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38 Cards in this Set

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free of microbes

axenic

what prevents most microbes, and most antibiotics from entering the brain?

blood brain barrier

how do pathogens access the CNS?

-through the breaks in the bones and meninges


-during medical procedures


-by traveling from peripheral neurons to the CNS (leprosy)

causative agents of bacterial meningitis? (5)

1) Haemophilus influenzae: leading cause prior to vaccine


2) Streptococcus pneumoniae: leading cause in adults


3) Streptococcus agalactiae: causes most cases of newborn meningitis (rare)


*4) Neisseria meningitidis: causes outbreaks in colleges, most common cause


5) Listeria monocytogenes: causes disease in fetuses, pregnant women, and immunocompromised indivicuals from contaminated foods

-only genus of Gram negative cocci that regularly causes disease in humans-diplococci

Neisseria

what two species of Neisseria are pathogenic to humans?

-Neisseria gonorrhoeae


-N. meningitidis: causes meningitis due to fimbriae, capsule, and LPS

symptoms of meningitis

-mild: influenza-like upper respiratory infection


-serious: sudden fiver, pounding headache and stiff neck due to inflammation


-petechiae


-can lead to encephalitis

diagnosis of meningitis

spinal tap

treatment of meningitis

intravenous antimicrobial drugs (Rifampin)

prevention of meningitis

vaccine available for meningococcal meningitis (Menactra)

another name for leprosy

Hansen's disease

causative agent for leprosy (hansen's disease)

Mycobacterium leprae


-only known pathogen to target nervous system

pathogenesis of leprosy (hansen's disease)

-Mycobacterium leprae grows best in cooler regions of the body (30 degrees C in the PNS and skin)


-bacteria will grow very slowly within phagocytes


-armadillos are the only other known host

transmission of leprosy (hansen's disease)

-person-to-person contact via respiratory droplets


-through breaks in the skin



two kinds of leprosy

-Tuberculoid leprosy


-lepromatous leprosy

-non progressive.-patients have strong immune system


-results in nerve damage and regions of skin that lose sensation



tuberculoid leprosy

-progressive tissue destruction caused my multiplication of bacteria in skin, mucous membrane, and nerve cells


-can result in loss of facial features, fingers, toes, etc

lepromatous leprosy

diagnosis of leprosy (hansen's disease)

-skin test with leprosy antigen


-observation of acid-fast rods in tissue samples

treatment of leprosy

-combination of antimicrobial drugs (sometimes lifetime)

prevention of leprosy (hansen's disease)

-limiting exposure to the pathogen


-prophylactic use of antimicrobial agents after exposure


-BCG vaccine provides some protection

characteristics of Clostridium bacteria

-gram positive, anaerobic, endospore-forming bacillus


-lives in soil, water, and GI tracts of animals



causative agent for tetanus

Clostridium tetani


-gram positive, spore-former

transmission of tetanus

-animal bites, rusty nails, broken glass, intravenous drug use, body piercing

where does tetanus come from?

found in intestines of many animals


-feces excreted into soil


-soil introduced to wound


anaerobic environment spurs vegetative growth

symptoms of tetanus (4)

-rapid developing muscle stiffness,


trismus: lockjaw


risus sardonicus: permanent grinning


opisthotonus: arching of back

treatment of tetanus

sedatives, dark quiet rooms, antitoxin & antibiotics



Prevention of tetanus

DTaP immunization: tetanospasmin toxoid, requires boosters

pathogenicity of tetanus (5)

1) spore into body


2) gets into anaerobic place


3) spore germinates, grows vegetatively


4) transcribes and translates gene for tetanospasmin


5) tetanospasmin gets into system and seeks out nerve cells

mechanism of tetanus

-tetanospasmin prevents the release of glycine (inhibitory NT) and other NTs needed to inhibit muscle contraction


-blocks relaxation pathway that follows contraction

causative agent of botulism

Clostridium botulinum


-gram positive, anaerobic spore-former (fish, bird, cow intestines)

three forms of botulism

1) food borne


2) infant


3) wound

course of infection in a baby for botulism (5)

1) baby inhales or ingests Clostridium botulinum endospores


2) endospores germinate in anaerobic environment of intestinal tract. Vegetative cells grow, reproduce and release botulism toxin


3) toxin absorbed into blood and circulated


4) botulism toxin produces constipation and weak cry


5) toxin paralyzes muscles, including neck muscles and the diaphragm

symptoms of botulism

-flaccid paralysis



pathogenicity of botulism

botulism toxin blocks release of acetylcholine

applications of botulism


-aligning eyes simultaneously


-uncontrolled eyelid closure

type A botulism can be used for


-strabismus


-blepharospasm

epidemiology of botulism



-infant botulism more common form

treatment of botulism (3)

-washing of intestinal tract to remove Clostridium


-administration of botulism immune globulin (BIG)


-antimicrobial drugs

prevention of botulism

destroying endospores in contaminated food


-heat foods to 90 degrees C for at least 10 years


-infants under 1 year shouldn't consume honey