selectins: C-type lectins 2. Integrins: Heterodimeric Receptors, ;2-Integrins 3. Cell Adhesion Molecules (CAMs): made of Ig Domains 4. Signaling Molecules: chemoattractant ; chemokine receptors |
What are the physical factors influencing lymphocyte/leukocyte migration? |
Blood Flow, Physical Barriers, and Ability to Detect Infection |
What mediates rolling and where are these components found? |
Selectins ; Carbohydrate Ligans; P ; E-Selectins on endothelial cells, L-Selectins on leukocytes, ligands on both |
T/F; If you are missing even part of the sLe molecule the leukocytes will not stick. |
True |
What are the two ways to see leukocyte rolling? |
Intravital Microscopy and Parallel Plate Flow Chamber |
Which Immunoserveillance disorder results in no binding to selectins? |
Incomplete Glycosylation of sLewx (LAD II is a Leukocyte Adhesion Deficiency) |
What does infection interacting with chemotactic receptors and ligands result in? |
Activates endothelial cells and lukocytes, causes "inside-out signaling", gradient-dependent migration of leukocytes |
What is the most common conformation of the ;2-integrins; what causes them to change conformation? |
closed/unactivated; expression of ICAM increases which results in inside-out signaling causing integrins to be in the open conformation and stick more tightly to the cell |
What type of integrin is expressed on neutorphils (PMNs) and Macrophages and is also called CR3 or CD18/CD11b? |
Mac-1 |
What is the result of missing functional CD18? |
CD18 is part of Mac-1; without it None of the CD's make it to the cell surface to be expressed, neither does CR4 (b/c CR4=CD18/CD11c) |
What molecules assist the leukocyte in diapedesis? |
Proteases: open space b/w the endothelial cells PECAM: helps trafficking of cell into tissue, expressed on neutrophil & endothelial cell Mac-1 & ICAM: interact to help pull cell through JAM: Junction Adhesion Molecules, expressed on endothelial cells, interact with integrin molecules (act as train tracks) |
What molecule mediates rolling only in lymph nodes & why? |
PNAd; b/c you don't want lymphocytes sticking to the rest of your endothelium |
Where does Naive Lymphocyte Homing occur? |
High Endothelial Venules (found only in lymph nodes) |

How can infection cause anemia? |
bacterial infections suppress erythropoietin production and the proliferation of erythroid progenitors; and also chronic infections impair iron utilization |
Lab results for Iron in anemia of chronic disease |
low sFe, reduced TIBC, and abundant stored Iron in tissue macrophages |
Cause of pure red cell aplasia |
B19 virus |
Infections that lead to aplastic anemia (4 viruses) |
hepatitis virus, CMV, EMV, and HSV |
Infections that lead to hemolytic anemia (2 parasites) |
Bebesia leads to cell lysis Leishmania causes production of oxidative metabolic products that lyse RBCs |
Bacterial toxins that might cause toxin production |
- alpha toxin in Clostridium perfringens - Capsular polysaccharide (PRP) of hameophilus influenza type B binds red cell surface and anti-PRP antibodies lyse the cell |
Parasitic infection which causes microcytic anemia |
iron deficiency anemia, associated with Hook Worm |
Infections that lead to megaloblastic anemia |
B12 deficiency accompanying D. Latum infection |
B19 presentation in various hosts (child, adult, chronic hemolytic anemia, immunocompromised patient, fetus) |
fifth's disease polyarthropathy transient aplastic crisis (TAC) PRCA Pure red cell aplasia congenital anemia, hydrops fetalis |
B19 virus and anemia (target; cell, presentation) |
erythroid progenitor cells;and erythroblasts, blood group antigen P erythema infectiosum, arthalgia, arthritis |
What is transient aplastic crisis, what is the presentation;and what infection is it associated with? |
TAC is the abrupt cessation of erythropoiesis reticulocytopenia, absent erthyroid precursors in the bone marrow and precipitous worsening of anemia B19 associated TAC is found in patients with underlying hemolytic disorders or in patients with high RBC turnover |
If a pregnant woman in her second trimester is exposed to parvovirus B19, what thest should be done first? |
obtain IgG and IgM serology ASAP |
What would each of the possible serology results of pregnant woman in her second trimester indicate/ - positive IgG result and negative IgM - positive IgG and IgM - negative IgG and positive IgM - negative IgG and negative IgM |
- indicates past infection (no risk to fetus) - indicates infection with in the last 1-120 days (possible risk to fetus) - indicates acute infection (higher risk to fetus) - indicates the mother is not immune and that no evidence of acute infection is noted.; Repeat the test in three weeks. |
Treatments for the following anemias: - pure red cell aplasia - aplastic crisis - HIV |
- intravenous immunoglobulin (IVIG) - packed RBCs - HAART |
Two target cells of Malaria parasites leading to anemia |
P.vivax binds Duffy blood group antigen P. falciparum binds to sialic acid residues on glycophorin A |
Babesia microti (transmission, population, acute and chronic presentation) |
tick-transmitted protozoan immunocompromised inclusions- tends to form ring froms in tetrads acute- malaise, headache, chills, sweating, periodic fatigue chronic- hemolytic anemia, renal failure |
Symptoms of Hook Worm infrection |
often asymptomatic iron (microcytic) deficiency anemia respiratory symptoms, itch, edema |
D. Latum (associated anemia, other symptoms, diagnosis) |
B12 deficiency leading to megaloblastic anemia salt craving, intermittent abdominal discomfort detection of large operculated eggs in stool or recovery of proglottids |
Bartonella bacilliformis (Gram stain, different disease presentations) |
gram-negative rods that penetrate RBCs carrion disease- acute febrile illness oroya fever- severe anemia verruga peruana- blood-filled nodules |
5 common features of H. pylori and C. jejuni |
- spiral or curved shape - gram negative rods - low G-C bqase ratio - inability to ferment or to oxidize carbohydrates - microaerophilic |
H. pylori (urease, H2S production, nitrate reduction, growth at 42 C, shape, size) |
positive negative negative negative spiral with 3 unipolar flagella 1 x 4 um |
C. jejuni (urease, H2S production, nitrate reduction, growth at 42 C, shape, size) |
negative positive positive positive bipolar flagella not very wide |
Describe the symptoms associated with a C. jejuni infection |
up to 10 stools/day bloody diarrhea RUQ pain- often only symptom |
Describe the symptoms of a C. fetus infection |
endocarditis, septic thrombophlebitis arthritis spetic abortion, meningoencephalitis, spontaneous peritonitis |
hyatid cysts in the liver |
Echinococcus granulosus |
biliary obstruction |
Ascaris lumbricoides |
Treatment of Campylobacter Infections |
fluid and electrolyte replacemnet empirical antibiotics for patients with high fever or bloody or frequent diarrhea erthromycin clears in 72 hours |
Virulent factor of H. pylori |
O-side chain resembles the blood group antigens so serve to protect the bacteria from immune clearance |
selequae of h. pylori |
gastric ulcers, MALT (mucus associated tissue lymphoma) |
treatment for H. pylori |
PPI clarithromycin beta-lactams |
bacteria found in scondary periotinitis caused by appendicitis perforation |
Prevotella melaninogenica |
Most important cause of endemic severe diarrheal illness |
Rotavirus group A |
Rotavirus (S/Sx, D, T) |
over a week duration ELISA/Latex agglutination in stool samples severe if ass. w/ dehydration and electrolyte imbalance vaccines are available |
Explain the role of the NSP4 protein in rotavirus in causing diarrhea |
intracellular release of Ca leading to diarrhea disrupts tight junction allowing for paracellular flow of H2O and electrolytes sitmulates the ENS |
Name three virulence factors of adenovirus |
inhibition of MHC I expression E proteins- block apoptosis by binding Rb and p53 VA-RNAS block interferon anti-viral response |
General characteristics of Enterobacteriaceae |
Gram-negative rods motile and facultative anaerobes LPS is the major cell wall antigen |
Distinguish between typhoid and non-typhoid serovars of Salmonella |
typhoid serovars: human-to-human, fecal-oral non-typhoid: animal or contaminated food handling |
Summarize virulence factors employed by Salmonella to establish infection |
attachment to epithelial cells by fimbriae; invade through M cells and enterocytes replication occurs in the endocytic vacuole; disseminated infection can occur enterotoxin produced |
Define; MacConkey Media |
bile salts and crystal violet inhibit gram-positive fermentation of lactose produces pink |
Describe EMB Media |
Eosin blue and methylene blue inhibit the growth of gram positives blue or green with lactose fermentation |
Discuss the mechanism by which Shigella invades intestinal epithelial cells |
invades M cells of the colon by type III secretion invades neighbor cells by comet-like actin tail IL-1 release and PMN migration causes further loss in cell integrity ; |
Define the mechanism of action of Shiga toxin |
AB subunit is cleaved by the protease furin the A subunit inhibits protein translation by cleaving 28S rRNA this causes cellular damage to intestinal epithelium |
ETEC (site of action, disease, pathogenesis ; virulence factors) |
small intestine Traveler's diarrhea enterotoxins stimulate hypersecretions of fluids and electrolytes, colonization factor antigens |
EHEC (site of action, disease, pathogenesis & virulence factors) |
large intestine hemolytic-uremic syndrome shiga toxin disrupts protein synthesis. A/E lesions on microvilli results in decreased absorption. Bfp, intimin adhesion |
EIEC (site of action, disease, pathogenesis & virulence factors) |
diarrhea which progresses to dysentery with bloody stools invasion mediated by invasive plasmid antigen |
Explain how SMAC media aids in the diagnosis of E.Coli. |
E. coli O157:H7 (EHEC) is the only E.coli strain that does not ferment sorbitol |
What is the cause of Hemolytic Uremic Syndrome? |
Shiga toxin form EHEC damages kidneys which release erythropoietin |
Yersininae enterocolitica (general characterisitics, source, CF, Labs) |
gram - rod, intracellular, cold tolerant contaminated meat gastroenteritis involving distal ileum, colon, and mesenteric lymph nodes, possible sequelae of autoimmune disorder lactose negative, urease negative, motility at cold temperatures |
After three days of vacationing in the city of Lima, Peru, a newly married couple fall ill with what appears to be the same condition. Both experience vomiting, watery diarrhea, nausea, and abdominal cramps. An analysis of their stool results in the isolation of gram-negative rods which produce colonies on MacConkey that are pink Which of the following is the most likely causative microorganism? |
E. coli (is a lactose fermenter) |
A 28-year-old woman complains of painful swelling of the right knee and and tender skin eruptions on both shins. For the past two weeks she has also had watery diarrhea that developed after she consumed some raw pork. She also complains of low-grade fever and mild abdominal pain. Both red and white blood cells were observed in her stool sample. A stool sample revealed a gram-negative rod that was only motile at temperatures below 30°C. Clear colonies on MacConkey agar |
Yersiniae enterocolitica ( motility below 30 C) |
A 16-year-old boy is brought to the emergency room by his parents, as he has been experiencing bloody diarrhea for 1 week. He also complains of not urinating often and blood in his urine when he does. His laboratory studies demonstrate an increased BUN and creatinine and the presence of gram-negative rods which produce beige colonies on SMAC and colonies on EMB as shown below (green). The condition is associated with infection by which of the following E. coli types? |
EHEC (beige on SMAC) |
A 36-year-old man comes to the emergency room because of the development of sudden nausea, vomiting, and diarrhea with blood and mucus, as well as crampy abdominal pain. He had just returned yesterday from a business trip to South America and has been experiencing these symptoms for two days. Leukocytes were found in his stools as well as a gram-negative non-motile rod. Growth on MacConkey media after 48 hours shows clear colonies. Which of the following is the most likely causative microorganism? |
Shigella dysenteriae (non-motile, non-lactose fermenter) |
A 3-year-old man presents with sudden-onset, crampy abdominal pain and diarrhea. The diarrhea is watery and contains mucus. The patient also complains of low-grade fever with chills, malaise, nausea, and vomiting. Careful history reveals that he had ingested partially cooked eggs at a poultry farm 24 hours before his symptoms began. Based on this limited information, which of the following microorganism would you most likely suspect? |
Salmonella enterica (sudden, mucus, poultry) |
A 3-month-old female infant was brought to the emergency department of a general hospital with a 5-day history of decreased activity, decreased oral intake, upper airway congestion, and general irritability. There was no history of fever or vomiting. During the previous 2 weeks, she had been constipated, and twice her mother had given a tablespoon of honey for treatment. The physical examination revealed dry oral mucosa, a sluggish pupillary response, and significant hypotonia. A gram stain of the fecal sample revealed a gram positive spore forming rod. Which of the following is the most likely diagnosis? |
C. Botulism (flaccid paralysis) |
A 67-year-old man presented with fever, abdominal cramping, and frequent diarrhea for four days. Three weeks before the current episode, he had undergone a hip replacement and was rehabilitating in an orthopedic unit. During the hospitalization, he developed a nosocomial pneumonia and was treated empirically with clindamycin. He gradually improved and was discharged a week before his current presentation, with maintenance oral antibiotics. Which of the following is the most likely diagnosis? |
Shigella sonnei (nosocomial infection) |
C. difficile (CF, and A and B toxins) |
pseudomembranous colitis A- enterotoxin--> recruits PMNs B- causes cytoskeletal damage |
C. perfringens (LF and A and B toxins) |
lechtinase enzyme destoys cells causes precipitate growth on egg yolk agar A enterotoxin disrupts ion transport B enterotoxin forms pores--> bloody diarrhea |
C. botulism (CF, source) |
1-3 days of weakness, blurred vision, and constipation flaccid paralysis canned foods |
Specifics about two forms of Bacillus Cereus |
emetic and diarrheal form diarrheal form lasts longer, from meat and is heat labile |
Giardia lambia (transmission, symptoms, E, D) |
fecal-oral diarrhea, increased fat and mucus in stool worldwide, primarily human-to-human transmission cysts (stain with Trichrome stain)and smiley-face trophozoite (stain with Kohn and Giemsa stain) forms are detected in feces |
What stain is diagnostic for Cryptosporium? |
acid-fast stain, it won't stain with trichrome |
What is the treatment for cryptosporidium infection? |
hydration, no drugs; are effective against crypto |
Cryptosporidium (Et, Sx, E, D); |
fecal-oral frothy BMs, anorexia, self-limiting, immunocompromised pateints cannot self cure oocysts, acid fast stain |
Balantidium coli (E, Sx, E, D) |
fecal-oral intermittent diarrhea with blood and pus, ulceration worldwide, swine #1 animal reservoir microscopic exam, bean-shaped macronucleus |
How does the O/P of E. histolytica read? |
trichrome stain shows ingested red blood cells |
E. histolytica (Et, Sx, E, D) |
fecal-oral dysentery, RUQ worldwide, human-to-human microscpic exam, motile trophozites PCR differentiate histolytica from dispar |
O/P of Ascaris lumbricoides |
large, mamillated coat and tapered end in fertilized egg |
O/P of stengyloides stercoralis |
muscular neck, distinguished from hookworm by mouth at one end and notched tail on the other |
O/P of schistosoma mansoni |
large spine projecting out of one side |
Life cycle of ascaris lubricoides |
ingested eggs travel to the lunges larvae break free in 3 weeks larvae pass and can be swallowed back into the small intestine |
O/P of trichus trichiura |
white worm , barrel shaped eggs with mucoid plugs at both ends |
Trichuris trichiura (Et, Sx, E, D) |
fecal-oral diarrhea, rectal prolapse in children Worldwide concentrated microscopic specimen |
Schistosoma mansoni (Et, Sx, E, D) |
skin penetration by cercariae from snails dermatitis, enlarged liver and lymph nodes, eosinophilia and dysentery South America and Africa schistosome eggs in stool and urine |

Innate immunity |
There is immediate maximal response, not antigen specific, and exposure results in no immunological memory |
Adaptive immunity |
Response is antigen dependent, there is a lag time between exposure and maximum response, antigen specific, exposure results in immunological memory, and recognition by antibody and T cell receptors |
Species resisitant |
Only affects certain animals or plants and not humans because our physiology is different |
Innate immunity |
Present at birth |
Adaptive immunity |
Acquired over time from exposure |
Skin (dermis/epidermis) |
Has chemicals that defend against pathogens. Perspiration secreted by sweat glands; sebum secreted by oil glands |
Mucous membranes |
Lines all body cavities open to environment, produces chemical that defends against pathogens |
Lacrimal apparatus |
Lysozymes that destroy bacteria |
Normal microbiota |
Microbial anatonism, makes it hard for pathogens to compete |
Plasma |
Liquid part of blood that carries blood cells, and plasma proteins which help with inflammation and blood clotting. Iron binding proteins bind to iron in blood which makes iron unavailable to pathogens |
Erythrocytes (RBC'S) |
Most numerous in body. Biconcave shape and transports gases |
Leukocytes (WBC'S) |
Used in immunity, broken into two catergories: granulocytes that contain granules and can exit the blood and agranulocytes which don't contain granules |
Granulocytes |
Broken down into Basophils, Eosinophils, and Neutrophils |
Agranulocytes |
Broken down into lymphocytes and monocytes |
Basophils |
Stain blue; not phagocytic, release chemical to cause inflammation |
Eosinophils |
Stain orange/red; phagocytic, high number in blood indicates allergic reaction or infection with helmin worms |
Neutrophils |
Stain light purple; phagocytic |
Lymphocytes |
Smallest WBC'S; nuclei covers almost entire cell, plays a part in adaptive immunity |
Monocytes |
Leaves blood stream and become macrophage and eat foreign pathogens |
Platelets |
Broken pieces of cells used for clotting; helps with inflammation |
Nonphagocytic killings |
Broken into 3 types: killing by Eosinophils, killing by natural killer lymphocytes, and killing by neutrophils |
Killing by Eosinophils |
Secrete antimicrobial chemicals, protect from helmins |
Killing by natural killer lymphocytes |
Secrete toxins that attack virally affected cells |
Killing by neutrophils |
Produce enzymes that create bleach with kills the bacteria |
Toll like receptors (TLRs) |
10 in body, proteins that are part of WBC'S and act as an early warning system. They detect pathogen associates molecular patterns (microbes). Very important because if they fail your immune system is compromised |
NOD proteins |
Proteins found on leukocytes that bind to certain things and cause cell death and other responses |
Interferons |
Protects us from viral infections. Broken into 2 types: type 1 (alpha and beta) 2hich is released within hours of infection to let neighboring cells know a virus is present and type 2 (gamma) which is activated by T cells and starts phagocytosis |
Complement |
Activation results in lysis of the foreign cell. Indirectly trigger inflammation and fever. Can be activated in three ways: classical pathway is activated by antibodies, alternative pathway is activated by exotoxins, and Lectin pathway is activated by molecules on bacteria |
Inflammation |
-itis / swelling |
Fever |
Body temperature over 37*C which enhances interferons and inhibits growth of some microbes and phagocytosis |
5 attributes of adaptive immunity |
Specificity, inducibility, clonality, unresponsive to self, and memory |
Specificity |
Responds to a certain shape |
Inducibility |
Activates only when pathogens are present |
Clonality |
Once induced, can clone cells to attack virus |
Unresponsive to self |
Your body does not attack itself |
Memory |
Will remember pathogen |
Lymph |
Watery liquid that carries toxins and pathogens out of the body |
Primary lymph organs |
Are WBC'S that mature in red bone marrow and thymus |
Secondary lymph organs |
Are the lymph nodes, spleen, and lymphocytes |
Antigens |
Shapes found on pathogens. 3 types: exogenous, endogenous, and autogenous |
Exogenous |
Responds to things on the outside |
Endogenous |
Pathogens that reproduce inside the cell |
Autogenous |
Produced from a normal cell process |
Epitopes |
3D shape on nucleus membrane that body recongnizes |
Function of B cells |
Secretion of antibodies |
Five antibody functions |
Neutralization, opsonization, oxidation, agglutonation, and ADCC |
Neutralization |
Neutralizes toxins and prevents it from attachment |
Opsonization |
Changes shape of antigen and activates phagocytosis |
Oxidation |
Produces oxidants that destroy cell |
Agglutonation |
Sticking them all together to get rid of them all at once |
ADCC |
Natural killer B cells that lyse cells |
Function of T cells |
To work against intracellular pathogens and cancer cells |
3 types of T cells |
Cytotoxin, helper, and regulatory |
Cytotoxin |
Directly kills other cells |
Helper |
Assist with activating B cells |
Regulatory |
Turns off the response tying to regulate immune system |
Major histocompatibility complex |
Holds pathogen in place for T cells at the antigen binding site |
Cell mediated immune responses |
Responds to intracellular pathogens and abnormal body cells. Antigen is present. MHC2 and epitote hols in place till T cell arrives and binds. T cell will differentiate and turns into a cell that can destroy pathogen. T cell makes clones of pathogen destroying cells and attaches to pathogens which causes them to lyse |
Antibody immune responses |
Helper t cells bind MHC and epitotes to pathogen. Makes clones. They activate and attach to B cells. B cells will then be activated and differentiate to make plasma cells to bind and destroy pathogen. |
T independent |
B cells that do not require helper T cells and are found in the interstitial fluid. |
T dependent |
B cells that require helper T cells and are found in the lymph nodes |
Immunological memory formed |
They are produced by B cell proliferation but does not secrete antibodies. These are long living ells that stay in the lymphoid tissue and initiates production if antigen is encountered again. This is important because your body will know how to fight that specific antigen much quicker subsequent times so they won't make you sick |
Naturally aquired (Active immunity) |
Is something you acquire from coming in contact with a certain pathogen |
Artificially acquired (Passive immunity) |
Is something you acquire an immunity from due to a vaccine |
5 different types of vaccines |
Attenuated, inactive, toxoid, combination, and gene technology |
Attenuated |
Live pathogens, can cause mild infection |
Inactive |
Whole or pieces of dead pathogens |
Toxoid |
Gives you modified toxins that won't cause the disease but will build up immunity |
Combination |
Combines pathogens |
Gene technology |
Takes genes and recombines them to make them safe |
Concerns and problems associated with vaccine safety |
Mild toxicity, risk of anaphylactic shock, residual virulence from attenuated viruses |
Mild toxicity |
Allergic reactions, injection site soreness |
Residual virulence from attenuated viruses |
A little sicker than normal. |
Debunked |
Allegations that certain vaccines can cause autism, diabetes, and asthma but research has debunked these allegations |

Faculative Intracellular Pathogens |
can live in host or freely |
Intracellular Pathogens |
seek refuge by invading host |
Pollutants that cause eutrophication |
nitrogen, phosphates |
Cold Seeps |
microbial communities at unheated benthic where methane and petroleum seep out |
Amensalism |
one species harms another (nonspecific) |
Synergism |
mutualism, but both species can thrive separately |
Syntropy |
feeding together of two species on something that wouldn't otherwise be digestable |
Metagenomics |
sequencing of genomes in an environmental community |
Pan-genome |
core genome and accessory genes present in isolates |
Core genome |
genes present in all sequenced genomes of species |
Hopanoids |
steroid-like molecules of bacteria membranes |
Serotyping |
identifying variations within subspecies of pathogen |
How technology spreads disease |
colonization of woods and rainforests transplants and transfusions modern meat-processing transportation |
Pandemic |
epidemic over large area |
Propagated Epidemic |
epidemic where infected spread disease to healthy |
Epidemic |
outbreak, high frequency over short period from one source; little transmission by infected |
Endemic |
low frequency of disease; normally present |
Epidemiology |
study of factors affecting illness and health of populations |
Survival strategies for pathogens of of cell, but still in host |
secretion of capsule manufacturing of proteins that bind to antibodies cause apoptosis of phagocytes alter cell surface (all to avoid detection and attachment of antibodies) |
Survival strategies for pathogens in cell |
use hemolysin to break out of phagosome secrete proteins to prevent fusion of phagosome with lysosome mature in acidic lysosome |
Vectors |
intermediates for pathogen transmission |
Fomites |
inanimate objects that relay pathogens |
Opportunistic pathogens |
cause disease in compromised host |
Primary pathogens |
cause disease in otherwise healthy host by breaching defenses |
Signature-tagged mutagenesis |
mutate pathogen and tag it inoculate host recover pathogen and determine which mutations prevented growth in host |
in vivo expression technology |
identify promotors that transcribe only when infecting a host |
Lipopolysaccharides |
endotoxin that activates inflammatory response that can also cause toxic shock |
AB toxin |
5 B subunits surround A and delivers A to host A subunit is toxic |
5 types of toxin function |
1. causes host cell membrane leakage 2. block protein synthesis 3. block 2nd messenger pathways 4. superantigens overactivate immune system 5. proteases cleave host proteins |
Pilus assembly |
protein secreted into periplasm secreted to site of assembly subunits strung together tips of pili bind to host |
Pili/Fimbriae |
hollow fibrils made of pilin with tips that bind to host prevents expulsion from host |
Pathogenicity island characteristics |
multiple genes associated with pathogenicity transferred as block from other organisms flanked by phage or plasmid genes different base ratio than other parts of genome |
Examples of virulence factors |
toxins, attachment proteins, capsules |
Lethal Dose (LD50) |
number of organisms to kill 50% of hosts |
Virulence |
frequency of lethal infections |
Infectious Dose (ID50) |
number of organisms to colonize 50% of host measure pathogenicity |
Exotoxin |
nonprotein; hyperactivates immune system |
Endotoxin |
toxic proteins; kills host to unlock nutrients |
Pathogenicity |
ability to cause disease |
Steps of Infection |
1. encounter 2. entry 3. establish infection 4. cause damage |
Benefits of biofilms to microbes |
protection from: predators phages biocides antibiotics immunophagocytes antibodies |
Biofilms |
community of bacteria enclosed in ECM |
Quorum sensing compounds |
oligopeptides (gram +) n-acyl homoserine lactones (AHLs) (gram -) Al-2 INTER species communication (gram +/-) |
Uses of quorum sensing |
adapt to availability of nutrients defense avoidance of toxins coordination of virulence to escape immune response and establish infection |
Quorum sensing |
ability of bacteria to communicate and coordinate behavior via small molecules (inter and intra species) |
Microbial predators |
protists, viruses, bacterial predators |
Tube worms and microbes |
worm takes up CO2 and H2S microbes must oxidize to make organic matter |
Metabolism of deep sea ocean vents |
producers oxides H2S for energy methanogens and methanotrophs prevent CO2 buildup hydrogen oxidizers convert H2 and S --> H2S |
Hawaiian bobtailed squid |
host for bioluminescent bacteria bacteria emit light to match moonlight to eliminate shadow on ocean floor undetectable by predators |
Microbes and coral |
bacteria and algae help coral fix N2, photosynthesis, protection against pathogens |
Rumen and microbes |
break down cellulose in anaerobic environment |
Arbuscular mycorrhizal fungi |
improve acquisition of phosphate, nitrogen, water reduce incidence of root disease |
Rhizosphere |
region of soil surrounding rocks |
Rhizoplane |
root surface |
Mycorrhizae |
fungal infection in plants that increase ability to absorb nutrients |
Rhizobium infection cycle |
legumes secrete flavanoids rhizobia express nod genes and enter cortical cells remains in symbiosome Rhizobia fix nitrogen; plant provides nutrients |
Chloroplast homolog |
cyanobacteria |
Mitochondria homolog |
rickettsiae |
Syntrophy |
both organisms combine metabolic capabilities to catabolize substances they couldn't alone |
Cycle leading to acid rain |
phytoplankton produce DMSP to protect against UV other bacteria convert DMSP-->DMS (volatile, acts as nuclei for cloud formation) DMS is hydrated to sulfuric acid, which falls as acid rain |
Characteristics of phosphorus cycle |
same oxidation state no gas intermediate soluble in oceans |
Dissimilatory nitrate |
used as and e- acceptor in e- transport chain |
Assimilatory nitrate |
used as nutrient |
Annamox |
anaerobic formation of N2 from ammonia and nitrite |
Denitrification |
cascade of anaerobic respirations converting nitrate-->N2 nitrate-->nitrite-->nitric oxide-->nitrous oxide-->nitrogen gas |
Nitrification |
ammonia-->nitrite-->nitrate oxidation makes nitrogen available to plants |
Nitrogen fixation |
nitrogen gas-->ammonia nitrogenase reduces nitrogen complex cofactors make it oxygen sensitive |
Methylotrophs (rxn too.) |
oxidize methane to CO2 CH4 + SO4 --> CO2 + H2S + OH- CH4 + H2O --> CO2 + 4H2 removal of H2 drives rxn to right |
Methanogenic Archaea |
break down trapped carbon compounds in anaerobic environments to CH4 |
Why viruses aren't "living" |
no cellular integrity only a protein and nucleic acid depend on host for survival and replication |
Dinoflagellates |
alveolate 2 long flagella red algal chloroplast secrete neurotoxins via extrusome |
Yeast classification |
unicellular fungi |
Growth of fungi |
growth material is secreted at hyphal tips |
Fungi food absorption |
must absorb as individual molecules |
Material of fungi walls |
chitin |
Alveolates |
ciliated protists |
Protist classifications |
amoebas, alveolates, heterokonts, euglenozoa, excavates |
Archaeal genomes |
circular, similar to bacteria |
Protein chemistry for increased stability |
ion pairs, acidic/basic residues, disulfide bridges, hydrogen bonds, hydrophobic interactions |
Archaeal lipids |
ether-linked, making it more resistant to acid and heat |
Gram-negative proteobacteria |
light-supplemented heterotrophs adaptable metabolisms |
Akinetes |
specialized pore cells survive desiccation and then germinate at better conditions |
Hormogonia |
short chains of motile cells |
Gas vesicles |
used for buoyancy to maintain position |
Carboxysomes |
carbon dioxide fixation location |
Thylakoids |
photosynthetic apparatus separate from plasma membrane |
Heterocysts |
cell part specialized in nitrogen fixing |
Cyanobacteria |
oxygenic phototrophs photolyze water to make oxygen photolyze hydrogen reduce sulfur compounds only bacteria producers |
Chloroflexi |
phototrphic, filamentous moderate thermophiles lots of membrane-bound chlorophylls |
Xerophile |
have little water activity |
Psychrophile |
live at low temperature environments |
Oligotroph |
live in low carbon environment |
Hyperthermophile |
live in high temperature environments |
Halophile |
lives in high salt environments |
Endolith |
live within rock crystals |
Prebiotic soup |
basic components from abiotic factors infused with electricity formed biomolecules |
Panspernia |
idea that life came from other planets |
Metabolism of early microbes |
sulfur-based anaerobic metabolism reduction of nitrate and sulfate |
Early Earth atmosphere |
CH4, CO2, N2, NH4+, H2S, FeS, CO, H2 |
Viroids |
infectious single strand RNA |
Koch's postulates |
microbe found in all cases, but not healthy microbe isolated and grown induce disease by introducing microbe can obtain microbe from diseased |
RNA World Theory |
RNA can: store info duplicate catalyze (ribosomes) later, DNA and proteins took over these roles |
Definition of Life |
structure and form catalytic activity self-replication membrane compartmentalization metabolism of energy |
Barophile |
live in high pressure environment |
Alkaliphile |
live in basic environments |
Acidophiles |
live in acidic environments |
Metabolist theory |
components of metabolism arose from self-sustaining abiotic rxns proteins and metabolism formed first |
Extremophiles |
species that grow in extreme environments |
Psychrophiles |
thrive at cold temperatures |
Paralogous proteins |
gene duplication and independent mutation of two protein lines |
Orthologous proteins |
proteins that diverge from one another in different species |
Proteobacteria resemble... |
mitochondria |
Endosymbiosis example: sea slug & chloroplasts |
sea slugs engulf chloroplasts chloroplasts perform photosynthesis |
Endosymbiosis example: aphids |
have symbionts that make essential amino acids for them |
Endosymbiosis example: amoeba and cyanobacteria |
cyanobacteria provides food amoeba provides protection |
Virulence factors |
help establish organism that can alter host functions to cause disease |
Immunopathogenesis |
when immune response to pathogen is contributing cause to pathology |
Genomic islands |
group of genes transferred together horizontally frequently linked to tRNA abnormal base-pair ratio flanked by genes similar to phage/plasmid |
Horizontal gene transfer |
DNA transfer via plasmids, transposons, bacteriophages with genes coding for metabolism, stress response, pathogenicity |
Vertical gene transfer |
parent-->child |
Reductive evolution |
loss or mutation of DNA encoding for unselected traits |
Shared ancestor (progenote) characteristics |
genetic code fueling pathways protein synthesis very inefficient |
When microbes originated |
3 billion years ago |
Requirements for phylogenetic marker study |
gene must be present in organisms studied gene can't be horizontally transferred gene must have conservation must be large enough |
Chemiosmotic theory |
redox reactions of e- transport chain store energy in proton gradients in mitochondria |
Lithotrophs |
feed on only inorganic minerals |
Archaea |
can survive extreme pH and temperatures |
Lichens |
algae live in fungus algae provides food fungus provides protection |
Stomalites |
layers of earliest microorganisms |
Types of microbes |
bacteria archaea eukaryotic microbes: yeasts, protists, algae |
Thermophile |
live in hot water branched off early |
Uses for Sugar |
carbon & energy sources, storage material, adhesives, parts of other structures, virulence factors, signaling |
Stabilizing forces of proteins |
hydrophobic interactions, hydrogen bonds, ionic interactions, disulfide bonds |
Lipid structure |
glycerol backbone with hydrophilic phosphate group and two fatty acid side chains |
Hopanoid |
planar, rigid structure within phospholipid bilayer; improves membrane stability |
Linkage in bacterial and eukaryotic membranes |
ester-linked |
Linkage in archaeal membranes |
ether-linked; more stable |
Membrane structure is stabilized by |
hydrophobic interactions, hydrogen bonds, negative charges on proteins and cations |
Diffusion |
passive transport through membrane from high to low concentration |
Facilitated diffusion |
passive transport flowing down concentration gradient via protein |
Symport |
transport of two molecules through same protein in same direction |
Antiport |
transport of two molecules through same protein in opposite direction |
ATP-binding cassette transporter |
active transporter hydrophobic channel and two proteins that bind ATP for uptake of particular molecule |
Group translocation |
active transport; intake of one molecule affects the uptake of others nearby via different proteins |
ATP synthase |
generates ATP through flowing of H+ ions |
periplasm location in gram+ |
between cytoplasm and peptidoglycan |
periplasm location in gram- |
between cytoplasm and outer membrane |
Functions of the periplasm |
has protein-folders, hydrolytic enzymes, used to adjust osmotic stress, transport, chemoreception, detoxification |
FtsZ function |
forms contractile ring for cytokinesis |
MreB function |
encircles cell; involved in cell division |
Cytoplasm functions |
involved in shaping, strength, transport, movement, chromosome separation, cell division, organization |
Carboxysomes |
CO2 concentrator that contains RubisCO that fixes CO2 |
Mitochondria |
catabolizes nutrients via TCA cycle to make ATP |
Chloroplast |
contains thylakoids (folds) where photosynthesis takes place; converts light to ATP & reducing power |
magnetosome |
bacteria that move along magnetic fields in order to maintain proper spacing in water column to live in environment with right amount of oxygen |
Gas vesicles |
filled by cell to manage level in water column |
Endospore |
cell structure that is resistant to heat, radiation, chemicals, dessication |
Capsule |
adds protection especially against phagocytes of immune system |
Outer membrane functions |
contains porins to allow passage of small molecules |
Peptidoglycan structure |
cross-linked glycopeptides; amide bonds between strings of amino acids and glucose derivatives |
location of peptidoglycan |
in bacteria; one molecule that surrounds entire cell |
Techoic acid |
stabilizes cell wall in gram+ bacteria |
S-layer |
lots of disulfide bonds, but function unknown |
Gram+ envelope structure |
polysaccharides and S-layer (protein) thick cell wall with peptidoglycan cross-links; thin periplasm; contains membrane |
Gram- envelope structure |
some have capsule of polysaccharide; outer membrane of lipopolysaccharide in outer leaflet; thin cell wall with fewer crosslinks; thick periplasm, plasma membrane |
Gram- outer membrane |
made of lipopolysaccharides contains O-polysaccharide antigen that determines virulence and can be altered endotoxin |
Cell wall structure |
made of peptidoglycan and sugar chains linked by amino acid polymer cross-links |
Archaeal cell wall |
made of peudomurien (like peptidoglycan); may have S-layer, ether linked |
Polar arrangement of flagella |
one flagellum on cell |
Lophotrichous arrangement of flagella |
many flagella on one end of cell |
Peritrichous arrangement of flagella |
multiple flagella at different places |
Difference between prokaryotic and eukaryotic flagella |
prokaryotic flagella rotate to move cell eukaryotic flagella whip to move cell |
Swarming Motility System |
movement across solid surface by hyperflagellated cells |
Swimming Motility System |
movement through liquid medium with flagella |
Type IV pili mechanism |
"cast & reel" mechanism |
Mechanisms of cell movement |
swarming, swimming, type IV pili, excretion of surface slime to slide across, rotary motors |
Mycoplasma |
cell wall-less bacteria; must live in host; tough membrane w/sterols |
Thermoplasma |
cell wall-less; low pH and high temperature environment; rigid membrane with tetra-ether lipids |
Gram Stain technique |
distinguishes gram+ and gram- bacteria add crystal violet to bacteria precipitate dye with I- extract precipitated dye this removes all dye from gram- gram positive still contains crystal violet due to the peptidoglycans that are present |
Macronutrients for microbes |
carbon, oxygen, nitrogen, hydrogen, phosphorus |
Sources of carbon |
CO2, sugar, organic acids, fatty acids, amino acids |
Nitrogen is needed for |
amino acids, nucleic acids, peptidoglycan layer |
Nitrogen sources |
amino acids, nucleic acids, nitrate, ammonia, nitrogen gas |
Phosphorus is needed for |
phospholipids, nucleic acids, ATP synthesis |
Phosphorus sources |
phosphate, degraded organics |
Micronutrients for microbes |
sulfur, potassium, magnesium, calcium, iron |
Sulfur needed for |
amino acids, vitamins |
Sources of sulfur |
sulfate, elemental sulfur, dihydrogen sulfide |
Potassium use |
acts as cell cation |
Magnesium use |
stabilizes ribosomes, cell membranes, nucleic acids required for ATP-dependent enzymes (forms complex w/ATP) |
Calcium use |
stabilizes walls and spores |
sodium use |
maintenance of osmotic balance |
iron use |
used by cell enzymes |
Trace elements needed by microbes |
transition elements |
Growth factors |
used by cell to make coenzymes |
Conenzyme of folic acid |
tetrahydrofolate |
Function of tetrahydrofolate |
synthesis of nitrogenous bases |
Coenzyme of biotin |
biotin |
Function of biotin |
CO2 fixation |
Coenzyme of lipoic acid |
lipamide |
Function of lipamide |
Decarboxylation of keto acids |
Coenzyme of Pantothenate |
coenzyme A |
Function of coenzyme A |
utilized in metabolism |
Coenzyme form of nicotinic acid |
NAD and NADP |
Function of nicotinic acid |
electron carrier |
Coenzyme form of pyridoxine |
pyridoxal phosphate |
Function of pyridoxine |
amino acid metabolism |
Coenzyme of Riboflavin |
FAD |
Function of FAD |
electron carrier |
Thiamine coenzyme |
TPP |
Function of TPP |
C2 unit carrier |
Cobalamin coenzyme |
adenosylcobalamin |
Function of adenosylcobalamin |
transfers methyl groups |
Photolithoautotrophs |
energy source: light carbon source: CO2 reducing power source: inorganics |
Photoheterotrophs |
energy source: light carbon source: organics reducing power source: organics |
Chemolithoautotrophs |
energy source: chemicals carbon source: CO2 reducing power source: inorganics |
Chemoheterotrophs |
energy source: organics carbon source: organics reducing power source: organics |
Chemo- |
gets energy from chemicals and organic compounds |
Process of division in spherical bacteria |
septation |
Division in Gram- rod-shaped bacteria |
Z ring forms when both nucleoids are present pulls membranes inward synthesizes new peptidoglycan |
Division in Gram+ rod-shaped bacteria |
Z-ring forms at middle peptidoglycan forms down middle |
Min protein function |
determines location of Z ring MinE depolymerizes MinCD, causing both proteins to oscilate back and forth when MinE runs out, MinCD complex reforms and causes Z-ring to form |
Influences on growth rate |
rate of catalysis, metabolism speed, nutrient availability, temperature, pH, gases available |
Growth rate constant |
rate of exponential growth |
Growth rate equation |
final # cells= initial # cells * 2^(# generations) |
Psychorphile |
lives in -5-10 degrees Celsius |
Mesophile |
lives in 10-45 degrees Celsius |
What temperature classification of bacteria infect humans? |
mesophiles |
Thermophile |
lives in 40-80 degrees Celsius |
Hyperthermophile |
lives in 80+ degrees Celsius |
How do cells adjust to cold temperatures? |
incorporate unsaturated fatty acids to increase membrane fluidity; express enzymes that are effective at low temperatures |
How do cells adjust to hot temperatures? |
incorporate saturated fatty acids, more sterols and hopanoids to decrease membrane fluidity; express enzymes resistant to denaturation; use chaperones to stabilize proteins |
Strict aerobes |
require oxygen |
Strict anaerobes |
don't use oxygen and are killed by it |
Facultative anaerobes |
can use oxygen, but can grow without it |
Aerotolerant anaerobes |
can survive in oxygen, but don't use it |
Microaerophiles |
require oxygen, but can't survive in atmospheric conditions |
How do cells adjust to acidic conditions? |
seal off membrane to prevent H+ ions from entering |
How do cells adjust to basic conditions? |
utilize other monovalent ions for cell processes; use antiport to expel ion and take up H+ ions |
Membrane-permeant organic acids |
weak acids that can enter cell membrane in uncharged form and then dissociate to cause decrease in pH |
Neutralophiles |
grow best in pH 5-8 |
What pH classification of microbes are pathogens? |
neutralophiles |
Acidophiles |
grow best in pH 0-5 tetraether lipids in membrane decrease H+ permeability |
Alkaliphiles |
grow best 9-11 diether lipids that prevent proton linkage expel Na+ ions to take up H+ |
How do cells prevent water loss? |
synthesize compatible solutes |
How do cells prevent water gain? |
release solutes |
Sterilization |
process where living cells, spores, viruses, are destroyed on an object |
Disinfection |
killing or removal of disease-producing organisms from inanimate surfaces |
Antisepsis |
removal of pathogens from surface of living tissues |
Sanitation |
reducing microbial population to safe levels |
Bactericidal |
antibacterial agents |
Germicidal |
chemical substances that kill microbes and pathogens |
Pasteurization |
heating food to temperature long enough to kill most heat resistant nonspore pathogens |
Decimal reduction time |
length of time it takes agent to kill 90% of population |
Decimal reduction time is affected by |
population size, population composition, agent concentration, duration of exposure |
targets of antiobiotics |
cross-link assembly in membrane, protein synthesis, nutrient synthesis, gene expression, DNA replication |
How microbes resist drugs |
add group to antibiotic to inactivate it, pump out antibiotic, lack molecular target of antibiotic, modify receptors so it is unrecognizable |
Bioremediation |
treatment of radioactive waste using genetically engineered bacteria |
Fe/Mn oxidation |
oxidize iron, making it insoluble (Fe2+-->Fe3+) gets carbon from CO2 |
Methanogenic archaea |
reduce CO2-->CH4 |
How to drive a reaction by altering concentrations |
increase reactants; decrease products |
Oxidant |
accepts electrons |
Reductant |
donates electrons |
Sign of redox potential that means oxidized form is more stable |
negative |
Sign of redox potential that means reduced form is more stable |
positive |
NAD+ |
accepts 2e- at once and 2H+ |
FAD |
accepts 1e- or 2e-, can also accept H+ |
one-electron carriers |
transition metal complexes that cannot accept protons |
Characteristics of energy carriers |
phosphorylated compounds or compounds with high energy bonds |
Types of high energy bonds |
anhydride bond, thioester bond, ester bond |
Holoenzyme |
complete enzyme |
What does catabolism achieve? |
chemical energy, reducing power, building blocks for biosynthesis |
oxidative phosphorylation |
synthesis of ATP by ion-driven ATPase; respiration substrate is passed from carrier to carrier to be reduced and eventually combines O2 and H+ to make water; generates proton motive force |
substrate level phosphorylation |
synthesis of ATP from ADP coupled with breakdown of bonds; fermentation |
NAD+/NADH |
energy carrier that donates and accepts 2-3 times more energy than ATP |
structure of NADH |
ADP attached to stable ring; ring has N base and sugar phosphate |
How NADH holds electrons |
aromatic ring is disrupted by addition of 2 electrons and H+; must transfer electrons to another carrier or substrate to reduce it |
FAD |
accepts 2e- and 2H+ to form FADH2 |
cytochrome |
extracts energy from electron by pushing protons out of cell; must tolerate/avoid oxygen |
ETS in steps |
1. protons & electrons brought to flavoprotein 2. electrons passed to Fe/S 3. Proton extruded to make PMF 4. electrons from Fe/S enter quinine pool 5. protons picked up from cytosol 6. electrons are brought to heme and Fe/S clusters of cytochromes 7. electrons from Fe/S centers are brought to heme 8. cytochrome oxidase transfers electrons to final acceptor and consumes protons from cytoplasm |
F0 mechanism of ATP synthase |
a-subunit port of entry for protons interacts with c unit to deprotonate amino acid residue neutralized c subunit can rotate and bring neutral c to exit where proton is lost, and then reprotonated |
F1 mechanism of ATP synthase |
active site on beta unit where ADP and phosphate loosely bind rotation of F0 drives this rotation rotation switches binding to tight state forming ATP Another rotation brings to open state to release ATP |
Proton motive force-driven ATP synthesis |
splits hydrogen to create protons and provide energy to make NADH and ATP |
Sulfur oxidizers |
oxidize sulfur to pump out H+ and drive production of ATP and NADH |
Iron oxidizers |
oxidize iron to pump out H+ and drive production of ATP |
Anaerobic respiration |
less efficient than aerobic respiration; still involves ETS, but O2 is not terminal acceptor |
Nitrate reducers |
nitrate-->nitrite, nirate-->nitrogen gas ineffective, toxic only used when oxygen is scarce |
hydrogenotrophic methanogenesis |
CO2-->CH4 CO2 is activated and then reduced by methanofuran Methanopterin reduces it twice more then forms CH4 |
Homoacetogenesis |
CO2-->acetate |
light-drive energy generation |
use light to make ATP & reducing power |
Light-driven proton motive force |
light hits compound to bring electron up an energy level electron flows down transport system to make NADPH or NADH enters a second photosystem to repeat and recycle electrons |
Capture of light in archaea |
involves retinal |
sensory rhodopsins |
drive archaeal cell away from damaging light and towards optimal absorbing light |
CO2 fixation |
gets reducing power from sulfur containing compounds (anaerobic) or water (aerobic) |
organotrophy |
organic compounds donate electrons |
organic respiration |
catabolism with inorganic or small organic electron acceptor using glycolysis, TCA cycle, ETS |
Lithotrophy |
inorganic compounds donate electrons |
methanogenesis |
anaerobic with inorganic donor and CO2 acceptor |
Photoautotrophy |
photolysis of water (aerobic) or others (anaerobic) using photosystems |
photoheterotrophy |
catabolism with light absorption supplements |
What do obligate fermenters lack? |
ETS |
Fermentation steps |
1. activate substrate 2. rearrange C skeleton 3. oxidize activated substrate 4. couple reaction to synthesize ATP 5. balance oxidation with reduction 6. excretion of products |
What glucose breakdown yields |
two 3-carbon sugars + 4H+ on NADH |
Glycolysis |
glucose 6-phosphate-->fructose 6-phosphate-(phosphorylation)->2 pyruvates, 2 net ATP, 2 net NADH |
Entner-Duodoroff (ED) pathway |
glucose 6-phosphate-(oxidation)->6-phosphogluconate-->1 pyruvate + 1 G3P-->G3P enters glycolysis , 1 net ATP, 1 net NADH, 1 net NADPH |
Pentose-phosphate shunt (PPS) |
glucose 6-phosphate-(oxidation)->6-phosphogluconate-(decarboxylation)->ribulose 5-phosphate (used for biosynthesis, or converted to pyruvate) makes 1 ATP and 2NADPH |
Amphibolic pathway |
can participate in both catabolism and anabolism, simply by reversing process |
Steps that regulate glycolysis |
involves steps that are not reversible |
How fermentation completes catabolism |
recycles e- carriers by transferring H's back to pyruvate products |
Mixed acid fermentation |
forms various products depending on pH |
Acetyl-CoA |
esterified coenzyme A to acetyl group |
Catabolism of fats |
uses lipases to generate acetyl-CoA that feeds into TCA cycle by dehydrating, then adding water and oxidizing to ketone |
Catabolism of aliphatic hydrocarbons |
addition of oxygen, then two oxidations |
Catabolism of aromatics |
attach CoA, removal of aromaticity, break ring, then oxidize |
Catabolism of proteins |
broken down to peptides then amino acids to feed into TCA cycle |
Cycles involved in CO2 fixation |
Calvin cycle, reductive TCA cycle, reductive acetyl-CoA pathway, methylotrophic strategy |
Calvin cycle steps |
1. 3CO2-->G3P 2. 1CO2-->rubisco-diphosphate -->6-carbon product-->2 G3Ps each cycle yields 1 G3P and spends 9ATP |
Reductive TCA cycle |
TCA cycle in reverse, but some enzymes are replaced because they can't run in reverse |
Methylotrophic strategy |
pick up CO2 to detoxify formaldehyde |
Biosynthesis of fatty acids |
CO2+acetyl-CoA-->malonyl CoA that then progresses to form fatty acid and kick off CO2 |
Rubisco |
fixes CO2, housed in carboxysome |
Where does nitrogen fixation occur? |
in cells that have differentiated into heterocysts so that O2 isn't there because nitrogen fixation is toxic in presence of oxygen |
Rhizobia |
fix nitrogen in symbiosis with legumes make leghemoglobin that binds to oxygen and prevent it from reacting with nitrogen fixation; also don't let ammonia freely float around |
Why do ensymes require metal cofactors? |
bind to active sites of enzymes; play structural roles |
Siderophores |
take up iron for bacterial cells; used by pathogens to survive and cause disease |
What's the difference between cofactors and coenzymes? |
coenzymes: organic, required by some enzymes for catalysis cofactors: inorganic, required for or increase rate of catalysis |
Nucleoside |
base + sugar |
Nucleotide |
base, sugar, phosphate |
Purines |
adenine and guanine; double-ring |
pyrimidines |
thymine, cytosine, uracil; single-ring |
Difference between RNA and DNA sugar |
ribose has 2' -OH group, so it's more easily cleaved |
What does double-stranding of DNA accomplish? |
protection from chemical attack; information redundancy; repair mechanisms |
Ribozymes |
RNA that catalyzes reactions |
Riboswitch |
mRNA with a UTR that binds to metabolite in order to hide a ribosome binding site, creating a terminator |
Helicase |
unwinds DNA |
Primase |
adds RNA priming strand |
DNA Polymerase III |
adds nucleotides during replication |
Sigma subunit of RNA polymerase recognizes what? |
-35 and -10 regions and binds to promoter |
Rho-independent termination |
G-C rich stem-loop forms, followed by a series of A's, causing the polymerase to fall off |
Rho-dependent termination |
polymerase stalls and Rho protein cleaves it off |
Wobble rule |
3rd nucleotide of a codon can bind to something else; G can bind to U or C; U can bind to A or G |
Polar mutations |
block translation, causing a stoppage in downstream transcription, since both occur at the same time |
Transition mutation |
conversion of a purine to another purine or pyrimidine to another pyrimidine |
Transversion mutation |
conversion of purine to pyrimidine or vice versa |
Effect of UV rays |
cause pyrimidine dimers to form |
Effects of X-rays and Gamma rays |
double-stranded breaks in DNA |
Effects of oxidation on DNA |
deamination, depurination, methylation |
Mismatch repair mechansim |
repairs base substitutions substitution is recognized by MutS; Excision is performed by MutL and MutH; repair is performed by Pol I |
Base excision repair |
removal of damaged bases, and then a separation of that gap |
Addiction System |
plasmid has a long-lived poison and a short-lived antidote; daughter cells that inherit the plasmid will survive because they have the antidote code, but ones that don't will die because the poison lingers from the parental cells |
Uncoating of Eukaryotic viruses |
can be uncoated upon attaching to membrane; can be uncoated once inside cell into an endosome (derived from cell membrane); can be uncoated upon attaching to nuclear membrane |
RNA-RNA polymerase |
involved in replication of RNA of viruses; doesn't proofread |
+RNA virus |
has ribosome that makes RNA-RNA polymerase |
-RNA virus |
needs to bring an RNA-RNA polymerase with it because it doesn't have a ribosome to transcribe RNA-RNA polymerase |
Viroids |
naked nucleic acid molecules that act as plant pathogens |
Prions |
single protein molecules that infect |
Histidine protein kinase |
senses stimulus; phosphorylates itself and transfers phosphate to response regulator |
phosphatase |
removes phosphate from response regulator |
What does membrane curvature control? |
where lipids are positioned and localization of some proteins |
What shapes membrane curvature? |
peptidoglycans |
Cardiolipin (CL) structure |
2 phosphate groups with side chains on each |
Where is cardiolipin found? |
found in bacteria and membranes related to mitochondria and chloroplasts at poles of septum |
What does cardiolipin do? |
destabilizes planar lipid bilayers |
How to bend bacteria |
use lysozyme to turn it into a sphere then confine them to microchambers; sphere membranes will then conform to curvature of the chambers |
MinD |
protein that inhibits division plane formation |

Pathogenic Gram-Positive Cocci and Bacilli |
Stain purple when gram-stained |
Staphylococcus is a _____ member of every human’s microbiota. |
Normal |
Staphylococcus is located: |
In nasopharynx On skin Colonizes the infant w/in hours |
Staphylococcus found in hospitals in |
Nurseries and surgical wards. |
Staphylococci live and reproduce on |
almost every square inch of human skin |
Staphpylococcus can be ______ pathogens causing anywhere from minor to life threatening diseases |
opportunistic |
Staphylococcus genus name comes from Greek term staphle meaning ______ |
“bunches of grapes” |
Coccus (pl.cocci) = |
spherical–shaped bacterial cell |
staph = |
staff or group (Cluster like grapes) |
Staphylococcus colonies appear |
cream colored, white to light gold, and “buttery-looking” |
Staphylococcus is Gram _____ |
positive cocci, nonmotile, facultative anaerobes |
Staphylococcus grows best when _____ present, but can continue to grow under ____ conditions. |
O2, anaerobic |
Staphylococcus is _____-tolerant |
salt |
Staphylococcus tolerates the ____ present on human skin |
salt |
Staphylococcus is tolerant of desiccation (capsule). What does this mean? |
allows survival on environmental surfaces such as fomites Object inadvertently used to transfer pathogen to new host: needle or coin |
Staphylococci are catalase positive or negative? |
positive |
Catalase Converts H202, (hydrogen peroxide) Into_____ and ____? |
H20 and 02 |
Staphylococci can disarm neutrophil’s and macrophage’s H2O2 with ______? |
catalase |
_______ is secreted by neutrophils and macrophages to kill bacteria |
Hydrogen peroxide |
To test for catalase: |
Inoculating loop is rubbed across a colony of Staphylococcus and mixed with H202 on a slide. If bubbles appear, the enzyme catalase must be present. So Staphylococcus is catalyst positive |
Staphylococcal infections range from the |
trivial to the rapidly fatal |
Are Staphylococcal infections easy to treat? |
No, They can be difficult to treat |
Why are Staphylococcal infections difficult to treat? |
Because staphylococci can acquire antibiotic resistance |
“Staph” infections result when staphylococci |
breach the body’s physical barriers. |
Entry of only a few hundred bacteria (ID) can result in |
disease |
Staphylococci are ______ in nature with about a _____ species part of our human flora |
ubiquitous, dozen |
How many species are commonly associated with staphylococcal diseases in humans? |
2 |
What are the 2 species commonly associated with staphylococcal diseases in humans? |
1.Staphylococcus aureus is one of the most common causes of infections 2.Less virulent,opportunist Staphylococcus epidermis may cause prosthetic implant infections |
Staphylococcus aureus is one of the most common causes of |
infections |
Less virulent, opportunist Staphylococcus epidermis may cause |
prosthetic implant infections |
Staphylococcus epidermidis is the______ of human skin |
Normal microbiota |
Staphylococcus epidermidis is the normal microbiota of human skin that can cause ? |
opportunistic infections to immunocompromised patients or when introduced into parts of body |
Staphylococcus aureus is located on |
skin, nares, mucous membranes (pharynx and vagina) |
What pigment is Staphylococcus aureus on sheep blood agar? |
Gold pigment |
Pathogenicity of Staphylococus (3 things) |
1.Cell wall structures that prevent phagocytosis 2. Enzymes 3. Production of toxins |
Cell wall structures that prevent phagocytosis (3 things) |
a. Protein A b. Bound coagulase c. Capsule/slime layer |
2. Enzymes (5 things) |
a. Coagulase b. Staphylokinase c. Hyaluronidase d. Lipase e. B-lactamses |
3. Toxins (4 things) |
a. Cytolytic toxins b. Exfoliative toxins c. Toxic-shock-syndrome (TSS) toxin d. Enterotoxins |
Staphylococcus aureus has Protein A which causes_____to bind upside-down _____ antigen. This _____ opponization and ________. |
antibody stems,S. aureus Inhibits, phagocytosis |
Staphylococcus aureus has ________ that converts fibrinogen into ______ that form clots around pathogen. |
enzyme coagulase, fibrin |
Fibrin clots ______ Staphylococcus aureus from phagocytic cells |
hide |
Staphylococcus aureus forms slime layer/capsule that prevents: |
Phagocytosis and Dessiccation |
Slime layer facilitates attachment of Staphylococcus to artificial surfaces such as (5 things) |
catheters, shunts, artificial heart valves and joints |
Coagulase triggers fibrin clotting, which hides the _______ |
Staphylococcus aureus |
Staphylokinase |
Dissolves fibrin threads in clots, allowing S.aureus to free itself from clots and spread to new location |
Hyaluronidase |
Breaks down hyaluronic acid, enabling S. aureus spread deeper between cells |
Lipases = |
digest lipids allowing Staphylococcus aureus to grow on surface of skin and sebaceous glands |
B-lactamase = |
penicillinase now in 90% of S. aureus strains and thus resistant to penicillin and cephalosporins |
Cytolytic toxins Disrupts the ______ ______ ______of a variety of cells such as |
mammalian cytoplasmic membrane Heart, skeletal muscle, renal cells, platelets |
Hemolysins damage |
RBCs |
Leukocidin lyses |
Leukocytes, Macrophages, and neutrophils |
Leukocidin provides S. aureus ______ from _____. |
protection from phagocytosis |
Exfoliative toxins = ET causes |
Exofoliation |
Exfoliative toxin dissolves |
desmosomes The patient’s epidermal layer of skin to slough off |
Toxic-shock-syndrome toxin symptoms |
High fever, rash, peeling of skin, vasodilation, drop in BP |
Staphylococcus aureus produces enterotoxin proteins which in turn stimulate which 4 things? |
Intestinal muscle contractions Nausea Intense vomiting Associated with staphylococcal food poisoning |
Staphylococcus aureus Enterotoxins are ____ stable |
heat |
Heat does not denature_____ protein |
enterotoxin |
cover dish dinner; take home leftovers; reheat = zap in microwave. This process Does not _______the Enterotoxin |
denature |
Staphylococcal Diseases categorized as which 3 things? |
1. Noninvasive Disease 2. Cutaneous Disease 3. Systemic Disease |
1. Noninvasive Disease |
Food poisoning Ingestion of Staphylococcus aureus contaminated food |
Ingestion of Staphylococcus aureus contaminated food Bacteria grow on food and secretes |
Enterotoxin that is heat stable |
Common cause of food poisoning? |
Staphylococcus aureus |
Food poisoning is caused by ______ rather than by ______ of the bacteria |
enterotoxin, invasion |
Food must remain at ________for several hours for bacteria to grow, reproduce, and produce toxin |
room temperature |
Enterotoxin causes ____, ____, ____ for how long? |
nausea, vomiting, diarrhea for 24 hours |
Reheating may kill ______ bacteria but does not inactivate _______. |
S. aureus, enterotoxin |
2. Cutaneous Disease Various skin conditions: name 6 |
Scalded skin syndrome Impetigo Folliculitis Sty Furuncles Carbuncle |
Staphylococcus aureus causes localized _______(pus filled lesions)lesions |
pyogenic |
Pyogenic = |
pus filled lesions |
Scalded skin syndrome = Exfoliative toxin causes: name 4 things |
Reddening of skin Large blisters Epidermis peels off in two days Subject to secondary bacterial infection |
Scalded skin syndrome = Exfoliative toxin Usually affects ______ of severed umbilicus & Older children with ______. |
neonates, skin infections |
Staphylococcus aureus causes 80% of |
impetigo |
impetigo is what and occurs on who? |
Small, flattened, red patches on face, limbs of children whose immune system is not fully developed |
impetigo mostly occurs on _____ as pus filled vesicles that crust over and become honey colored, wet, flaky. The pus is filled with ____ and ____ |
face, S. aureus and WBC |
Folliculitis = |
Infection of hair follicle |
Folliculitis Becomes red, swollen, and pus filled. When it occurs at base of eye in eyelash follicle it is called a |
Sty |
Furuncle = boil Penetrates into the ______? |
Large, painful, raised nodular extension of folliculitis to surrounding tissue. Penetrates into the subcutaneous layer |
Carbuncle = |
several furuncles coalesce |
Carbuncle |
Larger, deeper, more painful May have to be surgically drained Can be the size of baseball |
Carbuncle May cause____ and _____ as S. aureus spreads into underlying tissues may need ______. |
fever, chills, antibiotics |
S. aureus can cause a variety of potentially fatal _____ _____ When introduced to deeper tissues of the body such as ___, ____, ____, and ____. |
systemic infections Blood, heart, lungs, and bones |
3. Systemic Disease 6 things |
TSS Pneumonia Bacteremia Endocarditis Osteomyelitis Empyema |
Staphylococcus aureus produce _____ toxin |
TSS |
Staphylococcus aureus can grow in a _____ or _____ vagina and produce the toxin and cause______. |
wound,abraded Toxic shock syndrome |
can TSS occur in both males and females? |
Yes |
Toxic Shock Syndrome Toxin causes: |
Fever Vomiting and Diarrhea Red rash Loss of sheets of skin Low BP, shock Multi-organ failure due to shock |
TSS fatal in ____% cases. Why? |
5%, When BP drops so low O2 cannot be carried to vital organs and causes shock, death |
Staphylococcus aureus in blood is ______ and Accounts for half of all ______ infections |
Bacteremia , noscomial |
Staphylococcus aureus Bacteremia Causes: |
Furuncles Vaginal infections Infected surgical wounds |
Hospitalized patients with chronic disease that contract S. aureus bacteremia have a |
high mortality rate |
Staphylococcus aureus = Endocarditis |
Attacks lining of heart and valves |
Endocarditis is one of the consequences of _______. |
staphylococcal bacteremia |
Staphylococcus aureus = Endocarditis Symptoms are _____ and ______. |
nonspecific, flulike |
Staphylococcus aureus = Endocarditis Blood pumped from heart ______ which in turn makes the ____ drop. 50% patients do not |
drops, BP, survive |
Staphylococcus aureus in blood invades _____ causing______. |
lungs, pneumonia |
Mortality rate for staphylococcal pneumonia is _____%. |
50%. |
Staphylococcal pneumonia known to occur as secondary infection to |
influenza |
Staphylococcal pneumonia Particularly occurs in _____ and_______ patients |
infants,cystic fibrosis |
In 10% of patients with Staphylococcal pneumonia… The fluid filling the alveoli is _____, this condition is called ______. |
pus, empyema |
When Staphpylococcus aureusInvades a bone, it causes |
Staphylococcal osteomyelitis |
Staphylococcal osteomyelitis Signs and symptoms are: Inflammation of |
Bone marrow, diaphysis and periosteum Fever, Chills, Swelling and pain (Brake hip and get stahpylococcus aureus infection in bone) |
Diagnosis of Staphylococcus Infections |
Detection of Gram-positive bacteria Isolated from pus, blood, or other fluids |
Treatment: ______ is the drug of choice to treat staphylococcal infections. |
Methicillin |
Treatment:Since (1962) 1987 have: MRSA = |
methicillin-resistant Staphylococcus aureus |
Treatment: Since 2002 have: VRSA = |
vancomycin resistant S. aureus |
Prevention = some humans are carriers |
Hand antisepsis Proper cleansing of wounds and surgical openings Aseptic use of catheters or indwelling needles Appropriate use of antiseptics |
The Genus Streptococcus Is a diverse group of |
Gram positive cocci |
Streptococcus can be arranged in ____ or ______ |
Pairs or chains |
Streptococcus are arranged in pairs called |
diplococci |
Streptococcus are Arranged in chains like a strip of button candy called |
streptococci |
Streptococcus is Catalase _____ |
negative |
Most Streptococcus are _______ ________. |
facultative anaerobes |
Serological classification of Streptococcus is useful in _______. |
identification |
The Lancefield classification Developed by Rebecca Lancefield in 1938 was Based on ______ ______. |
serological classification |
The Lancefield classification puts various strains of Streptococcus into _____ different groups. |
19. |
Lancefield groups go from _____ to ____. |
A – S |
Lancefield groups A and B are ______ and ______. |
GAS and GBS |
GAS and GBS Include the significant streptococcal pathogens of _____. |
humans |
There are _____ species of Streptococci only a few (5) are ______ _______. |
Thirty, human pathogens |
Group A Streptococcus = |
Streptococcus pyogenes |
What do Group A (GAS) Streptococcus pyogenes look like? |
Looks like chain of purple pearls on slide |
Group A Streptococcus: GAS On blood agar plate, Streptococcus pyogenes forms ______ colonies surrounded by _____ of beta-hemolysis on blood agar plates. |
white, zone |
Streptococcus pyogenes lyse _____ leaving a ____ zone around ____ colony. |
RBC, clear, white |
What is the main representative of group A Streptococcus (GAS)? |
Streptococcus pyogenes |
What is the most serious streptococcal pathogen? |
Streptococcus pyogenes |
Streptococcus pyogenes has a number of Structures, Enzymes and Toxins that enable it to survive as a ______. |
pathogen |
Pathogenic strains of Streptococcus pyogenes form _____ |
capsules |
What are the structural components and enzymes of Streptococcus pyogenes? 5 things? |
1.Protein M (protein A in S. aureus) 2.Hyaluronic acid capsule 3.Streptokinase Enzymes 4.Hyaluronidase = spreading factor |
Protein M ________ complement. Thereby interfering with opsonization, phagocytosis, and lysis of bacteria. |
destabilizes, |
Hyaluronic acid capsule acts to ______ the bacteria |
camouflage(WBC cannot recognize) |
Streptokinase Enzymes ______ blood clots and _______ spread of Streptococcus pyogenes into ______ and _____tissue |
dissolves, facilitates, damaged and infected |
Hyaluronidase called the ______ ______, dissolves hyaluronic acid and facilitates spread of Streptococcus pyogenes into deeper tissue |
spreading factor |
What are Streptococcus pyogenes major Extracellular Toxins? 3 things |
Exotoxins Pyrogenic toxins/ Erythrogenic toxins Streptolysins toxins |
Streptococcus pyogenes :Pyrogenic toxins Stimulate______ and ______ cells to release cytokines/pyrogenes |
macrophages and helper T cells |
Streptococcus pyogenes :Pyrogenic toxins Stimulate ______ , causes ____ , and _____ toxic shock |
fever,rash and streptococcal |
Because Pyrogenic toxins cause blood capillaries near surface of skin to dilate producing a red rash known as ____ _____, Some scientist call the toxins _________ toxins |
(scarlet fever), Erythrogenic |
Streptolysins toxins Cause _____ of sheep blood agar. Clear zone around colony |
hemolysis |
Streptolysins toxins Lyses _____, _____ and _______Which interfere with O2 carrying capacity, Immunity, Blood clotting. |
RBCs, WBCs and Platelets. |
Streptolysins toxins also lyse other tissue cells such as |
Liver cells Cardiac muscle cells Kidney cells |
Humans are only significant reservoir of ___ to ____ % of population are carriers of virulent strains of Streptococcus pyogenes |
5-15% |
Streptococcus pyogenes Typically causes disease when: |
Competing normal flora is depleted Immunity is impaired When large inoculum enables it to get a foot hold (infectious dose) before antibodies form against it |
Streptococcus pyogenes Causes following diseases: KNOW these 7 |
Strep throat Erysipelas Streptococcal toxic shock syndrome Necrotizing fasciitis Scarlet fever Rheumatic fever Post streptococcal glomerulonephritis |
What is the Streptococcus pyogenes strain for Sore throat, strep throat, or tonsillitis ? |
Streptococcal pharyngitis |
Bacteriological or serological testare needed for a sure diagnosis of ______ _____ |
Streptococcal pharyngitis |
What is Streptococcal pharyngitis treated with? |
penicillin |
What is a Sequela? |
a condition following and resulting from a disease |
_____ is a morbid complication that follows a disease |
Sequela |
Some diseases leave sequela In the form of long-term or permanent |
Damage to tissues or organs |
Examples of Sequelas: Meningitis can result in _____ |
deafness |
Examples of Sequelas: Strep throat can result in _____ _____ |
scarlet fever |
Examples of Sequelas: Strep throat can result in _____ ______ disease |
rheumatic heart |
What is Pyoderma? |
streptococcal impetigo |
streptococcal impetigo is a localized _____ ______. |
ski |