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129 Cards in this Set
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how do these structures influence CNS infections
1. Bone/Meningies 2. BBB 3. subarachnoid pace |
1. compartmentalize infections
2. keeps pathogens AND AB/immune cells OUT 3. CSF from ventricles to spinal cord |
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tell me about the infection
1. Epidural 2. Subdural 3. Parenchymal |
1. assoiciated with osteomylitis, localized bc there is no disruption in dura/bone attachment
2. spread FAST bc dura and outer arachnoid are NOT attached 3. localized when bacterial, diffuse with viral infection |
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tell me about the disease
1. meningitis 2. encephalitis 3. abcess 4. toxicity |
1. meningitis- infection in subarachnoid space
2. inflammation of parynchema 3. in parynchema or elsewhere 4. exotoxin |
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what are some common causes of CNS disease
1. bacterial 2. fungi 3. Parasites |
1. strep pneumoniae, N meningiditis, H influenza B, E coli, Strep agalactine, listeria monocytogenes
2. Fungi: cryptococcus neoformans (bird poo) 3. Parasites/Amebea: Toxoplasma gondii, Angiostrangylus cantonenis, baylisarrcis procyonis, Taenia solium, echinococcus *also tick paralysis as "other" |
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what is the time frame of acute meningitis?
what are some causes |
Onset: hours to days
Virus, rickettsia, bacteria, spirochetes, protozoa, helminths *Infectious syndromes with resultant acute meningitis include parameningeal foci, infective endocarditis, viral postinfectious syndromes and postvaccination events **can also be noninfectious: tumor, medical procedures, meds, systemic illness |
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what is the time course of chronic meningitis?
what are some causes? |
one month and more!
**parasite, fungi, few bacteria, few virus |
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how do things get into the CNS and cause disease
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1. from blood
2. penetrating injury, congenital defects, shunts 3. contagious spread form nasal sinus, middle ear, etc 4. intraaxonal transport |
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what are some common community acquired meningitis
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**respiratory tract is colonized withL
Nisseria meningiditis strep pneumonia H influenzea |
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what are some common hospital acquired meningitis
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Iatrogenic procedures, altered immune status
GNR staph aureus other strep/staph |
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what is the pathogenesis of bacterial meningitis
mucosal colonization (common repspiratory tract) --> _____ ----> |
1. mucosal colonization
2. entry of pathogen into blood 3. blood carries it to BBB, penetrates 4. release of inflammatory cytokines 5. Diapedesis of WBC into CSF (purulent) 6. increased permiability of BBB 7. exudate! edema, increased intracranial pressure, altered blood flow |
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what are some signs and sx of CNS disease
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HA, fever, stiff neck, ocular pain, nausea, vomit, comfusion
**Hx of URI (often gets into CNS from colonized respiratory tract) |
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what are some lab findings when we ahve CNS disease
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Presence of any polymorphonuclear leukocytes or more than 5 WBCs of any type
decreased glucose and elevated protein b. Direct smear of CSF is examined with a wet mount, gram stain, or imaging according to suspected etiologies |
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in general what 3 methods are used to determine CNS disease
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1. rapid test for AG detection
2. gene amplification 3. blood cultures (eh, may not reflect what is going on in CSF. also takes a while to grow) |
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is CNS disease a big deal
how do you treat |
YES! EMERGENCY
**treat asap emperically but then get susceptibility data **drugs must penetrate BBB and be bactericidal |
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who gets purulent meningitis
what are the signs what is the treatment |
1 older kids and adults
2. irritable, severe HA, lethargy, fever, vomit, nuchal rigidity, photophobia, convulsions, coma (typical for bacterial meningitis) 3. treat AGGERSSIVE: lots of sequelae and death |
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does this describe bacterial or viral meningitis
intense acute congestion of meningeal BV nad purulent exudate in sulci |
bacterial
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what bacteria is commonly assocatied with purulent meningitis (seen in older kids and adults, sx typical for bacterial meningitis, treat AGGRESSIVELY)
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klebsiellia pneumonia
**often caused by an encapsulated organism |
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what neonatal and maternal factors influence a neonatal meningitis cause
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baby: immature immune system, low birth weight, immature organs
Mom: premature rupture of membranes, UG infection late, intrauterine infection early, |
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what are the sx of adult bacterial meningitis
what about neonatal meningitis |
Adult: HA, fever, nuchal rigidity, irritable, lethargic, nausea/vomit, convulsions, photophobia
NeoNate: Hyperthermia, CNS- lethargy, irritable, seizure GI- anorexia, vomit, nausea Respiratory- dyspnea, apnea, cyanosis |
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do infants recover well from neonatal meningitis
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nope, high mortality, sequelea are common
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what does CDC say for prevention of neonatal meningitis
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check mom for rectal or vaginal colonization with group B strep for ALL preggos nad AB prophylax moms who test +
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what are the common pathogens in neonatal meningitis (3)
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listeria monocytogenes
e coli streptococcus agalactiae |
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strep agalactiae
meningitis general info virulence found? |
causes neonatal strep
Group B, most b hemolytic virulence: capsule, hyluronidase, collagenase normal flora of vagina |
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what is the group B strep that is normal in the vagina and causes neonatal meningitis
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strep sgalactiae
**one of the more common causes of neonatal meningitis *has virulence factors that allow it to break through tissue- high mortality |
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tell me about early nad late onset disease assoicated with strep agalactiae (what type of meningitis)
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NeoNatal Meningitis
Early- infection transmitted during delivery- mom often had OB problmes. in first 5 days of life- bacteremia, oneumonia, meningitis Late- disease transmitted post partum. no OB problems. sx 7days-3 months- joint/bone infection, bacteremia with concomitant/fulminant meningitis |
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if your 2 mo baby gets meningitis from the most common cause of neonatal meningitis was it early or late onset diease. Were there maternal OB coplications, what other sx might there be
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strep agalactiase
late onset- passed post partum from mom (notmal flora) to baby no maternal OB complications may have bone/joint infections and bacteremia **more commonly an early onset with the infectionbeing transmitted during delivery |
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how is strep agalactiae dx (neonatal meningitis)
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isolation from sterile: blood, CSF, is difinitive
CAMP factor- hemolysis bc of interaction with b lysin (b hemolytic) DNA probe |
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other than strep agalactiae what else is commonly the source of neonatal meningitis
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E coli K1- encapsulated gram - bacillus
**from moms rectum to baby (the rectum to the vagina to the baby) |
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tell me about E coli K1
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encapsulated, gram -
goes from moms rectum to vagina to baby to cause neonatal meningitis |
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most community acquired meningitis is caused when, what is the exception
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most are winter: HIB, N meningiditis, S pneumoniae, S agalactiae
EXCEPTION: L monocytogenes- summer |
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what are the most common causes of community acquired meningitis
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1. HIB- infants
2. N meningitidis: infants- 19 yo 3. S pneumoniae- infants, kids, old ppl 4. L monocytogenes: newborns, predisposed adults **all are in wnter except listeria is in summer |
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tell me a little about listeria monocytogenes
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causes meningitis in neonates and old ppl in the summer
*gram + MOTILE coccobacillus *needs decreased O2 **can live in temps 0-50 (fridge!) **intracellualr- lives in epithelium and macro/mono |
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if you ID listeria in sample where might it be
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INSIDE ANOTHER CELL- facultative intracellular
**hides in epithelium and macrophages |
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at what temps does listeria grow
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0-5
**tons of replication at 4* |
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what are the cirulence factors assiated with listeria
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1. LPS like surface htat is ANTIPHAGOCYTIC, responsible for Compliment dependen hemolytic AB
2. Listeriolysin O is secreted and disrupts phagolysosome and inhibits AG precessing |
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what is listeriolysin O
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virulence fastor assoicated with listeria that inhibits AG processing and inhibits phagolysosome membrane
**the other virulence factor assoicated with listeria is the antiphagocytic LPS like surface |
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where do we find lysteria
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world wide in envirnment and animals
**plants, soil, poo, coleslaw, animal- hot dog, undercooked chicken, **sporadic and common source outbreaks |
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what is the pathogenesis of listeria
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1. eat it
2. invasion in GI (lives in epithelium and macro) 3. spread 4. disease: meningitis, encephalitis, septicemia 5. exit in poo *disease in renal transplant pts and cancer pts (can also be mild comprimise like preggo or URI) **in am immunocompetent host this wont cause disease |
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what happens with listeria in a baby
what about an adult |
Neonate:
acquired in utero--> death or pneumonia, seizure, high mortality acquired from moms genitals--> meningitis Adult: Competent: no disease Comprimised: renal transplant and cancer pts- brain stem inflammation, meningitis |
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when we say pts who get listeria are immune compromised (renal transplants, cancaer) what part of the immune system is effective in KILLING listeria
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immunity is T mediated- will kill stationary (not the replicating ones)
AB is only partial protection |
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if we think our pt has listeria what do you do
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1. tell the lab what we think
2. gram stain- unreliable, 3. culture 4. DNA probe |
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what diesase is caused by HIB
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epiglotitis
meningitis bacteremia penumona |
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tell me about the characteristic of HIB bacteria
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gram -
NON motile pleimorphic coccobacillua ENCAPSULATED- good for dx and prognosis Fastidious growth requirements: needs factor V and X, grown on chocolate agar or blood arag with s aureus that will lyse RBC and release V nad X |
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how is HIB grown
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fastidious, needs V nad X
grown on chocolate agar OR along with s aeurus- this lysis RBC so V and X are around |
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where is HIB found
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common in nasopharynx, normal flora (gram - non motile encapsulated)
spread by contact, secretions, aerosol |
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ok so HIB is nornal in nasopharynx, who is at RISK
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low SES, crowds, day care, siblings, no breast milk, parents who smoke
Native Alaskans, Native americans, immunodeficient- humoral deficiit |
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what is the virulence associated iwth HIB
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Encapsulated
Strain B is virulent (but not in vaccine) resistant to compliment degradation Cell envelope has lipooligosaccharide to help it attach |
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what is the pathogenesis of HIB
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1. colonized in nasopharynx
2. penetrate epithelium 3. gets in blood or lymph 4. SEEDS choriod plexus --> MENINGITIS |
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ok so we know HIB lives in the nose and can get into the choroid plexus to cause meningitis, what is the presentaiton
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get a URI or otitis media that spreads
insidious onset, then deterioration |
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how is HIB dx
do you need susceptibility tests |
1. gram stain (gram -, encapsulated)
2. Detect capsular AG in CSF or urine. can also direct prognosis 3. Culture is DIAGNOSTIC, bacteria in the blood is common 4. MUST do susceptibility tests |
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invasive haemophalus influenzea is what type
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B almost always
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what is a good way to prevent meningitis (2 ways)
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1. Conjugate Vaccine
2. Chemoprophylaxis of conntacts |
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what is the gram - non motile coccobacillus that is encapsulated. Capsular AG can be used to Dx and determine prognosis of disease. This pathogen is normally found in the nose and cab be vaccinated against with a conjugate vaccine
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HIB
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in what ways are HIB and pneumococcal meningitis (s. pneumoniae) simliar
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both are encapsulated
both have vaccines HIB- gram - S pneumonia gram + |
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give me the general characteristics of Strep pneumoniae
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causes pneumococcal meningitis in all ages, purulent
gram - lancet shaped fastidious diplococcus, encapsulated |
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what does the capsule do for HIB
what about strep pneumonia (pneumococcal meningitsi) |
HIB- Dx, prognosis.
Strep pneumonia- antiphagocytic, virulence! |
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if someone has recurrent meningitis what is the likely curprit
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penumococcal meningitis (strep pneumonia)
causes a purulent meningitis, all ages (old is common) *gram + lancet shaped diplococcus **may follow pneumococcal pneumonia, infection at another site, or appear with no antecedent infection |
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what predisposes someone for pneumococcal meningitis
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pneumococcal meningitis caused by strep penumonia
**multiple myeloma **sickle cell **cardiorespiratory disease **congenitial defect **no slpeen **head trauma |
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if you have MM, Sickle cell and no spleen what are you at risk for (meningitis wise of course)
if you are a kid whos parents smoke and you live in a crowded house with lots of siblings and spend time in daycare what meningitis are you looking at |
pneumococcal
HIB |
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what is the clnincal manifestation of penumococcal meningitis
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bacterial meningitis
onset/progression is acute (contrast to insidious onset for HIB) PURULENT! underlying CNS tissue and ventricles often infected |
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what is the dx for pneumococcal meningitis
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gram + lancet
mucoid a hemolytic colonies Optochin susceptiblity Bilie solubility Quelling |
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ok so we isolate a mucoid colony that is sensitive to optochin, soluble in bile and has a + quelling. The bacteria is gram + and lancet shaped.
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strep pneumonia
causes pneumococcal meningitis |
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how is pneumococcal meningitis treated
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Vaccine!
23 valent: use on ppl >65, and ppl who are susceptible (multiple myeloma, sickle cell, no spleen etc) 13 valent conjugate: HIGH risk, infants kids, old Penicillin G is DOC |
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tell me who gets the 23 valent and 13 valent pneumococcal vaccine
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23: all ppl >65, adn ppl with predisposing factors
13: conjugate vaccine. ppl at high risk: kids, old |
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what causes meningiococcal meningitis
what are the general characteristics |
Neisseria meningitidis
**gram -, bean shape, dipplococcus, **encapsulated **type B is NOT included in vaccine |
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might have been confused, what "B" is NOT included in its vaccine
Neisseria meningitidis Heamophilus influenzea |
Neisseria meningiditis- the bean shaped encapsulated cause of meningiococcal meningitis
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tell me about the ppl who carry Neisseria meningitis in their nose (contrast to HIB where ppl had it as normal flora without a problem)
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1. Transient bacteremia with fever and spontaneous resolution
2. Acute meningococcemia develops into meningitis |
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where do you find neisseria meningitidis? how is it spread
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HUMANS ONLY!! in the nose
Spread with close contact: more susceptible if your mucosa lost its integrity, college and military |
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what cause of meningitis is common in college nad military
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meningococcus meningitis caused by N meningitidis
**B has no vaccine |
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adrenal necrosis is common in what form of meningitis
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meningiococcal meningitis caused by N meningitidis
Waterhouse Friderichsen syndrome- hemorrhage into adrenal tissue |
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tell me about meningococcemia seen in N meningitidis carriers
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can eveolve into meningitis
Rash: petechiae, and pink macules. widespread erruption in HOURS DIC and shock can occur Waterhouse Friderichsen syndrome- hemorrhage into adrenal tissue |
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what is waterhouse Friderichsen syndrom
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hemorrhage into adrenal tissue, cause of adrenal necrosis assocaited iwth meningiococcal meningitis caused by N meningitidis
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if there was a sporadic epidemic case of meningitis at a local college what pathogen? what is the incubation and what can be a sequelae
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n meningitidis
<1 week dissemination in blood |
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what is the difffernece in how infants and older kids/adults present with meningococcal meningitis caused by N meningitidis
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Babies: lack of signs early on, then get apnea, seizures, and coma later
Adults: get the typical HA, vomit, and neuro signs |
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what meningitis has the characteristicpetechial leisions (what are they called) what are the other ways to dx this meningitis
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meningococcal meningitis (N meningitidis)
called meningococemia Dx with Capsular AG in CSF gram stain, culture blood/csf |
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we know strep pneumonia causes a purulent meningitis, does N meningitidis
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yep
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whats the tx for N meningitidis (meningiococcal meningitis)
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Penacillin G (same as for strep pneumonia)
**also control the infection with chemoprophylaxis of ppl who were exposed nad there is a vaccine |
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how is meningococcal meningitis prevented
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chemoprophylaxis of ppl exposed (recall that <1 week incubation)
vaccine |
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The most characteristic manifestation of meningococcemia is ...
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the skin rash
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parameningeal infections due to bacteria are what
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abcess: localized pus. often 2 to infection somewhere else, like otitis media or bacterial endocarditis
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is nervous tissue susceptible to bacterial invasion
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NO! its highly resistant
parameningial infections are not common Nervous tissue is highly resistant to bacterial invasion, i.e., damage to the brain is more likely to result from rupture of a mycotic aneurysm or cerebral infarction than it is to result from even a sustained bacteremia. |
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ok so we know its not common to get bacterial invasion into the brian, what things increase its liklihood
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chronic cerebral anoxia
infection of nearby bone septic embolization trauma |
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what are some common organisms in brain abcess
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1. Strep intermedius
2. bacteroides/Prevotella **often polymicrobial, anerobic |
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what is the most common obligate anerobe
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bacteroides
**common cause of brain abcess **does NOT have the enzymes required to destroy intermediates of O2 metabolism (OH, O-, H2O2) |
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will trauma lead to meningitis?
what about mastoiditis, otitis media, dental sepsis, bacterial endocarditis |
not meningitis but all can predispose to brain abcess
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bacteroides is assocaited with what, what are its virulence factors
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Brain abcess, most common obligate anerobe
**Neruoaminidase- **hyaluronidase- breaks CT **LPS to activate Hageman factor --> intiate intrinsic coaulation **polysaccharide capsule to prevent phagocytosis |
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what bacteria has LPS that activated haegman factor to activate the intirisic coagulation pathway
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bacteroides
also has neuroaminidase, hyaluronic acid nad a capsule that prevents phago |
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whats the pathogenesis of brain abcess
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1. bacteria enter the brain
2. inflammatory response 3. Progression of early and late cerebritis 4. capsule forms (early and late) 5. abcess is formed |
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what pathogen is involved in abcess
what predisposes whats the clinical presentation tx |
mixed infection with anerobic
infections near CNS manifestations based on LOCATION not organism type tx with surgery to drain |
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are brain abcesses the result of meningitis
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almost never
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tell me about the clinical manifestations of brain abcess
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based on LOCATIOn of abcess, not the type of organism
1. systemic reaction- low fever 2. Increased intracranial pressure- HA, 3. Damage of tissue: localized signs, aphasia, change in consciouness, nystagmous |
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hwo are brain abcesses dx
what is NOT sued |
high index of suscipiscion (nearby infection or recent trauma)
CT/MRI NO lumbar puncture |
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whats the tx for brain abcess
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dx with CT/MRI (NOT lumbar puncture) need a high index of suspicion to suspect this (recent trauma or nearby infection)
treat emperically, surgery to drain/excise |
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what is an intracrainial collection of pus btwn dura nad arachnoid
what pathogen |
subdural empyema 1
often anerobic streptococci, also staph adn enteric bacilli **usually bc of nearby infection or abcess rupture |
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what are some common ways to get subdural empyema 1
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usual cause is an infection of the paranasal sinuses or otitis media
Direct extension (erosion of bone) is more common with otitis media while indirect extension through the venous system (progressive thrombophlebitis venous sinuses and veins) is more common in paranasal sinus infection. |
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how does subdural empyema present
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acute onset, progression varies from hours to days,
high mortality dx with ct, cerebral angiography CSF is neg for bacteria |
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is CSF + or - for bacteremia in subdural empyema
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negative, its a localized infection. the bug wont spill into the CSF
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what is a mass of pus in the epidural space called
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spinal epidural abcess
**s aureus is common cause **Infections occur via direct extension from an infection site in adjacent tissues, by metastasis via the bloodstream, or by a perforating wound **In acute cases, there is purulent necrosis of the epidural fat **In chronic cases, the dura is gray and thickened. Epidural fat is replaced by granulation tissue |
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what bug causes spinal epidural abcess most often
2. how does the infection occur 3. acute vs chronic 4. presentation 5. dx |
1. staph
2. direct spread of infection from adjaent tissue, mets from blood, perforating wound 3. Acute- purulent necrosis of epidural fat Chronic: thick, grey dura and fat is replaced by granulation tissue **present with back pain, paralysis can occur and be permanent dx with CT or myelography |
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what is malignant external otitis
what is the pathogen clinical |
when you have an EAM infection that spreads to adjacent tissue and temporal bone
pseudomonas pain, +/- discharge, parotid involvement, paralysis of CN 6-12. death from meningitis |
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in what disease is it common to get paralysis of CN 6-12 and can die from meningitis
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malignant external otitis caused by pseudomonas
**its when the EAM is infected and the infection spreads to temporal bone and adjacent tissue |
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why is bacterial endocarditis associated with CNS disease
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vegetations can break off and have septic emboli to CNS
CVA- infarct, hemorrhage, ischemia toxic encephalopathy: confision, delirium, hallucinations |
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what are the 3 main diseases of peripheral nervous system
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leprosy
botulism tetanus |
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what are the 3 main granulomatous diseases
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TB
syphalis leprosy |
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if you dont want a person to feel bad that they have leprosy what can you call it
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hansens disease
**chronic bacteriosis due to mycobacterium leprae -acid fast, obligate intracellular: histocytes, macrophage, schwan cells but not in culture |
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where do mycobacterium leprae bacteria live
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histocytes, macro and schwann cells
*intracellular, acid fast bacillus |
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is leprosy restricted to humans?
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nope, carried in armadillos and monkeys too
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how is leprosy passed, who gets it? whats the incubation
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teenages in tropical areas (can affect all ages)
**usually skin infection but can be inhaled 5 year incubation |
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where is leprosy common in the US
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texas, ca, fl- near the coasts
**carried by armadillos |
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what is the pathogenesis of Mycobacterium leprae
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1. contact M leprae
2. mononuclear phagocytes nad schwann cells are infected 3. granuloma formation and nerve destruction **more common in cooler parts of body (face) |
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if you have a hypopigmented area that you cant feel is it no big deal
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it can be the first manifestation of leprosy
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what happens as we progress from Tuberculoid leprosy (TT) to lepromatous leproy (LL)
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increased number of bacilli in tissue
switch from CMI to AB mediated immune system |
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what type of leprosy is characterized by a granulomatous hypopigmented skin leision that lacks innervation
what about the one with raised skin leisions, secondary infections, paralysis, ischemia and deformity of hands/feet |
tuberculoid
lepromatous **we progress from TT to LL when bacillary load increases nad CMI switched to AB mediated |
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tell me about lepromatous leprosy
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the worse one
**raised skin leisions bc of so many bacilli in the histocytes nad macrophages **peripheral N destruction- anesthesi, paralysis, secondary infections, ischemia, distortion of hands and feet **multiple organ damage and death **AB mediated immunity, and lots of bacilli **can get lots of granulomas on the face or not |
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what is a leonie facie
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seen with lepramomatous leprosy (L)
wide nose |
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leprosy can damage the median and ulnar nerve such that its paralysed, waht does it look like
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messed up hand! this is why we have skeletal deformaties
progressive crippling effects of lepprosy metatarsals and phalangies are destroyed |
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whats borderline leprosy
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can have a combination of flat (TT) and raised (LL) leisions
widespread severe neuropathy can progress to TT or LL |
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how is leprosy dx
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1. Hx: do you live in the tropics or an area with lots of armadillos. contact with pts exposed to M leprae
2. biopsy leision and look for acid fast bacilli LOTS: miltibacillary (lot of bacilli in LL) Little: paucibacillary (little bacilli in TT) |
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is the lepromin skin test dx for leprosy
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nope, useful for prognosis
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what are the 2 biggies with obligate anerobes
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bacteroides- neonatal
Clostridium- (gram +) botulism, c diff, C perfringens- gas gangrene, food poision. C tetani |
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tell me about the clostridia
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gram +
live in environemnt and make spores, exotoxin causes disease |
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what is the gram + bacillus that forms spores in the environment and exotoxin causes disease
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clostridia
perfringes- gas gangrene, food poision difficile- pseudomembranous colitis tetani- tetnua boutulinum |
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tell me about the disease produced by c tetani
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one serotype
terminal spores (looks like a tennis racket) toxin production is plasmid mediated |
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tell me a bit about tetnus, where can you pick it up, who gets it
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its a gram + spore forming exotoxin producing clostridium
**found in soil and intestines (normal flora) of us horses etc **infants and IV drug users are at risk, not common in US but common elsewhere **us is seeing less and less cases each year, get a tetnus shot! |
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what is the pathogenesis of tetnus
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1. trauma introdices bacteria and makes ANEROBIC area
2. bacteria multiply and die, plasmid makes tetanospasmin which is released 3. tetanospasmin binds nerve endings and there is intra axonal transport to inhibitory neurons 4. inhibition of NT release 5. SPASMODIC mm contractions- toxin affects central motor control, autonomic control, NM junction |
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in what disease do you see risus sardonicus nad trismus and opisthotonos
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tetanus, its a fixed smile and lock jaw and rigid spine
with tetnus also see mm spasm (trismus) and rigidity, lung nad heart complications |
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where does tetnus toxin act
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1. NM junction
2. Central motor control 3. Autonomic fx |
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what are the clinical forms of tetnus
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1. Generalized
2. Neonatal- bacteria in the umbilicus, rare inUS common developing countries 3. Localized- happens when ppl arent immunized well, they get it in their limbs, its rare and resolves spontaneously 4. Cephalic- after head trauma only hte facial mm are affected |
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whats the best way to dx tetnus
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clinical signs and FAST!!!
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