Exam 2 Lectures 9-14 – Flashcards

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Factors Influencing Oral Microbiota (5)
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1. Salivary Flow
2. Antibiotics
3. Diet
4. Age
5. Gender
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Bacteremia
Relevance in Dentistry?
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Presence of bacteria in the blood.
Oral bacteria can become opportunistic pathogen, inflammatory response to oral bacteria may be risk for cardiovascular diseases.
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Primary Colonizers of tooth (4)
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1. Streptococci
2. Actinomyces
3. Spirochetes
4. Gram-negative anaerobes.
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Sore Throat (Pharyngitis)
1. Caused by? (Virus, Bacteria, Fungi)
2. Pathogen? Harmful agent3. Most susceptible4. Treatment
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1. Bacteria
2. Strep. Pyogenes. Erythrogenic Toxin.
3. Children 5-8 yrs. old
4. Penicillin and Erythromycin
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Enterococci (General Characteristics)
1. Common acquisition2. Reservoir for3. Harmful because?
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1. Nosocomial - as a result of treatment in a hospital
2. Reservoir of antibiotic resistance genes for other streptococci.
3. Harmful because they can be hemolytic (exotoxin)
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Streptococcus Pyogenes
1. Significance
2. Diseases
3. Virulence Factor
4. 3 Exotoxins and what they do
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1. Clinically the most important streptococci
2. Pharyngitis, Scarlet Fever, Necrotizing Fascitis, Toxic Shock Syndrome, Rheumatic Fever, Glomerulonephritis.
3. M-Protein, F-Protein, Exotoxins. M-Protein sticks out of cell membrane and is anti-phagocytic.
4. a.Pyrogenic Toxin - Causes rash in scarlet fever and causes streptococcal toxic shock disease
b. Streptolysin O/S - cell lysis
c. Streptokinase - dissolves clot - used as medication to treat strokes
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Impetigo
1. Causative Agent
2. Characteristic Symptoms
3. Treatment
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1. Streptococcus Pyogenes
2. 2-5 yr olds susceptible, skin ulcers, crusted skin lesions.
3. Penicillin
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Necrotizing Fascitis
1. Causative Agent
2. Characteristic Symptoms
3. Treatment
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1. Streptococcus Pyogenes
2. Deep soft tissue infection
3. Surgical drainage and aggressive antibiotic therapy
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Streptococcus Agalactiae
1. Where found2. Diseases caused3. Susceptible groups?
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1. Vagina and Urethral Mucosa
2. Meningitis, postpartum infections (endometritis)
3. Pregnant women - often treated with prophylactics
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Streptococcus Pneumoniae
1. Significance
2. Diseases
3. Virulence Factor(s)
4. Susceptible groups
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1. Most common cause of pneumonia and otitis media.
2. Pneumonia (inflammation of lungs), Otitis Media(middle ear infection), Meningitis (swelling of membranes covering brain and spinal chord)
3. Autolysin, activated by beta-lactam drugs and releases toxin that attacks mammalian cell membrane and lyses them
4. Undernourished, alcoholism, smoking, children for otitis media
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Meningitis
1. Causative Agent
2. Significance
3. Treatment
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1. Streptococcus Pneumoniae
2. High mortality rate.
3. Third generation Cephalosporins
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Diptheria
1. Causative Agent
2. Characteristic Symptoms
3. Treatment and Susceptible Groups
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1. Corynebacterium Diptheriae.
2. Diptheriae is an upper respiratory tract infection. Pharynx becomes swollen and may obstruct airway. If toxin enters blood can cause myocarditis(inflammation of heart muscle)
3. Since toxin is harmful, antibiotics only useful early on, then antitoxin must be used. Best treatment is prevention via vaccination.
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Vincent's Angina
1. Causative Agent
2. Characteristic Symptoms
3. Treatment
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1. Oral Spirochetes - often related to poor oral hygiene
2. "Trench Mouth" progressive painful infection with ulceration, swelling, and sloughing dead tissue
3. Penicillin, Metronizadole, removal of infected tissue.
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Whooping Cough
1. Causative Agent
2. Characteristic Symptoms
3. Treatment
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1. Bordetella Pertusis
2. Lower GI infection. Sudden outburst of coughing followed by rapid inhalation "whoop".
3. Erythromycin and vaccination.
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Bronchitis
1. Causative Agent
2. Characteristic Symptoms
3. Treatment
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1. Streptococcus Pneumoniae and H. Influenzae
2. Bronchitis is an inflammation of the lung tissue. Dry painful cough followed by green mucous excretion.
3. Antibiotics.
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Tuburculosis
1. Caused by2. Characteristic Symptoms3. Treatment
4. Special test
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1. Mycobacter Tuburculosis
2. Initially, flu-like symptoms that develop into calcified lung lesions and lung tissue destruction.
3. Isoniazid, Ethambutol, Rifampin, Streptomycin, Pyrazinamide
4. Skin test with injection of Purified Protein Deritavie of Mycobacterium, active disease or past infection produces hard lesion.
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Candidiasis
1. Causative Agent
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1. Opportunistic Pathogens - fungal infection found only in immunocompromised individuals
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Staphylococcus Aureaus
1. Where found2. Oxygen tolerancy3. Difficulties in treating?
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1. Skin, particularly moist skin, axilla, groins.
2. Facultative Anaerobe - produces catalase
3. Antibiotic resistance becoming very common
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Staphylococcus Aureus
1. Exotoxin causes what2. Common source of? Why3. Notable Structural Characteristics
4. Enzyme of clinical significance
5. Toxin
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1. Food poisoning, Toxic Shock Syndrome (Food Poisoning), Boils, Caruncles, Scalded Skin Syndrome
2. Nosocomial Infections - hospital workers become carriers. 20% of humans are carriers.
3. Capsule, Slime Layer, Teichoic Acid (Rigidity to cell wall), Protein A (binds IgG)
4. Hyaluronidase(hydrolyzes Hyaluronic acid in CT)
5. Enterotoxin causes food poisoning
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Boils and Carbuncles
1. What causes2. What are they3. How are they treated?
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1. Staphylococcus Aureus
2. Hair follicle infection - neutrophils cause pus formation. Carbuncles are just a really deep boil.
3. Boils require no treatment, Carbuncles require drainage and antibiotic treatment.
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MRSA
1. Stands for2. Two kinds? Which is more severe, Why3. What do they cause4. How treat each kind?
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1. Methicillin Resistent Staphylococcus Aureus
2. Hospital acquired and Community acquired - Hospital acquired bc strains are Beta Lactamase producing and possess altered PBP.
3. Hospital acquired causes serious infections requiring longer hospital stays, community acquired causes skin and soft tissue infections.
4. Community acquired - sensitive to antibiotics. Hospital acquired - newer antibiotics such as daptomycin, linezolid, synercid.
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Necrotizing Pneumoniae
1. What causes it? How is it acquired2. What is it?
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1. Staph Aureus. Usually aspiration of foreign materials.
2. Infection of lungs from aspiration of staph carrying substance.
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Staph Toxins
1. Toxins (5) What do they doa. alpha
b. beta
c. gamma
d. delta
e. PVL
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a. Alpha - form pores sodium influx
b. Beta - hot/cold lysis.
c. Gamma - lysis neutrophils and macrophages.
d. Delta - Produced by all staph - disrupts membrane, detergent action.
e. PVL - Lyses leukocytes by forming membrane pores, found in community acquired MRSA.
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Scalded Skin Syndrome
1. What causes it2. What is it?
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1. Exfoliatin toxin of Staph Aureus.
2. Exfoliatin attacks desmosomes in stratum granulosum and separates epidermal layer of skin.
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Toxic Shock Syndrome
1. Most common cause2. What is it? How developed3. What causes recurrence?
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1. Toxic Shock Syndrome Toxin and Enterotoxin B and C from Staph Aureus.
2. Fever-like symptoms, rash. Toxins act as superantigen and cause massive release of cytokines, macrophages, t-cells, Tumor Necrosis Factor.
3. Lack of antibocies against super antigen.
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Food Poisoning
1. What causes it2. What is it? Characteristic Symptoms
3. Treatment
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1. Enterotoxin from Staph. Aureus
2. Flu-like symptoms. Caused by eating contaminated food. Diarrhea, vomiting.
3. Fluid replacement and rest, no need for antibiotics.
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Staph Epidermidis
1. What does it cause2. How is it commonly acquired?
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1. Endocarditis of heart valves and artificial joints.
2. During valve replacement or surgery.
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Staph. Saprophyticus
1. What does it cause2. Structural features significant3. Treatment?
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1. Urinary Tract Infections.
2. Slime layer that helps adhere to urinary epithelium.
3. Easily treated with penicillins.
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Gas Gangrene
1. What causes it? Common acquisition.
2. Characteristic Symptoms
3. Treatment
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1. Clostridium Perfringens. Accidental contamination of wound or during surgery.
2. Excruciating pain, tissue damage, organism multiplies in tissue and destroys muscle mass.
3. Removal of dead tissue, antibiotics.
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Tetanus
1. What causes it? Structural features2. What is it3. Treatment
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1. Clostridium tetani - enters through broken skin. Endospores highly resistant, anaerobic thrives in wounds after closed.
2. Toxin called tetanospasmin causes excessive activity of motor neurons and result in muscular spasms.
3. Antitoxin, excision of infected area, immediate cleaning with peroxide.
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Wound and Burn Infections
1. Pathogens involved2. Treatment and Prevention?
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1. S. Aureus, E. Coli, Clostridium Difficile, Bacteroides Fragilis, Psuedomonas aeruginosa (Critical in Burn Infections)
2. Removal of infected area, antibiotic treatment, prophylactics.
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Psuedomonas
1. What are they? What do they form2. What do they cause3. Structural/Virulence characteristics?
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1. Gram-negative rods, colonize moist environments. Involved in biofilm formation.
2. Infections in wounds, burns, cystic fibrosis.
3. Endo and Exotoxins, pili for attachment.
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Helicobacter Pylori
1. Where do they live2. What do they cause? How3. Toxins
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1. Upper GI - adhere to gastric mucosal epithelial cells.
2. Stomach and Duodenal Ulcers, gastric cancers. The bacteria can weaken the protective coating of the stomach, allowing digestive juices to irritate the sensitive stomach lining.
3. Urease and CagA Protein - secreted into target epithelial cell.
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Enterobacteriaceae
1. Common strains2. Where do they live3. How do they produce disease?
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1. E. Coli, Salmonella, Shigella, Yersenia
2. Normal part of Gut Flora
3. They invade mucosal epithelium and produce toxins
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Dysentery
1. What causes it? How2. What are the symptoms3. Pathogenesis
3. How can it be treated?
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1. Shigella. Fecal-oral transmission, person person contact, food, water.
2. Bloody Diarrhea, severe intestinal cramping.
3. Invasion of colonic mucosal epithelial cells via actin-mediated motility. Shiga toxin produced by some strains. Very low infective dose, common in US and huge problem in developing countries.
4. Antibiotics
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Bacterial Type III Secretion Systems
1. What is it2. Which bacteria is it found in3. What effects does it have?
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1. Mechanism for directing effector proteins directly onto target cells
2. Gram-negative bacteria
3. Disrupts host cells signaling, disturbs inflammatory response, disturbs cytoskeletal structure.
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Acute Watery Diarrhea
1. What causes it2. Pathogenesis
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1. ETEC - Enterotoxigenic E. Coli
2. ETEC colonizes small intestine using fimbriae, and increases intracellular cGMP. Two toxins produced. HeatLabile (LT), and HeatStable (ST).
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Persistent inflammatory non-bloody diarrhea
1. What causes it2. Pathogenesis
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1. EPEC - Enteropathogenic E. Coli
2. EPEC colonizes small intestine. Once there, it adheres to intestinal mucosa and causes a rearrangement of the actin filaments. This deforms the cells causes inflammation, and ultimately causes diarrhea.
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Bloody Diarrhea and Hemolytic Uremic Syndrome
1. What causes it? - What is it2. Pathogenesis
3. Epidemiology
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1. EHEC - Enterohemorrhagic E. Coli. Bloody diarrhea leads to reduced platelet counts and breakdown of RBC's (HU-Syndrome)
2. EHEC colonizes colon fia fimbriae attatchment. It produces Shiga-toxin that elicits intense inflammatory response.
3. Most likely in children, and elderly, improperly cooked beef primary source of infection.
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Typhoid
1. What causes it2. Pathogenesis
3. Symptoms
4. Treatment
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1. Salmonella Enterica Serotype Typhi
2. Exposed to human source. Fimbriae attach, and perforate through intestinal wall and are phagocytyzed by macrophages where they can survive within.
3. Prolonged high fever that after 3 weeks leads to ulcers, hemorrhage.
4. Antibiotics, and 2 vaccines available.
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Acute gastroenteritis
1. What causes it2. What are the symptoms3. Pathogenesis4. Epidemiology?
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1. Salmonella Enterica non-typhi serotype
2. Abdominal cramps, diarrhea, fever. Progression to systemic infections.
3. Colonization of Small Intestine, invasion of epithelial cells. Type III secretion system (effector proteins injected directly onto target cells)
4. Acquired from animal sources, major etiologic agent of diarrhea in US
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Vibrios
1. Shape
2. Growing Conditions
3. Diseases
4. Toxins
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1. Curved Rods
2. Alkaline (pH 8-9.5) salt-water.
3. Cholera and Wound infections
4. Cholera Toxin and Toxin Coregulated Pilus
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V. Parahaemolyticus
1. Diseases caused
2. How acquired3. Where common?
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1. Dysentery, diarrhea, bowel inflammation
2. Ingestion of raw food
3. Cruise ships, Japan
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V. Vulnificus
1. Disease caused2. How and where acquired?
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1. Wound infection
2. Raw foods and exposure to contaminated seawater
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V. Cholerae
1. What does it cause2. Pathogenesis3. Epidimiology?
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1. Cholera - infection of small intestine that causes watery diarrhea.
2. Cells adhere to epithelial small intestine cells via pili. Produce Cholera toxin.
3. Common in India, Africa, South America.
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Campylobacter jejuni
1. Morphology2. Diseases3. Pathogenesis4. Epidemiology?
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1. Gram-negative curved rod (similar to vibrios)
2. Infections diarrhea.
3. Low infectious dose. Contaminated food, adhesion to intestinal mucosa, intracellular migration via microtubules. Outer membrae reacts with hosts myelin.
4. Frequent in developing world.
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Bacteroids
1. Common environment2. Virulence factors3. Diseases?
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1. Colon (25% of bacterial population)
2. Oxygen tolerant (though anaerobic), resistant to antibiotics, capsule, produce toxins.
3. Abdominal, peritonial abscess
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Clostridium Difficile
1. Diseases2. Pathogenesis3. Special test for diagnosis?
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1. Nosocomial diarrhea, psuedomembranous colitis (ulcerative disease)
2. Endospores on fomites produce enterotoxin and cytotoxin.
3. ELISA
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Clostridium Perfringens
1. Diseases
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1. Food Poisoning (Also Staph Aureus) -
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Frequent colonizers of Vagina (3)
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a. Lactobacilli
b. Beta Hemolytic Strep
c. Candida Albicans
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Fungi General Characteristics
1. Yeasts, shape, how many2. Moulds, shape, how many3. What is dimorphic4. What is Ergosterol5. Virulence Factors6. Type of infections (2)
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1. Oval Shaped, individual
2. Fillamentous, multicellular
3. Can change between mold and yeast
4. Lipid-based hormone that is present in fungal cell walls, common target of antifungal drugs.
5. Capsule, Dimorphism, Exotoxins.
6. Superficial (on skin athletes foot), Systemic (fungi penetrate physical barriers)
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Virulence Factors of Fungi (CHADM)
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Capsule - hides from antibodies
Hydrolytic Enzymes - tissue damage adn penetration
Adhesins - cell attatchment
Dimorphism - switch yeast and mould
Melanin - protects against UV
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Candidiasis Albicans
1. Diseases Caused2. Epidemiology
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1. Oral Thrush, Vaginal and Erythematous Candidiasis, PMC, Diaper Rash, angular chelitis, Candidial Leukoplakia.
2. Antibiotic patients, opportunistic pathogen that invades when normal flora is displaced.
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Psuedomembranous Candidiosis
1. What causes it2. What is it?
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1. Candididiasis albicans
2. Creamy-white plaques on tongue, cheeks.
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Angular Chelitis
1. What causes it2. What is it?
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1. Candidiasis Albicans
2. Inflammation at angle of mouth, seen in denture related candidiosis.
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Candidial Leukoplakia
1. What is it2. What causes it?
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1. White patches in oral mucosa that can't be rubbed off, can lead to cancer.
2. Candidiasis albicans.
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Predisposing factors for Oral Candidasis
(3)
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1. HIV infection
2. Drug Therapy
3. Diabetes Mellitus
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Systemic Candidiasis
1. What causes it2. Pathogenesis
3. Epidimiology
4. Treatment
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1. Candidiasis albicans
2. Entry into blood - attatches to endotnelial cells - transmigration(rearrangement of microtubules) - endocytosis. Usually in lower respiratory or urinary tract.
3. Broad spectrum antibiotics make more susceptible. Common nosocomial blood infection.
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Croptococcus Neoformans
1. What does it cause2. Virulence Factors3. Where is it found?
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1. Pneumonia like symptoms followed by meningitis.
2. Thick capsule that protects cells.
3. Found in pigeon droppings and soil.
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Histoplasma Capsulatum
1. What does it cause2. Where is it found3. What can it be treated with3.
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1. Respiratory illness
2. Soil contaminated with bat and poultry droppings
3. Though Fungal, Can be treated with antibiotics.
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Coccidiomyces Imitis
1. What does it cause? What are the symptoms2. Where is it found3. Treated with?
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1. San Joaquin Valley Fever - Lung infection. Fatigue, Cough, Fever, 60% of patients non symptomatic.
2. Southern US and Northern Mexico
3. Flucanozole and Amphotericine B (Antifungals)
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Dermatophytes
1. What are they?
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1. A group of fungi that live on skin and cause skin infections because of their unique ability to derive nutrients from keratinized material (hair, nails), cause athlete's foot, ring worm.
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Species of Dermatophytes and 1 fact (3)
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1. Tricophytum Rubrum - person to person
2. Tricophytum Tonsurans - person to person
3. Microsporum Canis - animals to people
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Aspergillosis
1. What causes it2. What is it?
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1. Aspergilus Fumigatus
2. Fungus ball that colonizes in a healed lung scar. Pulmonary aspergillosis is an allergic reaction to fungus in lungs.
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Mycotoxins
1. Types (TEACO)2. Where are they common?
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1. Trcothecenes, Ergot alkaloids (LSD), Aflatoxin, Citrinin, Ochratoxin.
2. Common in underdeveloped nations and potential weapon for bioterrorism, suspect in indoor moulds.
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DNA Viruses use what for replication? (2)
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1. Host cell enzymes for transcription.
2. Unusual RNA polymerase or regulatory protein to circumvent host transcription machinery.
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Polymavirinae Characteristics (2)
1. Where does it replicate2. What type of DNA3. What do they cause?
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1. Replicates in nucleus
2. DS, circular, supercoiled
3. Tumors at multiple sites in experimental animals.
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Adenovirus
1. What does it cause2. How, when?
3. Where is latent virus isolated4. Virulence factor?
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1. Conjuctivitus - swelling of eye, Pharyngitis, Pneumonia, Gasteroenteritis, Myocarditis
2. Fecal-oral route, early in life.
3. Tonsils
4. Group-specific antigen associated with capsid protein
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Enterovirus (AKA)
1. What does it cause?
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AKA Coxsackie Virus
a. Asymptomatic at onset
b. Encephalitis (inflammation of brain)
c. Pulmonary edema
d. Hemmorhage.
e. Respiratory infections
f. Pediatric myocarditis
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HPV
1. How is it transmitted2. What does it cause3. Process of formation
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1. Sexually transmitted
2. Genital warts, cervical cancer.
3. a. infect basement membrane
b. cells proliferate and keratinize
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Herpesvirus
1. Where do they replicate and what2. What is involved in Latency3. Stages Chickenpox (MPFC)
4. Where do chickenpox infect? What do they develop into?
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1. In the nucleus, capsid and large numbers of enzymes used for DNA replication.
2. Latency Associated Transcript (LAT), repressor for E1 gene.
3. (Mary Poppins Flies Cheery), Macule, Papule, Fluid-Filled Vesicle, Crusting
4. Basal root ganglia, shingles.
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Poxviridae (AKA)
1. What are two subfamilies2. Unique characteristic3. Where does smallpox vaccine come from?
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AKA - Smallpox Virus
a. Vertebrate pox viruses (chordopoxvirinae)
b. Insect pox viruses (entemopoxvirinae)
2. Only DNA virus that replicates outside the nucleus
3. Vaccinia Virus -
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Hepadnavirus (AKA)
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Hepatitis B Virus
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PicoRNAvirus (Name disease)
1. Enterovirus
2. Cardiovirus
3. Rhinovirus
4. Apthovirus
5. Hepatovirus
6. What does CPE do7. What are all receptors8. What happens in the canyon?
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1. Polio
2. Encephalomyocarditis Virus
3. Cold Virus
4. Foot and Mouth Disease
5. Hepatitus A
6. Shuts down host protein synthesis
7. Super IG family
8. Receptor binding site
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