Test 2b Flashcards
Listeria monocytogenes
- Main Biological Features
a. gram positive regular (stain uniformly + don’t assumer pleomorphic shape)
b. Non spore forming Bacilli
c. coccobacilli to long filaments
d. lack capsules, 1-4 flagella
e. resistant to cold, heat, salt, pH extremes, + bile
d. avoids humoral immune system
e. typically found singly or in short chains
f. grows in refrigeration - Clinical Manifestations
Listeriosis- most cases associated with dairy products poultry and meat
a. often mild or subclinical in normal adults - mechanisms of disease
a. ability to replicate in the cytoplasm of cells after inducing phagocytosis; avoids humeral immune system - Transmission
a. primary reservoir is soil and water; animal intestines
b. can contaminate food and grow during refrigeration, does not change taste or smell
c. amino compromised patients, Fetuses, Neonates; Affects brain and meninges-20% death rate
d. replicates with in the cytoplasm of the host cell after inducing its own phagocytosis - prevention
a. pasteurization and cooking - treatment
a. Rapid diagnostic test using ELISA, immunofluorescence, and DNA Analysis
b. antibiotics
Erysipelothrix rhusiopathiae
- main biological features
a. gram-positive rod widely distributed in animals and the environment
b. primary Reservoir-tonsils of healthy pigs
c. zoonotic pathogen - transmission
Enters through skin abrasion - clinical manifestations
-septicemia
-endocarditis
Multiplies to produce erysipeloid, dark red lesions - prevention
Vaccine for pigs
Thorough cleaning of wounds - treatment
Antibiotics
Cornyebacterium diptheriae
- main biological features
-gram-positive the regular bacilli
-Gray biofilm
-nonmotile, non capsulated: pleomorphic, stain unevenly - clinical manifestations
-Diphtheriae
-toxemia
-endocarditis - Mechanisms of disease
Two stages of disease:
Local infection(primary infection)-upper respiratory tract inflammation
-sore throat, nausea, vomiting, Swollen lymph nodes
-pseudomembrane formation(Gray biofilm) can cause asphyxiation
-cutaneous(secondary infection) - mechanisms of disease
-diptherotoxin production and toxemia
–Target organs primarily partners - transmission
-reservoir of healthy carriers
-children in crowded + unsanitary conditions
-respiratory droplets from carriers or infected - prevention
Toxoid vaccine series and boosters - treatment
-antitoxin
-antibiotic
Genus Propionibacterium
- man biological features
- irregular: pleomorphic, stain unevenly
- gram-positive, non-spore forming bacilli
- Propionibacterium acnes most common
- Graham positive rods
- zero tolerance our anaerobic
- non-toxigenic
- come resident of pilosebaceous glands - clinical manifestation
- Acne
- occasionally eye and artificial joint infections
Mycobacteria; acid-fast bacilli
- main biological features
- not gram stain organisms
- gram-positive irregular bacilli
- strict aerobes
- Produce catalase
- possess mycolic acids and a unique type of peptidoglycan
- no capsules, flagella, or spores
- slow growth
Mycobacterium tuberculosis
- main biological features
-tubercle bacillus
-see mycobacteria; acid-fast bacilli - clinical manifestations
-tuberculosis
–primary tuberculosis-beginning, exudative phase
–secondary tuberculosis(reactivation/ reinfection) body encapsulates, can’t destroy, cells form physical barrier granuloma, creates latency(violent coughing, Bloody sputum)
–disseminated (extrapulmonary) tuberculosis
Damage to kidneys, Long bones, genital track, brain, and meninges, grave consequences - mechanism of disease
-no exotoxins or enzymes that contribute to infectiousness
-complex waxes and cord factor that prevent destruction by lysosomes and macrophages - transmission
-Airborne respiratory droplets
-disease of Poor cultures
-weak immune system, Poor nutrition, lung damage, poor access to medical care, genetics - prevention
Vaccine - treatment
-6 to 24 months of at least two drugs from a list of 11
Mycobacterium leprae
- main biological features
- see mycobacteria; acid-fast bacilli
- acid-fast rods
- strict parasite, slowest growing of all species - clinical manifestations
- lepromatous leprosy, deep nodular infection, severe disfigurement
- tuberculoid leprosy, shallow lesions, damaged nerves - mechanism of disease
- not highly virulent
- can live and grow within macrophages
- Schwann cells
- wax like other mycobacterium for protection - transmission
- mechanical vectors, in contact with a leprotic
- inhalation of droplet nuclei - prevention
- WHO trial vaccine
- surveillance of high-risk populations
- chemoprophylaxis of healthy persons in close contact - Treatment
- Long term combine therapy, five years or lifelong
- increased and resistant strains
Non-tuberculosis mycobacteria
M. avium complex
M. marinum
M. avium complex
-third most common cause of death and AIDS patients
-soil bacteria through respiratory tract
-treatment requires two or more combined drugs, several months to years
M. marinum
- water and inhabitant; lesions developed after scraping on swimming pool concrete
-localized nodule, ulcerates, and drains
-can require long-term treatment, typically clears up spontaneously
Aerobic gram-negative non-enteric bacilli
Pseudomonas
Brucella
Bordetella
- large diverse group of nonspore forming bacteria
- wide range of habitats, large intestines(enteric), zoonotic, respiratory, soil, water
- most not medically important; some are true pathogens, some are opportunist
- all have outer membrane lipopolysaccharides of the cell wall, endotoxin
Pseudomonas-opportunistic pathogens
Pseudomonas aeruginosa
- main biological features
-small gram-negative rod with a single polar flagellum
-produce oxidase and catalase
-use aerobic respiration, Do not ferment carbohydrates
-Many produce water soluble pigments
-resistant to soaks, dies, Quaternary ammonia disinfectants, drugs, drying
-protease, amylase, pectinase, Cellulase positive
-grapelike odor, greenish blue pigment
-can degrade natural substrates, like oil spill cleanup/ clearing pesticides - clinical manifestations
-infections in patients with severe burns, neoplastic disease, cystic fibrosis
,-leads to endocarditis, bronchopneumonia, or meningitis
-healthy persons acquire skin rashes, UTIs, ear infections - mechanism of disease
-pili that aid in attachment of bacteria to host cells
-phagocytosis resistant slime layer, contribute to biofilm formation
-enzymes that degrade host issues
-exotoxins the damage/destroy neutrophils and lymphocytes
-the lipopolysaccharide layer of the outer membrane also causes endotoxic shock - transmission
-invasive medical procedures or weakened defenses
-contaminate ventilators, mops, bathrooms - Prevention
-difficult because so resistant - treatment
-drug sensitivity testing a necessity
-multidrug resistant
-effective drugs cephalosporins, Third and fourth generation
Brucella and Brucellosis
- main biological features
- Tiny gram-negative coccobacilli
- two species:
- -Brucella Abortus (cattle)
- -Brucella suis (pigs) - clinical manifestations
- brucellosis, Multi fever, undulant fever, Bang disease(zoonosis- transmitted to humans from the infected animals) - Mechanism of disease
- ability to survive and grow inside of macrophages
- Macrophages transport pathogen into the bloodstream - Transmission
- occurs through contact with blood, urine, placentas, and consumption of raw milk and cheese in animals
- slaughter houses, Livestock handling, a veterinarian - prevention
- animal vaccine available
- Testing and eliminating the infected animals
- pasteurization of milk
- potential for germ warfare - Treatment
- Antibiotics for six weeks
Bordetella pertussis
- main biological features
- small, gram-negative coccobacillus
- found singly or in pairs
- Encapsulated and nonmotile - clinical manifestations
- whooping cough(two stages)
- -catarrhal stage-you can still there in airways, coughing, sneezing
- -paroxysmal stage-persistent coughing, followed by deep inhalations
- bronchitis(acute respiratory syndrome) - mechanism of disease
- fimbraelike adhesion molecules, bind to ciliated respiratory epithelial cells
- exotoxins destroy host cells after bacterium has bound - transmission
- Direct contact with inhale droplets or aerosols given off during coughing stage of infection
- Half between birth and four years of age - Prevention
- Vaccination and booster (DTaP) - treatment
- One-week standard therapy of antibiotics
Pertussis toxin
Pertussis toxin
- G protein adds ribose
- ribose switches G protein to on position
- Adenylate and cyclase add enzyme
- cAMP= messenger in cell
- kinases go crazy
- ion channels
- ions and water (disturbs water transfer
Enterobacteriaceae Family(create sugar cravings)
- main biological features
- small, Nonspore forming gram-negative rods
- inhabit soil, Water, decaying matter,, and occupants large bowel of animals including humans
- most frequent cause of diarrhea through enterotoxins
- enterics, Account for almost 50% of nosocomial infections w/ Pseudomonas sp.
- facultative anaerobes, Grow best in air
- all fermented glucose, reduced nitrate to nitrite, Oxidase negative, And catalase positive
- coliforms and non-coliform
- coliforms the lactose fermenters(intestines primarily)
- Non-coliforms non lactose fermenters - clinical manifestations
- gastroenteritis
- Severe diarrhea - mechanism of disease
- resistant to drying, disinfectants, and drugs
- most frequent cause of diarrhea through enterotoxins
- H- flagellar Ag
- K- capsule or fimbrae Ag
- O- somatic or cell wall Ag- all have
- endotoxins- LPS - transmission
- contaminated food or water - prevention
- donate contaminated food or water - treatment
- Replenish electrolytes and water loss
Eschericha coli
- main biological features
-Small, motile, gram-negative rod’s
-most common aerobic and non-fastidious bacterium in the gut
Multiple pathogenic strains
-Enterotoxigenic-causes severe diarrhea, Self resolving in two to four days, no blood, heat labile toxin, and heat-stable toxin, and fimbrae
-enteroinvasive-inflammatory disease of the large intestine common crosses intestinal wall, Blood in stool
-enteropathogenic-can cause ulcers, infantile diarrhea, crosses intestinal wall
-enterohemmorhagic-0157:H7 strain, causes hemorrhaging and kidney damage, most dangerous, destroys walls of vascular system, crosses intestinal wall,(H.U.S., hemolytic uremic syndrome- anemia caused by destruction of red blood cells and acute kidney failure(uremia) caused by SHIGA toxin
-plasmid transfer - clinical manifestations
-diarrhea
-Infantile diarrhea
-Travelers diarrhea
-H.U.S.
-50-80% of UTIs - mechanisms of disease
-Capsule
-LPS endotoxin
-individual strains possess heat labile and heat stable toxins and shiga toxin - Transmission
-consumption of spoiled food and water
-sewage
-Fecal matter - prevention
–Water treatment
-Pasteurization
-proper food preparation - treatment
-pepto-Bismol
-Self-limiting
-HUS use antibiotics not always effective though