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238 Cards in this Set
- Front
- Back
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organism that causes folliculitis
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Staphlococcus epidermidis and aureus
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organism that causes rocky mountain spotted fever
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Rickettsia rickettsii (intracellular bacterium)
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folliculitis is a disease of...
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the skin and wounds
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rocky mountain spotted fever is a disease of...
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the skin and wounds
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symptoms include: infection of hair follicle, carbuncles, boils
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folliculitis
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symptoms: non-itchy rash on trunk and appendages on or after day 3
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rocky mountain spotted fever
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severe cases of this disease cause the respiratory, CNS, GI, & renal systems to fail
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rocky mountain spotted fever
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outermost layer of the skin is
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keratinized
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defenses of the skin it is covered with _______ and ________
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salt and sebum
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trauma to any tissue of the body
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wound
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normal skin microbiota include
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Malassezia, staphylococcus, Micrococcus, && Diphtheroids
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gram-positive cocci, arranged in clusters
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Staphylococcus
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Staphylococcus is tolerant of (4)
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salt, desiccation, radiation, && heat
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accounts for up to 90% of the bacteria on the skin
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S. epidermidis
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more virulent of the two staphylococcus species
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aureus
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grows in nasal passages and moist skin folds
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S. aureus
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coagulase
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immunological disguise used by staphylococcus
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hyaluronidase
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promotes spread by breaking glue (staphylococcus)
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staphylokinase
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promotes spread by dissolving clots (staphylococcus)
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b-lactamase
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resistance to some antibiotics (staphylococcus)
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lipases
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provides source of nutrition on surface of skin by breaking down lipids (staphylococcus)
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capsule
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staphylococcus; helps attachment of biofilms
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protein A
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inhibits opsonization and complement casscade (staphylococcus)
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cytolytic toxins
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damage cytoplasmic membranes (staphylococcus)
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hemolysins, leukocidins, leukotoxin
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cytolytic toxins
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exfoliative toxin, toxic shock syndrome toxin, staphylococcal enterotoxins
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staphylococcus, folliculitis
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tends to be localized
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folliculitis
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transmitted by direct contact and fomities
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folliculitis
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progression of folliculitis
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zit, furuncle, carbuncle
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can cause bacteremia
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(bacteria in the blood stream) staphylococcus
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diagnosis: gram-positive bacteria in graplike arrangements isolated from pus, blood, or other fluids
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folliculitis
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test used to differentiate between staphylococcus aureus and staphylococcus empidermidis
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coagulase test (aur has epi doesnt)
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treatment: get rid of pus
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folliculitis
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treatment: dicloxacillin
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folliculitis
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MRSA, VRSA
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drug resistant staphylococcus aureus
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prevention: proper cleansing of wounds
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folliculitis
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tick vector
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rocky mountain spotted fever; rickettsia rickettsii
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brought into cell through endocytosis but escapes phagosome
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rickettsia rickettsii
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reproduces slowly and is released via exocytosis
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rickettsia rickettsii
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antropods become infected by feeding on blood or transovarial passage
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rocky mountain spotted fever
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trasmitted to humans through bites and feces
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rocky mountain spotted fever
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typically dormant in salivary glands of tick
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rickettsia rickettsii
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infects cells lining small blood vessels
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rocky mountain spotted fever
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damage to blood vessels: loss of intravascular fluid into tissue spaces, low blood volume, low blood flow, disordered function of tissues
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rocky mountain spotted fever
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5% mortality rate even with treatment
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rocky mountain spotted fever
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recovering patients may experience paralysis, hearing loss, and secondary infections
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rocky mountain spotted fever
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petechiae
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blood hemorrhaging into tissues; rocky mountain spotted fever
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mortality rate 20-25% without treatment
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rocky mountain spotted fever
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rash on soles or palms, sudden fever, and headache
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rocky mountain spotted fever
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treatment: doxycycline, tetracycline, or chloramphenicol
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rocky mountain spotted fever
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rocky mountain spotted fever is bacterial or viral
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bacterial
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folliculitis is bacterial or viral
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bacterial
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chickenpox and shingles are caused by
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by VZV (herpesvirus)
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signs and symptoms: highly infectious, incubation time 2-3 weeks, malaise, lesions on back and trunk that spread to face, necks, and limbs
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varicella chicken pox and shingles
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progression of lesions in varicella chickenpox and shingles
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lesions begin as macules, then papules, dry up and crust over,
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signs and symptoms: virus becomes latent in sensory nerves, stress, aging, immune supression cause virus to reactivate, stays on one side
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herpes zoster chicken pox and shingles
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treatment: acetominophen and antihistamines
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relief of symptoms for chickenpox
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treatment: loose-fitting clothing, bedrest, acyclovir
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shingles
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attenuated vaccine (2) then live vaccine
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chickenpox and shingles
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controls voluntary muscles, perception, and "thinking"
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cerebrum
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controls manyinvoluntary body movements
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cerebellum
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controls breathing, heart rate, BP
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brain stem
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extends from the brain stem to the lumbar region
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spinal cord
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2 cell types of the CNS
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neuroglia and neurons
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provide support, insulation, nutrients, phagocytize microbes
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neuroglia
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carry nerve impulses
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neurons
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outer membrane protecting the brain and spinal cord
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meninges
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circulates around the brain and spinal cord between the layers of the meninges
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cerebrospinal fluid
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protects the CNS from chemical injury
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blood-brain barrier
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axenic environment
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CNS; no normal micrbiota
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can be caused by over 50 species of bacteria
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meningitis
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meningitis is a bacterial or viral disease
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bacterial
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5 species that cause 90% of bacterial meningitis
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streptococcus pneumoniae
peisseria meningitidis haemophilusinfluenzae listeria monocytogenes streptococcus agalactiae |
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gram-positive coccus; usually in pairs
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streptococcus pneumoniae
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normal flora of throat that colonize lungs, sinuses, and middle ear opportunistically
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streptococcus pneumoniae
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leading cause of meningitis in adults
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streptococcus pneumoniae
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capsule
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streptococcus pneumoniae and staphylococcus aureus/epidermidis
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pathogenic members of streptococcus pneumoniae produce
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IgA protease and pneumolysin
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__________ in cell wall binds to receptorso n cells in lungs, meninges, and blood vessel walls
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phosphorylcholine
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gram-negative diplococci
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neisseria meningitidis
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92 strains known
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streptococcus pneumoniae
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13 antigenic strains
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neisseria meningitidis
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known as meningoccus
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neisseria meningitidis
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have fimbriae and polysaccharide capsule
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neisseria meningitids
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contain lipid A and sugars that allow bacteria to bind to human cells
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Neisseria meningitidis
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nasopharyngeal colonization
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streptococcus pneumoniae
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opportunistically colonize lungs, sinuses, and middle ear; move to meninges via bloodstream
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streptococcus pneumoniae
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stimulates endocytosis by endothelial cells
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phosphorylocholine
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spreads via respiratory droplets
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neisseria meningitidis
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attached to non-ciliateed columnar epithelial cells of nasopharynx w/fimbriae
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neisseria meningitidis
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enters the CNS through bloodstream
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streptococcus pneumoniae
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inflammation of spinal meninges puts pressure on surrounding nerves and muscles
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bacterial meningitis
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can result in deafness, blindness, behavioral changes, coma, and death
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infection of the brain (encephalitis)
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can kill w/in 6 hours
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meningococcal menigitis
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like RMSF can cause petechiae
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bacterial meningitis
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present in mouths and throats of 75% of humans but bad if in bloodstream
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streptococcus pneumoniae
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mortality rate up to 20 times that of meningitis caused by other organisms
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streptococcus pneumoniae
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humans are reservoir
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neisseria meningitidis
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carrier state may last few days to few months and is highest in older children & young adults
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neisseria meningitidis
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only type of bacterial meningitis that becomes epidemic
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neisseria meningitidis
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mortality is 100% if untreated; 10% if treated
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neisseria meningitidis
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diagnosis from culturing bacteria from CSF following spinal tap
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bacterial meningitis
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prompt treatment reduces mortality to less than 15%
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bacterial meningitis
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prevention: Pneumococcal polysaccharide vaccine (PPV)
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streptococcus pneumoniae
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prevention: polysacharide conjugate vaccine (PCV)
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streptococcus pneumoniae
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those who have close or prolonged contact w/bacterial meningitis patient should receive ______ antibiotics
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prophylactic
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bacteria/viruses more readily cross the blood-brain barrier
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viruses
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90% of viral meningitis is caused by members of the genus
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Enterovirus
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very small, nonenveloped, RNA viruses
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enteroviruses
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often spread from person to person via fecal contamination of food, water, or hands
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viral meningitis
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replicates in respiratory or gastrointestinal mucosa and kills target cells
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viral meningitis
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incubation period 3-7 days and patients recover completely after 7-10 days
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viral meningitis
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contagious from onset of signs and symptoms for up to 1-10 days
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viral meningitis
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treatment: no specific treatment, bed rest, fluids, fever/headache meds
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viral meningitis
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thrombocytopenia in 50% of patients
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rocky mountain spotted fever
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erythrocytes, leukocytes, platelets
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formed elements
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liquid part of blood
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serum
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pumps blood to lungs
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right ventricle
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blood from lungs
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left ventricle
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organism that causes lyme disease
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borrelia burgdorferi
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gram-negative spirochete
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borrelia burgodorferi
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burrows into tissues
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borrelia burgodorferi
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changes BLPs
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borrelia burgodorferi
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releases endotoxin when it dies
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borrelia burgodorferi
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white-footed mouse is reservoir
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borrelia burgodorferi (lyme disease)
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hard ticks of the genus Ixodes are the vectors
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borrelia burgodorferi (lyme disease)
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caused mostly by nymph rather than adult ticks
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lyme disease
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BLPs appear to initiate pathogenesis
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lyme disease
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mimics many other diseases
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lyme disease
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red rash resembling bull's eye, malaise...etc
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phase 1 of lyme disease
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seen only in 10% of cases, neurological symptoms, meningitis, encephalitis, cardiac dysnfunction
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phase 2 of lyme disease
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severe arthritis, rarely if ever fatal
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phase 3 of lyme disease
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most-reported vector-borne disease in U.S.
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lyme disease
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treatment: antimicrobial drugs like doxycycline or penicillin
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phase 1 of lyme disease
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treatment of later phases is difficult b/c symptoms are often caused by the immune system
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lyme disease
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used to have vaccine
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lyme disease
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caused by the human herpes virus 4 or epstein-barr virus
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infectious mononucleosis
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enveloped, DNA virus
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HHV4 or EBV
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may plya a role in chronic fatigue syndrome, Hodgkin's lymphoma, and oral hairy leukoplakia
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EBV
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transmitted thru saliva
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EBV
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starts in nasopharyngeal epithelial cells then through lytic replication spreads to salivary glands and oropharyngeal lymphoid tissues
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EBV
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possible development of cancers
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late events of EBV
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mild in kids resembling regular cold
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infectious mononucleosis
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95% of Americans are infected with this by age 30
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EBV
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diagnoisis: based on large, lobed B lymphocytes and neutropenia
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infectious mononucleosis
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checks for antibodies to EBV
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monospot test
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this organism causes malaria
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plasmodium
p.ovale p.vivax p.malariae or p.falciparum |
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most fatal strain of malaria caused by
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p. falciparum
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sporozoites injected, reach liver, enter blood stream while some stay in liver
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exoerythrocytic cycle of malaria
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merozoites penetrate erythrocytes; become trophozoites that phagocytize hemoglobin; erythrocytes lysed
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erythrocytic cycle of malaria
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Anopheles mosquito feeds on infected human and ingests gametocytes; gametocytes become zygotes which become ookinete that penetrate the mosquito's gut wall and become oocyst; make sporozoites and go to salivary glands
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sporogenic cycle of malaria
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reproductive cycle occurs w/in red blood cells, hiding parasite from immune surveillance
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malaria
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secretome injects toxins into host cells
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malaria
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change in body chemistry attracts other mosquitos
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malaria
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extreme fever, large scale erythrocyte lysis, renal failure, dark urine
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malaria
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adherence of erythrocytes to lining of capillaries causing tissue death, low blood flow, and hemorrhages
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malaria
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when tissue death occurs in brain
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cerebral malaria
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sickle-cell trait
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resist penetration by Plasmodium
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Hemoglobin C
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unknown protective mechanism
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merozoites penetrate erythrocytes; become trophozoites that phagocytize hemoglobin; erythrocytes lysed
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erythrocytic cycle of malaria
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Anopheles mosquito feeds on infected human and ingests gametocytes; gametocytes become zygotes which become ookinete that penetrate the mosquito's gut wall and become oocyst; make sporozoites and go to salivary glands
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sporogenic cycle of malaria
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reproductive cycle occurs w/in red blood cells, hiding parasite from immune surveillance
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malaria
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secretome injects toxins into host cells
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malaria
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change in body chemistry attracts other mosquitos
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malaria
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extreme fever, large scale erythrocyte lysis, renal failure, dark urine
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malaria
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adherence of erythrocytes to lining of capillaries causing tissue death, low blood flow, and hemorrhages
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malaria
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when tissue death occurs in brain
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cerebral malaria
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sickle-cell trait
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resist penetration by Plasmodium
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Hemoglobin C
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unknown protective mechanism
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gneetic deficiency of glucose6phosophate dehydrogenase
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inhibits trophozioite replication
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lack of duffy antigens
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required for attachment of P. vivax
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fever chills diarrhea headache pulmonary or cardiac dysfunction w/recurrent 2-3 day cycle
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malaria
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anemia, weakness, fatigue, severe jaundice
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malaria
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if victim survives, immunity develops
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malaria
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diagnosis: trophozoites and other stages in blood smears; case history, including travel history, vital
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malaria
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can be treated w/standard drugs like chloroquine and pyrimethamine
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malaria
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can be treated w/melfoquine, doxycycline, hydroxycholorquine, or comination of atovaquone and proguanil
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malaria
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can be treated w/artemisinin
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malaria
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based on chinese herbal treatment and cures 90% of patients w/a single dose w/in days
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artemisinin
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antifever medication and blood transfusions may be required
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malaria
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un patented pill used to treat
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malaria
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microbes usually not present in this part of the respiratory system
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lower
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diphtheroids
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in nose and nasal cavity
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many organisms colonize this part of the respiratory system
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upper regions of pharynx
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streptococcal respiratory diseases are caused by
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streptococcus
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gram-positive, faculatively anaerobic cocci in chains or pairs
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streptococcus
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differentiated by Lancefield grouping
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streptococci
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streptococci group A
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s. pyogenes
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major cause of bacterial pharyngitis and scarlet and rheumatic fevers
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streptococcal pyogenes
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found in fimbriae
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M protien
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major cause of antigenic shift and drit
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M protein
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M protein
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virulence factor of s pyogenes
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hyaluronic acid capsule
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s. pyogenes; disguise and inhibits phagocytosis
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streptokinases
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s. pyogenes; lyse fibrin clots
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C5a peptidase
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s. pyogenes; decreases movement of WBC to infection site
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pyrogenic (erythrogenic) toxins
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s. pyogenes; act as superantigens
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streptolysins
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s. pyogenes; lyse RBC, WBC, and platelets
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hyaluronidase
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s. pyogenes; digest host connective tissue hyaluronic acid and its own capsule
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typically occur when normal microbioate are depleted, large inoculum is introduced, or adaptive immunity is impaired
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streptococcal respiratory diseases
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exogenous secondary invader
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streptococcal respiratory diseases
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strep throat
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streptococal pharyngitis
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back of pharynx red, swollen lymph nodes, abscesses over tonsils, fever, malaise, can cause laryngitis and bronchitis
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streptococcal pharyngitis (strep throat)
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caused by s. pyogenes strain carrying lysogenic phage of erythrogenic toxins
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scarlet fever
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1-2 days of pharyngitis then toxins released: fever, rash, tongue red, rash gone then skin sloughs off
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scarlet fever
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acute glomerulonephritis and rheumatic fever are complications of
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untreated strep throat
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glomerulonephritis
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kidneys
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damage to heart valves and muscle
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rheumatic fever
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spread via respiratory droplets
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scarlet fever and strep throat
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5-15% of people are carriers for this
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streptococcal diseases
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treatment: penicillin or erythromycin or cephalosporin
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streptococcal respiratory diseases
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prevention: antibodies against M proteins and immediate treatment
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streptococcal respiratory diseases (rheumatic fever)
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tuberculosis is caused by
|
mycobaterium tuberculosis
|
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non-endospore forming, gram-positive rod w/cell walls containing mycolic acid
|
mycobacterium tuberculosis
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directly responsible for unique characteristics of pathogen
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mycolic acid
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slow growth, protected from phagocytosis, capable of intracellular growth, resistant to gram staining, drugs, and desiccation
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mycobacterium tuberculosis
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cord factor
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produced by virulent strains of mycobacterium tuberculosis
|
|
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toxic to mammalian cells
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mycobacterium tuberculosis
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can remain viable for long periods in aersol drops
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m. tuberculosis
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organism not particularly virulent
|
m. tuburculosis
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typically occurs in children and involves the formation of tubercles in the lungs
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primary tuberculosis
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|
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organism ruptures tubercule; active infection; spreads through lungs
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secondary tuberculosis
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macrophages carry pathogen via blood and lymph to variety of sites; consumption
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disseminated tuberculosis
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|
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minor cough, mild fever; breathing difficulties, fatigue, malaise, chest pain, wheezing, cough up blood
|
TB
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kills 4 ppl a minute in Asia and Africa
|
TB
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treatment: INH, rifampin, and other drugs for 2 months followed by 4 months of INH and rifampin alone
|
TB
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treatment: MDR strains
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TB
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treatment: DOTS-health care workers observe patients to ensure they take medications
|
TB
|
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BCG vaccine
|
TB
|
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influenza virus caused by
|
orthomyxoviruses types A and B
|
|
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plemorphic envelope
|
influenza
|
|
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glycoprotein spikes of neuraminidase and hemagglutinin
|
influenza
|
|
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hydrolyzes mucus in lungs thereby providing access to pulmonary epithelial cells
|
neuroaminidase
|
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binds to pulmonary epithelial cells and triggers endocytosis
|
hemagglutinin
|
|
|
two processes for mutations in influenza virus
|
antigenic drift or antigenic shift
|
|
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symptoms are produced by cytokines released as part of the immune response to the virus
|
influenza
|
|
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signs and symptoms: sudden fever, pharyngitis, congestion, dry cough,myalgia, recovery in 1-2 weeks
|
influenza
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transmitted by inhalation or self inoculation
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influenza
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treatment: oseltamivir and Zanamivir
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influenza
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