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111 Cards in this Set
- Front
- Back
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what are the common bacterial agents of CNS diseases
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Strep pneumo
N. meningitidis H. influenzae type b E. coli Strep agalactae L. monocytogenes |
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what are the common fungal agents of CNS diseases
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cryptococcus neoformans
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what are the common parasitic agents of CNS diseases
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amebae
Toxoplasma gondii angiostrongylus cantonensis Baylisascaris procyonis Taenia solium echinococcus spp. |
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deffinition of chronic meningitis
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infection of 4 or more weeks
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general signs and symptoms of CNS infections
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N/V
fever/headache stiff neck ocular pain confusion History of URI |
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what is purulent meningitis
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>2 yrs old
–Irritability, lethargy, severe headache, fever, vomiting, nuchal rigidity, photophobia, convulsions, coma aggresive treatment essential -10% mortality - 30 to 50% neur sequelae |
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what are the signs and symp of a neonatal meningitis
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hyperthermia (typical)
hypothermia lethargy, irritability, seizures anorexia, vomiting, distention, diarrhea dyspnea, apnea, cyanosis |
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what is the prognosis for neonatal meningitis
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10-60% mortality
survivors gen have perm defects |
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what are the CDC reccomendations for preg mothers at 35 - 37 weeks
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screen vagina and anus for group B strep
treat with prophylaxis if positive (not needed if planning cesarian and water has not broken) |
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Group B strep characteristics
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B-hemolytic
hyaluronidase collagenase |
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Group B strep, interesting stats
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leading cause of neonatal meningitis
50% mortality 80% transmited during delivery |
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early vs late onset of neonatal meningitis
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early
- obstetric complications - infection w/in 5 days - bacteremia, pneumo, meningitis Late - no obstetric complications - 7days to 3 months post birth - bone and joint infect, bacteremia, meningitis |
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diagnosis of neonatal group B strep meningitis
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Definitive diagnosis requires isolation from blood, CSF, and/or the site of suppuration
presumptive tests: CAMP factor, Ag detection, DNA probe, CHO group |
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what is the main group B strep causer of neonatal meningits
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S. agalactae
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strain types associated with E. coli meningitis and etiology of infection
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encapsulated (K1) strains
colinization of mothers vagina from rectum |
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what bacteria causes summertime meningitis in newborns and predisposed adults
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L. monocytogenes
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which bacteria typically infects infants during late winter and early spring
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H. influenzae type b
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which bacteria typically cause meningitis in the winter
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N, meningitidis
S. pneumonia S. agalactae |
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characteristics of L. monocytogenes
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G- motile coccobacilli
can grow at low temps facultative intracellular pathogen |
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virulence factors for L. monocytogenes
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antiphagocytic LPS-like surface protein
listeriolysin O - disrupts phagolysosome membrane |
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epidemiology of L. monocytogenes
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ubiquitous
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pathogenisis of L. monocytogenes
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ingestion
penitration of epi cells (immunocompramised) intra and extracellular multiplication systemic infection |
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clinical neonatal L. monocytogenes infections
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stillbirth/abortion
or pneumonia, seizures, skin lesions, high mortality (in-utero) meningitis if aquired in vaginal tract during birth |
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clinical adult L. monocytogenes infections
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leading cause of meningitis in cancer and renal xplant pts
brainstem encephalitis (classic) |
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diagnosis of L. monocytogenes
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*alert the lab*
culture with tissue homogenization tumbling motility with hanging drop prep DNA probe |
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what does H. aegypticus cause
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conjunctivitis
brazillian purpuric fever |
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what does H. ducreyi cause
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chancroid
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what does H. influenzae b cause
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Hib causes meningitis, epiglottitis, bacteremia classically
also, otitis media, sinusitis, tracheobronchitis, pneumonia |
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characteristics of Hib
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G- coccobacilli
non-motil fastidious |
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at risk populations for Hib
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Native Americans and inuits
immunocompramised |
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virulence factors for Hib
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compliment resistant capsule
LOS proteins |
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pathogenisis of Hib meningitis
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normal flora of nasopharynx
penitration of epi migrate to blood or lymph seeding of choroid plexus meningitis |
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what are the clinical manifestations of Hib meningitis
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Preceeding URI and or otitis media
insidious onset of classic meningitis sympt |
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diagnosis of Hib
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Gram stain of CSF
detection of capsular CHO (any fluid) culture |
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prevention of Hib
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conjugate vaccines
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Gen characteristics of S. pneumoniae
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G+ lancet shaped, non-motile, diplococcus
antiphagocytic capsule |
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who is most likely to get a S.pneumoniae meningitis
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elderly, but all ages are susceptible
most common in pts with recurrent meningitis |
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what is a differentiating characteristic for the clinical manifestations of S. pneumoniae meningitis
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typical meningitis features, but
marked purulent meningits - inflamm exudate involving underlying CNS tissue and the ventricles |
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diagnosis of S. pneumoniae
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Gram stain
mucoid, a-hemolytic colonies Optochin susceptible, Bile soluble, quellun rxn |
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treatment of S. pneumoniae
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Penicillin G (or VK)
23-valent vaccine for 65+ 13 valent vaccine for high risk |
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what is the cause of meningiococcal meningitis
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N. meningitidis
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characteristics of N. meningitidis
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fastidious, gram-negative, kidney bean-shaped diplococcus
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who are the reservoirs for N. meningitidis
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Humans are the only reservoir
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where do you typically find N. meningitidis
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nasopharynx
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what are the characteristics of Meningococcemia
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may or may not evolve into meningitis
skin rash (petechiae) DIC and shock can occur Waterhouse-Friderichsen syndrome in children (hemorrhage into adrenal tissue) |
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what is different about infantile meningiococcal meningitis
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no early symptoms of disease
presents with late symptoms of apnea, seizures, and coma adult = early signs (rash) + typical meningitis presentation |
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diagnosis of Meningococcal Meningitis
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Characteristic petechial lesions=meningococcemia
•Gram stain of CSF •Cultivation of blood, CSF •Detection of capsular polysaccharide in CSF |
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treatment and prevention of meningiococcal meningitis
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Penicillin G (doc)
chloramphenicol or 3rd gen cephalosporins polysaccharide-protein conjugate quadrivalent vaccine (children, military, college, asplenics, travelers, during epidemics) |
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what are the characteristics of parameningial infections caused by bacteria
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abscesses
subdural empyema dural sinus infection thromboses external otitis endocarditis |
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what is the most common obligate anaerobe that causes a brain abscess
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Bacteroides fragilis
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what causes parameningeal infections
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they are rare
secondary to adjacent infection some systemic, local, brain, immune defect is usually present, making the indivdual susceptible to this |
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where would you most likely find an brain abscess, secondary to an otitis media or mastoiditis infection
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temporal lobe or cerebellum
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where would you most likely find an brain abscess, secondary to dental sepsis
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frontal lobe
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what are the virulence factors for Bacteroides fragilis
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neuraminidase
Hyaluronidase LPS polysaccharide capsule |
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pathogenisis of a Brain abscess
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entry and inflammitory response
early --> late cerebritis early --> late capsule formation abscess |
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clinical manifestations of a brain abscess
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almost never the result of a bacterial meningitis
low grade fever headache c progressing severity aphasia, impaired conciousness, nystagmus, etc |
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diagnosis of a brain abscess
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CT or MRI
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treatment of brain abscesses
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Antibiotic
surgical aspiration or excision |
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what is the causitive agent of a pyogenic brain abscess
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mixed organism infection
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subdural empyema features
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pus btw dura and arachnoid layers
anaerobic Strep most common (Staph and enterics to lesser extent) usually caused by paranasal sinus infection or otitis media high mortality CT and cerebral angiography CSF usually neg |
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spinal epidural abscess features
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epidural space
Staph aureus most common (strep and enterics too) infection from adjacent tissue, blood, perforating wound |
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clinical symptoms of a spinal epidural abscess
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severe back pain
radicular pain to the trunk or extremities leads to permanent paralysis and high mortality hours(acute) to months (chronic) diagnosed via CT |
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what is malignant external otitis
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External auditory canal infection that progresses to adjacent tissues and the temporal bone
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what is the usual suspect for malignant external otitis
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Pseudomonas
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clinical manifestations of malignant external otitis
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rapidly evolving pain c or w/o discharge
swelling of the parotid paralysis of CN VI-XIII death caused by progression to meningitis |
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diagnosis of malignant external otitis
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Pseudomonas culture
MRI or CT |
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what are the major infections of the PNS
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Leprosy
Botulism Tetanus |
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what are the "big 3" granulotomatious diseases
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TB
Syphilis Leprosy |
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when was the leprosy vaccine liscensed in India
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1998
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when did Hansen discover the leprosy bacilli
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1873
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characteristics of Mycobacterium leprae
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acid fast bacilli
obligate intracellular org grows in histocytes, Macs, Schwann cells |
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reservoirs for Leprosy
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monkeys and armadillos
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what is the most likely route of infection for leprosy
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the skin
resp and other routs possible |
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what is the usual incubation period for leprosy
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5yrs
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why was there a spike of leprosy in the US in the 80s
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indo-chinese refugee influx
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where do you typically find leprotomatious lesions?
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on the cooler parts of the body
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what are the clinical signs of leprosy
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earliest sign, hypopigmented macule (may be numb)
tuberculoid, lepromatious, or borderline leprosy will then develop depending on the CMI response tuberculoid to lepromatious is a switch from CMI to AMI (and they say based on bacterial "titer") |
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what are the clinical signs of tuberculoid leprosy
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•Skin lesions are granulomatous and hypopigmented, with raised edges and a flattened, dry center
•Peripheral nerve invasion results in anesthesia at the involved areas |
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what are the clinical signs of lepromatous leprosy
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•Skin lesions are raised, and the histiocytes and macrophages contain many bacilli
•Peripheral nerve destruction with anesthesia and eventual trauma, secondary infection, paralysis, ischemia, and distortion of hands and feet •In untreated cases, there is multiple organ involvement and death |
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what is a common finding in progressive lepromatous leprosy
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gross destruction and penciling of apendages (fingers, toes, nose)
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where is leprosy endemic
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tropical areas
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how do you diagnose leprosy
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observation of acid fast bacilli in skin lesions
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C. perfringens causes
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gas gangreen and food poisoning
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C. difficile causes
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pseudomembranous colitis
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C. tetani causes
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tetanus
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C. botulinum causes
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botulism
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what is the epidemiology of C. tetani
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soil
GI tract of humans, horses, others |
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who are the high risk groups in the US
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newborns and IV drug users
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pathogenesis of tenanus
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trauma that establishes anaerobic conditions
bacterial multiplication and release of tetnospasmin protein bind to nerve endings, intra-axonal xport to inhib neurons inhibition of neurotransmitter release spastic paralysis |
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what are the cardiac complications of tetanus
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hypo/hypertension
tachy |
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what are the respiratory complications of tetanus
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asperation pneumonia
atelectasis |
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where do the bacteria enter in neonatal tetanus
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the umbilicus
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what is localized tetanus
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disease only affects the limbs and resolves spontaneously
inadequately immunized person |
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what is cephalic tetanus
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head trauma induced
only involves facial spasms very rare |
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prevention and treatment for tetanus
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DTaP or Tdap (toxoid)
- 4 doses, starting at 2 mo - 10 yr boosters HTIG (human tetanus Ig) IV penicillin |
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what is the most potent exotoxin known to man
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botulism toxin (neurotoxin)
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what is the etiology of C. botulinum
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soil
GI of birds, fish, mammals |
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what are the typical sources of C. botulinum infections
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home canned foods (or dented store cans)
infant botulism due to honey ingestion wound botulism from deep puncture wounds or IV drug use isolated cases of GI botulism |
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what type of C. botulinum is predominant in the US
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A in the West
B in the East |
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in botulism food poisoning, is the bacteria causing the disease?
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no, the preformed toxin is
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what does the botulism neurotoxin block
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blocks Ach release at myoneuronal jxns and PNS inhibition
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clinical features of botulism
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flacid paralysis
respiratory paralysis and death |
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mortality rates for type A, B and E C. botulinum
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A-32%
B- 17% E-40% |
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CN palsy's typically seen in botulism
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diplopia
dysphagia dysphonia |
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clinical diagnosis of botulism, cardinal features used to differentiate it from other neurological problems
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no fever
symmetric neurological dysfunctions pt is responsive HR is normal or slower (hypotension) no sensory deficits except blurred vision confirmatory ddx is toxin in the feces or culture of bacteria |
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treatment of botulism
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elimination of the bacteria or toxin source
removal of unabsorbed toxin antitoxin admin supportive therapy |
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where do we get the antitoxin from?
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hyperimmunized adults
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how are both the tetanus and botulism toxins released
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autolysis of the bacteria
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what is the tetanus toxin production governed by?
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plasmid encoded
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what is the botulism toxin governed by
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it is bacteriophage encoded
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how many serologic types of botulism toxins are there? tetanus?
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B- 8
T- 1 |
