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88 Cards in this Set

  • Front
  • Back
Name the three bacteria (genus and species) which cause most cases of pediatric otitis media.
Streptococcus pneumoniae
Moraxella catarrhalis
Haemophilus influenzae
Name three bacteria which are major causes of bacterial meningitis in adults or children with normal immune systems.
Streptococcus pneumoniae
Haemophilus influenzae
Neisseria meningitidis
Which psychrotrophic bacterium is spread via contaminated food or drink and causes diseases such as meningitis and bacteremia in immunocompromised individuals? What other diseases can this bacterium cause, and what specific groups have a high risk of infection?
1. Listeria monocytogenes
2. Neonatal and in-utero disease
3. Pregnant women and newborns
Distinguish between tuberculoid and leprotamous leprosy. How is the immune response different? How do the symptoms differ?
Tuberculoid leprosy: Non-progressive form, strong cell-mediated immune response therefore able to kill cells infected with bacterium, symptoms are regions of skin that have lost sensation as a result of nerve damage

Leprotamous leprosy: Progressive form, weak cell-mediated immune response in which the bacterium can multiply in skin and nerve cells, gradually destroying tissue and leading to loss of facial features, digits and other body structures
Distinguish between food infection and food intoxication. How do symptoms of food intoxication generally differ from food infection? What is the incubation period of food intoxication vs. food infection?
Food infection - living organism are consumed; Heat-liable; enterotoxin; symptoms include diarrhea, usually NO vomiting; incubation 12-24 hours; duration more than 24 hours.

Food intoxication - reults from consumption of microbial toxin (preformed toxin); heat-stable enterotoxin, symptoms includ vomiting and nausea; incubation is 1-6 hours; duration is less than 24 hours.
Name three organisms that cause food poisoning via food intoxication.
xxx
Name three organisms that cause food poisoning via food infection
Bacillus cereus, Staphylococcus aureus, Campylobacter jejuni
Describe the mechanisms of action of tetanus toxin and botulism toxin.
Botchulism toxin blocks the fusion of the vesicles with the neuron's cytoplasmic membrane, thereby preventing secretion of the neurotransmitter into the synaptic cleft; as a result the muscle does not contract.

Tetanus toxin blocks the inhibitory neurotransmitter. As a result, motor neurons controlling the antagonistic muscle are not inhibited, but instead ca generate nerve impulses that stimulate muscle contraction.
Why are patients with certain heart conditions treated prophylactically with antibiotics prior to many dental procedures?
Because Viridans streptococci normally inhabit the mouth, pharynx, GI tract, genital tract and urinary tract. They are opportunistic that up on entering the bloodstream can cause meningitis and endocarditis
Which bacteria are common causes of toxic shock syndrome?
Staphylococcus aureus, Group A strep
Which bacteria can cause endocarditis?
Staphylococcus aureus, Viridians strep, Strep. pneumoniae
What are the four classes of pathogenic E. coli and what are the characteristics of each class? Which class causes the most severe infections? Why are anti-diarrheal medications and antibiotics contraindicated when treating these infections?
EPEC - Traveler's diarrhea
ETEC - Infant diarrhea
EIEC - Dysentary
(MOST SEVERE) EHEC - Hemmorhagic colitis, Hemolytic uremic syndrome

Anti-diarrheal meds. and antibiotics contradict because for example, E. coli, is mediated by exotoxins called enterotoxins.
Name some organisms which can cause UTIs. Which bacteria is the most common cause of non-nosocomial UTI? Which bacterial species cause infection-induced kidney stones? How?
E. coli, Enterococcus, Klebsiella pneumonia, Proteus mirabilisi, Proteus vulgaris

Most common cause is E. coli

Infection-induced kidney stones are Proteus mirabilis in the presence of urea, which releases a large amount of enzyme urease, which breaks into CO2 and NH3. NH3 raises the pH of urine in the bladder and kidneys such thta are normally souble a normal acidic pH of urine precipitate often around bacteria cells to form infection induced kidney stones.
What is the infectious dose for shigellosis? Tuberculosis? S. aureus infections?
Shingellosis - 10
TB - 10
S. aureus - few 100
Which bacterium is a common opportunistic pathogen of burn patients and cystic fibrosis patients?
Pseudomonas aeruginosa
Which bacterium was associated with fatal wound infections following Hurricane Katrina?
xxx
How does actin polymerization by intracellular pathogens such as Listeria and Rickettsia contribute to their pathogenesis?
The pathogen polymerizes the host cell's actin molecules to form stiff actin filaments that lengthen and push the bacterium through the cytosol to the cell's surface where it forms a pseudopod. A neighboring macrophage then endocytizes the pseudopod and the pathogen once again "tunnels" its way out of the phagosome to continue its intracellular parasitic existence with new host cell
Production of extracellular enzymes is a common virulence mechanism. What role would the following extracellular enzymes play in pathogenesis: IgA
found in tears, mucous membrane secretions and breast milk where is agglutinates and neutralizes antigens
Production of extracellular enzymes is a common virulence mechanism. What role would the following extracellular enzymes play in pathogenesis: protease
Digests into amino acids outside a microbe's cell wall; in inflammatory reactions, chemicals released by mast cells that activate viral enzyme that makes HIV virulent.
Production of extracellular enzymes is a common virulence mechanism. What role would the following extracellular enzymes play in pathogenesis: hyaluronidase
breaks down hyaluronic acid which is a major component of the matrix between cells
Production of extracellular enzymes is a common virulence mechanism. What role would the following extracellular enzymes play in pathogenesis: coagulase
triggers blood clotting. cell-free coagulase does not act on fibrin directly, but instead combines with a blood protein before becoming enzymatic abd cinverting fibrinogen ti fibrin threads.
Production of extracellular enzymes is a common virulence mechanism. What role would the following extracellular enzymes play in pathogenesis: lipase
lipases digest lipids, allowing the pathogen to grow on the surface of the skin and in oil glands.
Production of extracellular enzymes is a common virulence mechanism. What role would the following extracellular enzymes play in pathogenesis: DNAse
enzyme that degrades DNA
pharyngitis (strept throat)
a. Streptococcus pyogenes
b. Respiratory droplets
c. Fever, malaise, headache, red pharynx, swollen lymph node and pus-containing abcesses covering tonsils
d. Mediated by exotoxins? Yes
a) Pyrogenic toxins
b) Erythrogenic toxins produced by some chains, which is the cause of a rash (scarlet fever)
e. No Intracellular pathogens
f. No vaccine
necrotizing fasciitis
a. Group A Strep. (S. pyogenes)
b. Respiratory droplets; Enters through breaks in the skin
c. Toxemia, failure of many organs, and death of more than 50% of patients
d. Strep. secretes enzymes and toxins that destroy muscle and fat tissues.
e. Intracellular pathogens. No
f. No vaccine
osteomyelitis
a. S. aureus
b. invades the bone through a traumatic wound or via the blood during bactermia
c. inflammation of the bone marrowand the surrounding bone causing pain in the infected bone with a high fever.
d. Coagulase - triggers blood clotting; Staphylokinase - dissolves fibrin threads in blood clots; hyaluroindase - breaks down hyaluronic acid a major component of cell matrix; lipase - digests lipids; B-lactamase - breaks down penicillin
e. Not Intracellular pathogen
f. No vaccine
scalded skin syndrome
a. S. aureus
b. invades the bone through a traumatic wound or via the blood during bactermia
c. Reddening of the skin that usually begins near the mouth and spreads over the entire body. Followed by large blisters that contain clear fluid lacking bacteria or WBCs (because the disease is caused by a toxin released by bacteria growing on the skin).
d. Coagulase - triggers blood clotting; Staphylokinase - dissolves fibrin threads in blood clots; hyaluroindase - breaks down hyaluronic acid a major component of cell matrix; lipase - digests lipids; B-lactamase - breaks down penicillin
e. Not Intracellular pathogen
f. No vaccine
tetanus
a. Clostridium tetani
b. Innocluated from environment into puncture wounds
c. At onset tightening of the jaw and neck muscles (lockjaw), sweating, drooling, grouchiness, and constant back spasms, as spreads heartbeat irregularities, fluctations in blood pressure, extensive sweating, unrelenting contractions, and death because patients cannot exhale.
d. Tetanus toxin which is composed of 2 polypeptides held together by a disulfide bond. The heavier of the 2 polypeptides binds to a receptor on a neuron's cytoplasmic membrance. The neuron endocytizes the toxin, removes the lighter of the 2 polypeptides and transports it to the CNS. There the small polypeptide enters an inhbitory neuron and blocks the release of inhibitory neurotransmitter. e. No Intracellular pathogen
f. Yes there is a vaccine
botulism
a. Clostridiuum botulinum
b. Ingestion (improperly canned food); environment (wound)
c. Symptoms - 3 types (foodborne, infant and wound)Foodborne, weak, dizzy, dry mouth, blurred vision, constipation, abdominal pain and progressice paralysis that eventually effects the diaphragm. Infant, colnization in GI tract, crying, constipation and "failure to thrive". Wound, usually after 4 or more days, same as foodborne, but no gastrointestinal symptoms
d. Botulism toxins (there are 7) which are quaternary -protein that prevent the inactivation of the toxin by stomach acid
e. Not a intracellular
f. No vaccine
gas gangrene
a. Clostridium perfringes
b. innoculation of spores form enviroment; ingestion of spores
c. Symptoms include intense pain, swelling, and tissue death at site of infection, then production of foul-smelling gaseous bacterial waste products, then within a week shock, kidney failure and death can occur.
d. C. perfringens produces 11 toxins that lyse erythrocytes and leukocytes, increase vascular permeability, reduce blood pressure and kill cells, resulting in irreversible damage.
e. Not Intracellular
f. No vaccine
pseudomembranous colitis
a. Clostridium difficile
b. Oppoortunistic during antimicrobial therapy, particularly clindamycin
c. Exploding diarrhea potentially perforating the colon and leading to a massice internal infection and death
d. Toxin A, Toxin B, and Hyaluronidase (breaks down hualuronic acid which is the major component of cell matrix), work together to cause hemorrhagic necrosis of the intestinal wall.
e. Not intracellular
f. No vaccine
anthrax
a. Bacillus anthracis
b. Inhalation, ingestion or innoculation of spores
c. (3 possible clinical manifestations) 1. Gastrointestinal - intestinal hemorrhaging and eventually death. 2. Cutaneous anthrax - painless, solid, raised nodule forms on the skin at the site of infection, then nodule spreads to form an eschar. 3. Inhalation anthrax - endospores germinate get into blood stream and cause toxemia with fatigue, malaise, fever, aches and cough ... leading to high fever and labored breathing.
d. Anthrax toxin which is composed of 3 distinct polypeptide components that in combination are lethal.
e. Not intracellular
f. Yes vaccine available
tuberculosis
a. Mycobacterium tuberculosis
b. Aerosols
c. Small, hard nodules develop in lungs
d. Siderophore (iron-binding proteins); cord factor (cell wall component that produces stands of daughter cells that remain attached to one another in parallel alignments and inhibits migration of neutrophils and is toxic to mammalian cells.
e. Yes, Intracellular pathogens?
f. Vaccine available
leprosy
a. Mycobacterium leprae
b. Direct contact, nasal secretions
c. Tuberculoid leprosy: Non-progressive form, strong cell-mediated immune response therefore able to kill cells infected with bacterium, symptoms are regions of skin that have lost sensation as a result of nerve damage

Leprotamous leprosy: Progressive form, weak cell-mediated immune response in which the bacterium can multiply in skin and nerve cells, gradually destroying tissue and leading to loss of facial features, digits and other body structures
d. No
e. Yes it's an intracellular pathogens
f. BCG vaccine gives SOME protection
streptococcal pneumonia
a. Streptococcus pneumoniae
b. Respiratory droplets; superinfection
c. Productive cough, severe chills, slightly bloody septum, and chest pain.
d. Phosphorylcholine (binds to receptors on cells in thelungs, meninges and blood vessel walls and stimulates the cells to engulf the bacteria), capsule (protects them from digestion after endocytosis), protein adhesion (poorly defined protein that mediates binding of the cells to epithelial cells fo the pharynx), pneumolysin (binds to cholesterol in the cytoplasmic membranes or ciliated epithelial cells, producing pores that result in lyses of the cells), IgA protease (destroys IgA)
e. Not intracellular
f. Vaccine available
listeriosis
a. Listeria monocytogenes
b. Respiratory droplets
c. In elderly and immunodep. flu-like symptoms, when pathogens enters bloodstream causes meningitis, leading to death. Will also cause premature births, miscarriages, still birth and meningitis in newborns if pregnant women are infected.
d. Catalase, Listeriolysin (pore-forming protein that aforms hole in phagosome membrances releasing bacteria into host cell), Actin polymerase (forms a "tail" to push the bacteria into a pseudopod that is endocytized by a new host cell).
e. Yes, is Intracellular
f. No vaccine
scarlet fever
a. Group A Strep. (S. pyogenes)
b. Respiratory droplets; Enters through breaks in the skin
c. Usually accompanies strep. pharyngitis, rash that typically starts on chest and spreads across body, tounge turns strawberry red, skin sloughs off.
d. Pyrogenic toxins released by the pathogen triggers a diffuse rash
e. Not intracellular
f. No vaccine
rheumatic fever
a. Group A Strep. (S. pyogenes)
b. Respiratory droplets; Enters through breaks in the skin
c. A complication to untreated Group A strep. pharyngitis, leads to damage of heart valves and muscle
d. Strep. secretes enzymes and toxins that destroy muscle and fat tissues.
e. Not intracellular
f. No vaccine
neonatal meningitis
a. Group B strep.
b. Direct contact
c. Permanent neurological damage, including blindness, deafness, and severe mental retardation
d. Proteases (catabolize proteins), hemolysins (lyse RBCs), deoxyribonuclease ( ), and hylauronidase (breaks down hylauronic acid which is the major component of cell matrix).
e. Not intracellular
f. Yes, vaccine
diphtheria
a. Corynebacterium diptheriae
b. Respiratory droplets; skin contact
c. Sore throat, localized pain, fever, pharyngitis, oozing of intercellular fluid
d. Diphtheria toxin (2 polypeptides. One binds to the growth factor receptor triggering endocytosis. Once toxin is inside these cells, proteolytic enzymes cleave the toxin releasing the second polypeptide int othe cytosol, destroying the elongation factor (a protein needed for synthesis of polypeptides in eukaryotes).
e. No intracellular
f. Yes, DPT
gonorrhea
a. Nisseria gonorrhoeae
b. STD
c. In men, painful urination and pus discharge. Asymptomatic in women.
d. Catalase, Oxidase, IgA protease.
e. Not Intracellular
f. No
meningococcal meningitis
a. Nisseria menigitidis
b. Direct contact; respiratory droplets
c. stiff neck, flu-like
d. Catalase, Oxidase, capsule, LPS, IgA protease
e. Not intracellular
f. Yes, vaccine
hemolytic uremic syndrome
a. E. coli
b. ingestion
c. severe kidney disorder
d. Type III secretion system (injects 2 types of proteins into intestinal cells), shing-like toxin (inhibits protein synthesis in host cells)
e. Not intracellular
f. No vaccine
salmonellosis
a. Salmonella typhimurium and S. entertidis
b. contaiminated foor or water
c. Nonbloody diarrhea, nausea and vomiting, fever, muscle pain, headache and abdominal cramps.
d. No toxins
e. Yes, intracellular
f. No vaccine
typhoid fever
a. Salmonella typhi
b. Contaminated food, or water; Human reservoir - gallbladder
c. Fever, headache, muscle pains, malaise, and loss of appetite.
d. Type III secretion system (complex structure composed of 20 different polypeptides, ultimately forms a channel through which bacterial proteins are introduced into the host cell.
e. Intracellular
f. Vaccine
shigellosis
a. Shigella
b. Contaminated food, direct contact, flies
c. Abdominal cramps, fever, diarrhea and purulent bloody stools
d. Shiga toxin - stops protein synthesis in its host's cells
e. Not intracellular
f. A live, annenuated vaccine, but causes symptoms of mild diarrhea and fever
bubonic plague
a. Yersinia pestis
b. Flea bites
c. High fever, swollen lymphnodes called "buboes", called "Black death" because of darkening of dead skin.
d. Virulence plasmids that code for adhesions which allow for pathogen to attach to human cells and then injects proteins that trigger apoptosis in macrophages and neutrophils
e. Not intracellular
f. No vaccine
pneumonic plague
a. Yersinia pestis
b. Person-to-person; aersols
c. within a day, feve, malaise, pulmonary distress
d. Virulence plasmids that code for adhesions to which allow for pathogen to attach to human cells and then injects proteins that trigger apoptosis in macrophages and neutrophils.
e. Not intracellular
f. no vaccine
chancroids
a. Haemophilus ducreyi
b. STD
c. In men, genital ulcers, pain. Asymptomoatic for women
d. Fimbrae (aids in adhesion), toxin (kills epithelial cells).
e. No intracellular
f. No vaccine
whooping cough
a. Bordetella pertusis
b. Respiratory droplets
c. Usually pediatric, deep coughs with distinct whoop
d. Tracheal cytotoxin (at low levels inhibits the movement of cilia on cells and at high levels causes the expulsion of cells from trachea lining), Dermonectotic toxin (cusese localized constriction and hemorrhage of blood vessels resulting in cell death and tissue deconstruction), Adenylate cyclase toxin (triggers increased mucus production and inhibits leukocytes movement, endocytosis and killing), Pertusis toxin (interferes with ciliated epithelial cells metabolism, resulting in increased mucus production (adheasion)).
e. Not intracellular
f. Yes, an (aP - acellular pertussis)
Legionnaire’s disease
a. Legionella pneumophilia
b. Aerosols, but not person-to-person
c. Fever, chills headache, dry nonproductive cough, and pneumonia
d. No exotoxins?
e. Yes, intracellular
f. No, vaccine
Lyme disease
a. Borrelia burgdorferi
b. Tick bite
c. Red rash "bull's eye" within 30 days, malaise, headaches, dizziness, stiff neck, fever, chills, muscle and joint pain.
d. unknown
e. Not intracellular
f. No vaccine
Staphylococcus aureus
1. Diseases caused - Food poisoning, Scalded Skin syndrome, TSS Syndrome,
Cutaneous infections, Bacteremia, Osteomyelitis,
Endocarditis
2. Identifying properties - Gram + cocci clusters, Catalase +, Coagulase +,
Ferment mannitol, Salt tolerant
3. Route of Transmission - Person-to-person, Contact with contaminated objects
4. Virulence - Coagulase,
Glycocalyx (sticky external sheath of prokaryotic cells), TSS toxin, Exfoliative toxin (causes dissolution of epidermal intercellular bridge proteins that hold adjoining cytoplasmic membranes together), Enterotoxin (stimulate intestinal muscle contractions, nausea, and intense vomiting), hyaluroindase (breaks down hyaluronic acid which is the major component of cell matrix), Lipase (breaks down lipids), B-lactamase (breaks down PCN)
5. Treatment - Methicillin, vancomycin for MRSA
Group A Streptococcus
(Streptococcus pyogenes)
1. Disease caused -
pharyngitis, Scarlet fever,
Pyoderma, TSS, Necrotizing fasciitis, Rheumatic fever,
Glomerulonephritis
2. Identifying properties - Beta-hemolytic, Gram + cocci chains, Catalase –, Surface antigens
3. Route of trans. - Respiratory droplets
4. Virulence - Hyaluronic acid, capsule, Pyrogenic toxins stimulate macrophages and helper T lymphocytes to release cytokines that in turm stimulate (3 types - fever, widespread rash and shock), Streptolysins (proteins that lyse RBC,WBC and platelets which interferes with the oxygen-carrying capacity of the blood, immunity and blood clotting), Erythrogenic toxin (causes blood capallaries near the surface to dilate producing a red rash).
5. Treatment - Penicillin, Cephalosporins, Azithromycin
Group B Streptococcus
(Streptococcus agalactiae)
1. Diseases - Neonatal meningitis, Neonatal pnemonia
2. Identifying prop. - Gram + diplococci, Beta-hemolytic, Catalase –, surface antigens
3. Trans. - Direct contact
4. Virulence - Capsular antigen (
5. Treatment - Penicillin G,
Cephalosporins
Viridans Streptococci
1. Diseases - Dental caries,
Endocarditis
2. Identifying - Gram + cocci, Alpha-hemolytic w/ green pigment
3. Route of trans. - Normal flora
4. Virulence - none
5. Treatment - Penicillin
Streptococcus pneumoniae
1. Diseases- Pneumonia, otitis media, Bactermia, Endocarditis, Meningitis
2. Identifying - Gram + diplococci, Alpha hemolytic, Catalase -
3. Route of trans. - respiratory droplets
4. Virulence - Superinfection, Phosphorylcholine,
Capsule, Protein adhesion,
Pneumolysin, IgA protease
5. Treatment - Penicillin
6. Prevention - Vaccine
Enterococcus
1. Diseases - UTI, Bacteremia
2. Identifying - Gram + chains, Salt tolerant
3. Route of trans. - Direct contact, Superinfection
4. Virulence - none
5. Treatment - Vancomycin
Bacillus anthracis
1. Disease - Cutaneous anthrax, Gastrointestinal anthrax, Inhalation anthrax
2. Identifying - Gram + bacilli, Form endospores,
Aerobic
3. Trans. - Inhalation, ingestion, or inoculation of spores
4. Virulence - Anthrax toxin
5. Treatment - Ciprofloxacin,
Antiserum
6. Prevention - Vaccine is available
Bacillus cereus
1. Diseases - Food intoxication (Emetic form),
Food infection (Diarrheal form)
2. Identifying - Gram + bacilli, Form endospores,
Aerobic
3. Trans. - Ingestion of pre-formed toxin, Ingestion of bacteria
4. Virulence - Heat-stable enterotoxin, Heat-labile enterotoxin
5. Treatment - Supportive care
Clostridium perfringens
1. Diseases - Gas gangrene,
Food poisoning
2. Identifying - Gram + bacilli, Form endospores,
Strict anaerobes
3. Trans. - Inoculation of spores from environment,
Ingestion of spores
4. Virulence - 11 different toxins
5. Treatment - Penicillin; Removal of dead tissue
Clostridium difficile
1. Diseases - Diarrhea, Pseudomembranous colitis
2. Identifying - Gram + bacilli, Form endospores,
Strict anaerobes
3. Trans. - Opportunistic during antimicrobial, therapy, particularly clindamycin
4. Virulence - Exotoxin A & B
5. Treatment - Discontinue broad-spectrum antibiotic therapy

Severe cases: antibiotic treatment (metronidazole)
Clostridium botulinum
1. Diseases - Botulism (food poisoning, Wound infection, Infant botulism
2. Identifying - Gram + bacilli, Form endospores,
Strict anaerobes
3. Trans. - Ingestion (improperly canned food), Environment (wound)
4. Virulence - Botulism toxin, Anti-toxin
5. Treatment - Wash intestinal tract, No honey for infants
Clostridium tetani
1. Disease - Tetanus
2. Identify - Gram +, Form endospores, Strict anaerobes
3. Trans. - Inoculated from environment into puncture wounds
4. Virulence - Tetanus toxin, Anti-toxin
5. Prevention - Tetanus toxoid vaccine
Listeria monocytogenes
1. Diseases - Meningitis,
Bacteremia, Neonatal and in-utero disease
2. Identify - Gram + coccobacilli, Psychrotroph,
Intracellular pathogen of macrophages, Catalase +
3. Trans. - Ingestion, Transplacental
4. Virulence - Listeriolysin-O, Actin polymerization
5. Treatment - Penicillin or erythromycin
6. Prevention - Risk groups avoid nonpasteurized dairy products & cold deli meats
Corynebacterium diphtheriae
1. Diseases - Diphtheria: Pseudomembranous necrosis of throat, systemic toxemia
2. Identifying - Slender Gram + bacilli, Aerobic
3. Trans. - Respiratory droplets or skin contact
4. Virulence - Phage encoded toxin gene, Diphtheria toxin: inhibits protein synthesis
5. Treatment - Penicillin or erythromycin



Anti-toxin (passive immunity)



Vaccination -- DTaP
Mycobacterium tuberculosis
1. Disease - Tuberculosis
2. Idnetify - Acid-fast bacilli, Intracellular pathogen, Slow growth, Strict aerobe
3. Trans. - Aerosols
4. Virulence - Catalase, peroxidase, Cord factor,
Siderophore
5. Combination therapy: isoniazid, ethambutol, rifampin, pyrazinamide
6. Prevention - BCG vaccine –other countries
Mycobacterium leprae
1. Disease - Leprosy
2. Identify - Acid-fast bacilli, Cannot be grown in artifical media (mice, armadillos), Intracellular pathogen
3. Trans. - Direct contact, nasal secretions
4. Virulence - Tuberculoid: high cell-mediated response,
Leprotamous: lack of cell-mediated response
5. Treatment - Clofazamine, dapsone, & rifampin combination therapy
Neisseria gonorrhoeae
1. Disease - Gonorrhea, Neonatal conjuncitivis
2. Identify - Gram – cocci,
Catalase +, Oxidase +, Do not ferment maltose
3. Trans. - STD
4. Virulence - IgA protease
5. Treatment - Broad spectrum antibiotics, Prophylaxis of neonatal conjunctivitis
Neisseria meningitidis
1. Disease - Meningitis
2. Identify - Gram – cocci,
Catalase +, Oxidase +, ferment maltose
3. Trans. - Direct contact, Respiratory droplets
4. Virulence - Capsule, LPS,
IgA protease
5. Treatment - Penicillin, cephalosporin
6. Prevention - Vaccine
Moraxella catarrhalis
1. Disease - Otitis media, Sinusitis, Pneumonia, bronchitis
2. Identify - Gram – cocci,
Oxidase +
3. Trans. - Direct contact, Respiratory droplets, Superinfection
4. Virulence - Iron-binding proteins, Resist complement
5. Treatment - Antibiotics
Escherichia coli
1. Disease - EPEC, ETEC, EIEC, EHEC, Gastroenteritis, dysentery, Hemorrhagic colitis, HUS, UTI
2. Identify - Gram – bacilli, Ferments lactose
3. Trans. - Contaminated water or food, Improper hygiene (UTIs)
4. Virulence - Virulence genes on plasmids or phage,
Exotoxins, Enterotoxin, Type III Secretion, Shiga-like toxin
5. Treatment - Supportive therapy; HUS often requires dialysis; Antibiotics and antidiarrheals are counter-indicated

Antibiotics for UTI
Klebsiella pnemoniae
1. Disease - Pneumonia, Bacteremia, Meningitis,
UTI
2. Identify - Gram – bacilli, Ferments lactose
3. Trans. - Direct contact or contaminated objects
4. Virulence - Concern with
Immunocompromised and alcoholics, Capsule
5. Treatment - Antibiotics
Proteus mirabilis
1. Disease - UTI, Kidney stones, Wound infections, nosocomial
2. Identify - Gram – bacilli, Urease +, Swarm on agar
3. Trans. - Direct contact or contaminated objects,
Superinfection
4. Virulence - Urease
5. Treatment - Antibiotics
Proteus vulgaris
1. Disease - UTI, Kidney stones, Wound infections, nosocomial
2. Identify - Gram – bacilli, Urease +, Swarm on agar
3. Trans. - Direct contact or contaminated objects, Superinfection
4. Virulence - Urease
5. Treatment - Antibiotics
Salmonella typhimurium & S. enteritidis
1. Disease - Salmonellosis
2. Identify - Gram – bacilli, Do not ferment lactose, Produce H2S
3. Trans. - Contaminated food or water
4. Virulence - Type III Secretion, Capsule, LPS, Endotoxin
5. Treatment - Supportive therapy
Salmonella typhi
1. Disease - Typhoid fever
2. Identify - Gram – bacilli, Do not ferment lactose, Produce H2S
3. Trans. - Contaminated food or water; Human reservoir: gall bladder
4. Virulence - Type III Secretion, Endotoxin, Capsule
5. Treatment - Chloramphenicol & sulfonamides; May require choleocystectomy
6. Prevention - Vaccine: Short term immunity
Shigella
1. Disease - Shigellosis (Dysentary)
2. Identify - Gram – bacilli
3. Trans. - Contaminated food, direct contact, flies
4. Virulence - Type III Secretion, Enterotoxin,
Shiga toxin
5. Treatment - Antibiotics and antidiarrheals are counter-indicated
Yersinia pestis
1. Diseases - Bubonic plague, Pneumonic plague
2. Identify - Gram – bacilli
3. Trans. - Flea bites,
Direct contact with infected animals, respiratory droplets
4. Virulence - Type III Secretion
5. Treatment - Antibiotics
Haemophilus influenzae
1. Disease - Meningitis, Otitis media, Sinusitis, bronchitis / Pneumonia
2. Identify - Gram – bacilli, Obligate parasites – require heme and NAD+
3. Trans. - Respiratory droplets
4. Virulence - polysaccharide capsule, fimbrae, IgA protease
5. Treatment - Antibiotics
6. Prevention - Hib Vaccine
Haemophilus ducreyi
1. Disease - chanchroid
2. Identify - Gram – bacilli, Obligate parasites
3. Trans. - STD
4. Virulence - Fimbrae
5. Treatment - Antibiotics
Bordetella pertusis
1. Disease - Whooping cough
2. Identify - Gram – bacilli, Aerobic
3. Trans. - Respiratory droplets
4. Virulence - Filamentous, hemagglutinin, Pertussis toxin, Tracheal toxin,
Lethal toxin, Adenylate cyclase toxin
5. Treatment - Erythromycin (1st & 2nd stage)
6. Prevention - Vaccination, DTaP
Pseudomonas aeruginosa
1. Disease - opportunistic infections, Nosocomial infection, Burn and wound infections, Cystic fibrosis patients
2. Identify - Gram – bacilli, Aerobic
3. Trans. - Direct contact,
Environment
4. Virulence - Resistant to many antibiotic
Legionella pneumophila
1. Disease - Legionnaire’s Disease
2. Identify - Gram – bacillus, Fastidious
3. Trans. - Found in water,
Intracellular parasite, Aerosols (Not person-to-person)
4. Virulence - Survive in environment inside amoebas
5. Treatment - Quinolones,
Macrolides
Mycoplasma pneumoniae
1. Disease - Walking pneumonia
2. Identify - Smallest free-living microbe, Lack cell walls, Sterols in cell membrane
3. Trans. - Nasal secretions
4. Virulence - Attachment to base of cilia on respiratory epithelial cells
5. Treatment - Macrolides,
Tetracycline
Borrelia burgdorferi
1. Disease - Lyme Disease
2. Identify - Gram – spirochete, Microaerophilic
3. Trans. - Tick bite
4. Virulence - Host immune response causes symptoms in later stages
5. Treatment - Doxycycline, tetracycline – 1st stage
Vibrio vulnificus
1. Disease - Necrotizing faciitis, Bacteremia
2. Identify - Curved gram – rods, Halophilic – salt water
3. Trans. - Ingestion of contaminated shellfish,
Inoculation into wounds
4. Virulence - Capsule, Fimbriae, Cytotoxins
5. Treatment - Tetracycline, Cephalosporins, Wound debridement
Campylobacter jejuni
1. Disease - Food infection -- gastroenteritis
2. Identify - Curved gram – rods, Microaerophilic
3. Trans. - Ingestion
4. Virulence - Motility, Cytotoxin, Enterotoxin, usually self-limiting
1/1000 cases à Guillain-Barre