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Micro > CNS intro > Flashcards

CNS intro Flashcards

1
Q

Mass Lesions/Abscesses

A

Abscess – S. aureus, anaerobes

neurocysticercosis (cysts) – Taenia solium

toxoplasmosis –(pseudocyts) - Toxoplasma gondii

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2
Q

Neurotoxic diseases

A

CNS – tetanus – Clostridium tetani (rare only due to vaccination)

PNS – botulism – Clostridium botulinum
(rare only due to proper food handling)

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3
Q

Peripheral Nervous System (PNS) diseases

A

Leprosy – Infection of sensory nerves – Mycobacterium leprae

Guillain-Barre’ Syndrome – demyelination of PNS - autoimmune disease –Campylobacter jejuni

Botulism – toxin inhibits nerves at the neuromuscular junction –Clostridium botulinum

Myasthenia gravis

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4
Q

Prion disease

A

new variant Creutzfeldt-Jacob Disease: Prion of bovine spongiform encephalitis

Creutzfeldt-Jacob Disease (CJD). Human Prions

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5
Q

Common cause of purulent/pyogenic meningitis: bacteria

A

Neisseria meningitidis
Streptococcus pneumoniae
Haemophilus influenzae, type b

Streptococcus agalactiae
Escherichia coli K1
Klebsiella pneumoniae
Listeria monocytogenes

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6
Q

Bacterial encephalitis and/or mass lesions

A

Mycoplasma pneumoniae
Listeria monocytogenes
S. aureus
anaerobic [mixed] infections

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7
Q

viral encephalitis

A

HSV-1
arborviruses
rabies
polio

non-polio enteroviruses:
Echovirus
Coxsackie virus
enterovirus 68-71

HIV
JC virus
measles (rare only due to vaccination of humans) -SSPE
VZV 
CMV
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8
Q

Bacteria are most common cause of typical - purulent/pyogenic meningitis

A 
Streptococcus agalactiae
Escherichia coli K1
Klebsiella pneumoniae
Listeria monocytogenes
Streptococcus pneumonia
Neisseria meningitidis
Haemophilus influenzae, type b
Mycoplasma pneumoniae.
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9
Q

Viruses are the most common cause of meningitis (over all) and the cause of aseptic/viral meningitis

A 
HHV 6,7
NPEs
arbovirus
HSV-2
LCMV
HIV
Mumps virus, unless countries immunize against it.
polio, ditto
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10
Q

tetanus

A

not meningitis, tetanus is a neurotoxemia, like botulism

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11
Q

Fungi that cause meningitis

A

Cryptococcus neoformans & C. grubii. (Cryptococcosis)

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12
Q

Other causes of meningitis

A
  1. Lyme disease - B. burgdorferi.
  2. M. tuberculosis.
  3. syphilis - T. pallidum.
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13
Q

Encephalitis:

A

Viral cases have high mortality and incidence of severe neurological sequelae

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14
Q

Diffuse epidemic diffuse encephalitis in the summer/fall months:

A

Arbovirus:

Eastern equine encephalitis (EEE) virus.

Western equine encephalitis (WEE) virus.

Venezuelan equine encephalitis (VEE) virus.

St. Louis encephalitis (SLE) virus.

Powassan encephalitis (POW) virus.

California encephalitis serogroup: Jamestown canyon, La Cross viruses.

Colorado tick fever virus.

Mountain fever in Colorado virus.

West Nile encephalitis (Africa, Europe, USA) virus

Others: HSV-1 and the non-polio enteroviruses

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15
Q

year-round viral encephalitis

A

Herpes Simplex virus HSV (HSV-1 esp) sporadic, usually- focal encephalitis

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16
Q

non-polio enteroviruses

A

a. ECHO viruses,
b. Coxsackie viruses,
c. enteroviruses 6871.

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17
Q

other viral encephalitis agents

A
  1. Lymphocytic choriomeningitis virus (LCM).
  2. HIV - HIV-1-associated cognitive/motor complex (AKA AIDS Dementia Complex).
  3. Cytomegalovirus (CMV).
  4. Rabies virus (rare only due to vaccination of dogs and cats).
  5. Polio, measles, mumps viruses (rare only due to vaccination)
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18
Q

Focal Viral encephalitis:

A
  1. HSV-1(usually, not always) sporadic, focal encephalitis all year round.
  2. Rabies virus – Rabies (rare only due to vaccination of dogs and cats)
  3. Polio viruses (rare only due to vaccination of humans)

arboviruses and non-polio enteroviruses

Encephalomyelitis: WNV, Polio

CMV
VZV
JC virus and PML

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19
Q

bacterial agents of encephalitis

A

a. Mycoplasma pneumoniae.

b. Listeria monocytogenes

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20
Q

fungal agent of encephalitis

A

Cryptococcus neoformans var. grubii

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21
Q

Slow virus encephalitis diseases:

A

HIV - HIV-1-associated cognitive/motor complex (AKA AIDS Dementia Complex).

Progressive multifocal leukoencephalopathy (PML): polyomaviruses – papovavirus: JC
virus severe T-cell suppression/AIDS or transplant pt.

Subacute, sclerosing panencephalopathy (SSPE): Measles (Rubeola virus, rare in US (exc. immigrants)

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22
Q

protozoan agents of Meningoencephalitis/Mass lesions:

A

toxoplasmosis: Toxoplasma gondii.

amoebic meningoencephalitis:

a. Naegleria fowleri.
b. Acanthamoeba spp.
c. Balamuthia mandrillaris.
d. Vahlkampfia spp.
e. Hartmanella spp.

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23
Q

helminth agents of Meningoencephalitis/Mass lesions:

A

Neurocysticercosis – Taenia solium.

Cystic Echinococcosis-hydatid cyst – Echinococcus granulosus or multilocularis.

Raccoon Round Worm Encephalitis/Baylisascariasis – Baylisascaris procyonis.

Toxocaria – Toxocaria cannis or cati.

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24
Q

Peripheral neuropathies/Bell’s palsies, acute facial paralysis

A

HSV-1, VZV, B. burgdorferi

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25
Q

Guillain-Bare’ syndrome

Most common cause of generalized paralysis in US caused by
the host’s immune response to a mucosal infection of

A

GI tract - C. jejune;

RT

a. influenza virus
b. Chlamydia spp.;

G-UT - Chlamydia sp.

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26
Q

6? classes of CNS-PNS infections

A 
Meningitis - CNS
Encephalitis - CNS
Mass Lesions/Abscesses – CNS 
Neurotoxic diseases 
Peripheral Nervous System (PNS) diseases
Prion disease
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27
Q

Meningitis - CNS: agents

A

viruses are the most common cause

bacteria are 2nd most common cause – 7 major agents

fungus are less common – Cryptococcus neoformans var. grubii

protozoa are less common – Toxoplasma ghondii, Naegleria fowleri

*Tetanus mimics some S & S of meningitis but tetanus is a neurotoxemia, like botulism.

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28
Q

meningitis is..

A

Meningeal inflammation resulting from an infection within the subarachnoid space

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29
Q

encephalitis is…

A

Inflammation of the brain parenchyma

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30
Q

focal encephalitis agents

A

primarily HSV-1 – HSV-1 disease is treatable by antiviral therapy

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31
Q

diffuse encephalitis

A

primarily arbovirus- supportive tx only

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32
Q

Encephalomyelitis

A

encephalitis with myelitis (spinal chord inflammation) – caused by poliovirus and West Nile virus – supportive therapy only

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33
Q

Mass Lesions/Abscesses – CNS –

A

Lesion is macroscopic in size and of sufficient mass/volume to press against the normal brain tissue → increased intracranial pressure →focal seizures

CT scan showing ring-enhancing (mass) lesion supports the diagnosis

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34
Q

Fungi: three common agents

A

Cryptococcus – a meningoencehalitis

Candida. - meningitis

Coccidioides immitis – a meningoencehalitis

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35
Q

parasites usually cause a..

A

meningoencephalitis

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36
Q

most common CNS parasites

A
  1. Toxoplasma gondii (protozoan - Toxoplasmosis).
  2. Taenia solium, agent of neurocysticercosis (NCC; helminth).
  3. Echinococcus granulosus or multilocularis (Cystic Echinococcosis-hydatid cyst)
  4. Baylisascaris procyonis (Raccoon Round Worm Encephalitis/Baylisascariasis)
  5. Toxocaria cannis or cati (Toxocaria)
  6. Naegleria fowleri predominate agent
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37
Q

other CNS parasites

A

Acanthamoeba spp.
Balamuthia mandrillaris.
Vahlkampfia spp.
Hartmanella spp.

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38
Q

encapsulated agents

A 
S. pneumoniae;
S. agalactiae,
H. influenzae, type b;
N. meningitidis
E. coli K1, 
K. pneumoniae,

Cryptococcus neoformans var. neoformans.

*require B cells (not crypto)

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39
Q 
CMI required
(facultative or obligate intracellular agents)
A 
Listeria monocytogenes.
Toxoplasma gondii.
Cryptococcus cytomegalovirus CMV
Mtb
JC virus and PML
HIV
LCMV.
E. coli K1??
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40
Q

predisposing factors: immunodificiency

A

immunodificiency:

T cell.
B cell.

Terminal complement deficiency (C5-9) and N. meningitides

Long-term corticosteroid therapy. Immunosuppression of solid organ transplant (SOT) patient.

Cancer due to chemotherapy or form of cancer, e.g., lymphoma
AIDS.

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41
Q

predisposing factor: chronic or debilitating disease

A

Advanced HIV/AIDS.
Sickle cell disease.
Lymphoma/cancer.

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42
Q

need high index of suspicion with oldies bc…

A

often hypothermic so don’t manifest with fever.

neck arthritis so already manifest with nuchal rigidity.

dementia masks lethargy and irritability.

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43
Q

newborns should be..

A

routinely tapped because so few S/S in this age group

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44
Q

nosocomial meningitis from..

A

Intraventricular catheters (IVC) and cochlear implant

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45
Q

Carriage is in nasopharynx and humans are only HOST for these bac

A

S. pneumoniae;
H. influenzae, type b;
N. meningitidis,
S. agalactiae (also in vagina, GIT, skin).

*Humans are only host for Mycobacterium tuberculosis

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46
Q

Carriage is in nares for this bac

A

Staphylococcus aureus

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47
Q

Carriage in humans is primarily on mucosal surfaces for these bac

A

endogenous anaerobic flora

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48
Q

Carriage in humans is primarily in the colon for these bac

A

Streptococcus agalactiae,
E. coli
K. pneumoniae
Listeria monocytogenes

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49
Q

Carriage in humans is primarily in the colon with migration to the vagina and vaginal colonization and migration to urethra → cystitis for these bac

A

Streptococcus agalactiae,
E. coli
K. pneumoniae

*can infect fetus: neonatal infection

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50
Q

Animals and/or humans are RESERVOIR for these bac

A 
E. coli K1.
K. pneumonia.
L. monocytogenes.
M. leprae.
S. agalactiae,

Staphylococcus aureus: both but primarily humans

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51
Q

other bacteria

A

C. tetani, (soil reservoirs),
C. botulinum. (soil, water, animal reservoirs)
L. monocytogenes (ubiquitous).

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52
Q

viral agents: zoonosis

A

Arboviruses – animals (mammals and/or birds) and arthropods (mosquito or tick).
Rabies virus– mammals.
LCMV – mammals, especially rodents

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53
Q

viral agents that humans are sole reservoir for:

A 
enteroviruses
measles virus
herpes viruses: HSV-1, HSV-2, HHV-6, HHV-7, 
CMV
HIV.
JC and BK viruses. 
mumps virus
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54
Q

other agents and epidemiology

A

Cryptococcus neoformans (soil and animal [bird] reservoirs) – fungus

Toxoplasma gondii (animal reservoir) – protozoan

Taenia solium (pig and humans reservoir) – tape worm.

Echinococcus granulosus or multilocularis (Cystic Echinococcosis-hydatid cyst)

Baylisascaris procyonis (Raccoon Round Worm Encephalitis/Baylisascariasis)

Toxocaria cannis or cati (Toxocaria) in cat or dog round worm

Amoebic meningoencephalitis: mainly Naegleria fowleri – warm water reservoir.

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55
Q

zoonosis

A

Arboviruses – animals (mammals and/or birds) and arthropods (mosquito or tick).
Rabies virus: Bat mostly, raccon-East Coast, skunk-mid-West in US – Dog,WW
LCMV from rodent.
Listeria monocytogenes.
Mycobacterium leprae?
Toxoplasma gondii (cysts bearing larvae),
Echinococcus granulosus or multilocularis (Cystic Echinococcosis-hydatid cyst)
Baylisascaris procyonis (Raccoon Round Worm Encephalitis/Baylisascariasis)
Toxocaria cannis or cati (Toxocaria)
Bovine spongiform encephalopathy prion (AKA new variant Creutzfeldt-Jacob Ds).
C. botulinum
*Cryptococcus neoformans (animal-bird mechanical vector)

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56
Q

Consumption of tainted food:

A 
Bovine spongiform encephalopathy prion.
Taenia solium (cysts bearing larvae) – not directly to CNS, indirectly.
Toxoplasma gondii (cysts bearing trophs or bradyozoites).
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57
Q

Fecal-oral route / food is contaminated with feces

A

Taenia solium (ova) neurocysticercosis from human,
Toxoplasma gondii (ova) Toxoplasmosis from cat litter, soil.
enteroviruses (polio, ECHO & Coxsackie viruses, enteroviruses 68→71).
Listeria monocytogenes from many sources.
LCMV from rodent.
Echinococcus granulosus or multilocularis (Cystic Echinococcosis-hydatid cyst)
Baylisascaris procyonis (Raccoon Round Worm Encephalitis/Baylisascariasis)
Toxocaria cannis or cati (Toxocaria)

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58
Q

In utero (vertical) transmission:

A

Streptococcus agalactiae (less common than during parturition)

Listeria monocytogenes (more common than during parturition)

Non-polio enterovirus (Coxsackie, Echoviruses, enteroviruses 68→71).

LCMV.
Toxoplasma - Toxoplasma gondii.
rubella.
CMV.
HSV
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59
Q

During parturition:

A

Streptococcus agalactiae (more common than In utero transmission)
Listeria monocytogenes,
E. coli
K. pneumoniae
Herpes virus and CMV (more common In utero transmission)

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60
Q

Inhalation of infectious dust:

A

Cryptococcus neoformans.

LCMV

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61
Q

Agents of CNS disease associated with familial/close –contact outbreaks include

A 
hib.
meningococcus. (N. meningitis)
Non-polio enterovirues.
T. solium – if someone is shedding ova.
Very rare, very, very uncommon agents that can cause outbreaks in USA are:
 a. M. leprae (lepromatous form)
 b. mumps virus
 c. measles virus
 d. rabies virus
 e. polio virus
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62
Q

anaerobes

A

endogenous flora

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63
Q

arboviruses

A

exposure to mosquito; Ticks for two agents

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64
Q

Cryptococcus neoformans

A

bird droppings

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65
Q

HSV-1

A

disease is reactivation of latent infection

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66
Q

HSV-2

A

sexual contact

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67
Q

HIV

A

blood or bodily fluids

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68
Q

LCMV

A

exposure to rodents, droppings, secretions, fluids

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69
Q

Listeria monocytogenes

A

animal exposure, food

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70
Q

Measles virus – SSPE

A

human, exposure before 1-y-of-age

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71
Q

Mumps

A

human exposure to agent

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72
Q

Mycobacterium leprae

A

human or animal exposure

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73
Q

Mycobacterium tuberculosis

A

human exposure

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74
Q

Neisseria meningitis

A

human exposure, terminal complement deficiency

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75
Q

nonpolio enteroviruses

A

human feces

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76
Q

Naegleria fowleri

A

exposure to fresh water with algae

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77
Q

polio enteroviruses

A

human feces

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78
Q

rabies virus

A

animal exposure, bat (USA) Dog (WW)

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79
Q

Staphylococcus aureus

A

Another person

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80
Q

Streptococcus agalactiae

A

low birth weight infant, rupture of membranes >24h before delivery, colonized vaginal canal

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81
Q

Streptococcus pneumoniae

A

congenital CSF leak

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82
Q

Taenia solium ova

A

human feces

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83
Q

Taenia solium cysticerci

A

undercooked or uncooked meat- pork

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84
Q

Toxoplasma gondii ova

A

cat feces

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85
Q

Toxoplasma gondii pseudocyst

A

raw or uncooked meat

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86
Q

??? are rare occurrences compared to other causes of morbidity and mortality, even among infectious diseases

A

Meningitis and encephalitis
M>E
viral>bacterial (less than 50%)
but viral not definitively dx

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87
Q

most common viral agents (children–>adults) in order

A

ECHO and Coxsackie viruses
then the arbovirues
HSV-2

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88
Q

Diffuse encephalitis>focal encephalitis

A

arboviruses: Most common agents of diffuse encephalitis

HSV-1: Most common agent (50%) of focal encephalitis

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89
Q

Most common agents of meningitis (viral)

A

Non-polio enteroviruses (ECHO viruses and Coxsackie viruses).
HHV-6, HHV-7

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90
Q

Less common agents of meningitis (after NPEs and HHV-6, 7)

A

Arboviruses – late summer→early fall seasonality, meningitis and diffuse encephalitis.
HSV-1 – no seasonality—focal encephalitis.
HSV-2 – if manifesting with primary symptomatic infection (genital herpes) – meningitis.
LCMV – if winter seasonality and history of rodent exposure – meningitis.
Polio (late summer and early fall seasonality, meningitis primarily young children → adults) and Mumps (rare due to vaccination)

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91
Q

the most frequent cause of bacterial meningitis in infants, children, adolescents, and young adults in the United States

A

Meningococcal disease

3000 cases> 60% of the 3,000 cases are in individuals > 11 y-o-age and this age group has the highest mortality rate 25% versus 10 to 14% overall

11% to 19% of survivors are left with long-term disabilities: hearing loss, cognitive impairment, renal failure, limb amputations

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92
Q

the highest case mortality rate for any bacterial agent of meningitis
and
the most common infectious agent associated with patients with recurrent meningeal infections.

A

S. pneumoniae

About 1/2 of all cases of meningitis in the US are nosocomial-acquired meningitis

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93
Q

bacteria: year round seasonality

A

S. agalactiae.
E. coli K1
K. pneumoniae

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94
Q

bacteria: summer seasonality
protozoan: ?

A

L. monocytogenes

Neglaria fowleri

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95
Q

bacteria: late winter-early spring seasonality

A

H. influenzae type b
N. meningitidis
S. pneumoniae

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96
Q

viral: year-round seasonality

A 
HHV-1
HHV-2
HHV-6; -7
CMV
HIV
Rabies
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97
Q

viral: Late summer and early fall seasonality

A

ECHO viruses and Coxsackie viruses
Polio virus
Arboviruses

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98
Q

viral: winter seasonality

A

LCMV

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99
Q

Congenital infections – The unborn child’ s infection is acquired in-utero and results in a diseased child at birth

A

TORCH agents:

TOxoplasma
Rubella
Cytomegalovirus [CMV]* (most common)
Herpes simplex virus [HSV]) -2 or -1

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100
Q

TORCH test -

A

a test to detect a congential (AKA intrauterine infection) infection in a neonate via presence of specific IgM in chord blood

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101
Q

the leading cause (by far) of infection and morbidity in the neonate

A

CMV infection

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102
Q

neonates: Highest incidence of infection and morbidity among procaryotes

A

S. agalactiae

103
Q

neonates: highest incidence of infection andmorbidity of all agents.

A

cytomegalovirus (CMV)

104
Q

other causes in neonates

A

E. coli K1
K. pneumoniae
L. monocytogenes
herpes simplex virus (HSV) 2 or 1
non-polio enterovirus (Coxsackie & Echoviruses)
Human herpes virus-6 and –7. (HHV-6 and HHV-7)

105
Q

Infants and young children – all agents

A 
HH-6, HH-7
non-polio enterovirus (Coxsackie; Echoviruses).
N. meningitides
S. pneumoniae	
Mycobacterium tuberculosis.
Arboviruses
LCMV.
Mumps.
106
Q

Adolscents →Elderly:

A 
non-polio enterovirus (Coxsackie and Echoviruses).
Arboviruses.
N. meningitides,
S. pneumoniae
L. monocytogenes – those over 50-y-o-age.
Mycobacterium tuberculosis.
LCMV.
Mumps (Adolscents).
107
Q

viral by age

A

Neonate: CMV (#1), HSV-2, 1, Non-polio enteroviruses

6 m-o-age up to 2-y-o-age HHV-6 & HHV-7.

2-y-o-age and older:

a. Non-polio enteroviruses.
b. HSV-1
c. Arboviruses.
d. HSV-2.
e. LCMV.

108
Q

Bacterial Agent by Age:

nenonate

A

S. agalactiae (most common)
E. coli K1
L. monocytogenes
K. pneumoniae K1, K2 (least)

109
Q

Bacterial Agent by Age:

Infant to adult

A

N. meningitides (most common)

S. pneumoniae

110
Q

Bacterial Agent by Age: elderly

A

N. meningitides,
S. pneumoniae
L. monocytogenes

111
Q

Pathogenesis – Portal of entry for CNS disease

Secondary invasion of the CNS follows

A

bacteremia.
viremia.
fungemia.
parasitemia.

Entry into the subarachnoid space occurs via sites of minimal resistance:

choroid plexus.
dural venous sinuses.
cribriform plate.
cerebral capillaries.

112
Q

Direct entry via damage to integrity of the CNS:

A

Penetrating injuries of the skull or spinal column.
congenital defects
*most common cause for both is S. pneumoniae, Hib, GAS

Ventricular shunts.

All children with cochlear implants, esp. those with implants with a positioner (rubber wedge) are at increased risk of infection for > 2 y post-implantation

113
Q

Contiguous spread along vascular channels from:

A

Nasal sinuses – Naegleria fowleri.
Malignant otitis externa (P. aeruginosa) or otitis media.
Mastoid.
Sites of parameningeal infection, e.g., epidural abscess.

114
Q

Intra-axonal transport (retrograde flow) inside nerves:

A

rabies.
herpes.
polioviruses.
tetanus toxin.

115
Q

Signs and symptoms of meningitis in the neonate are the same as those for neonatal sepsis and encephalitis, but are not the same as the adult and include

A

Fever.
Lethargy.
Poor feeding
GI disturbance (vomiting/diarrhea)/abdominal distension.
Respiratory abnormalities (e.g., dyspnea, cyanosis)
Cardiac abnormalities (tachycardia).
Bulging fontanelle (indicates pressure on brain), ONLY if CNS infection

116
Q

Signs and Symptoms of any (bacterial, fungal, viral, etc.) meningitis in persons >2 y-o-age

A

Irritability
lethargy
fever

Others:
severe headache,
nuchal rigidity,
vomiting,
pressure on eyeball.
photophobia
meningeal inflammation/irritation
117
Q

Meningeal inflammation/irritation elicits a protective response (5 different signs) to prevent stretching of inflamed, hypersensitive nerve roots:

A

Nuchal rigidity – meningismus, (e.g., The inability of a patient to place their chin to their chest passively without involuntary muscles spasms preventing it).

Kernig sign - extension of the leg at the knee when patient is supine with the thigh flexed at the hip → marked pain and resistance to extension of the leg.

Brudzinski sign - rapid flexion of the neck while patient is supine → involuntary brisk flexion of the knees.

Opisthotonos - head drawn backward, spasm of back muscles.

Tripod position (aka Amoss or Hoyne signs) knees and hips flexed, back arched lordotically, neck extended, and arms brought back to support the thorax.

118
Q

S/S indicative of progression of severe symptoms indicate progression to meningoencephalitis:

A 
decline in consciousness.
focal cerebral abnormalities (hemiparesis, monoparesis, aphasia)
Seizures.
convulsions.
coma.
119
Q

Maculopapular rash

A 
non-polio enteroviruses (ECHOvirus, Coxsackievirus, enteroviruses),
arboviruses
HSV.
S. pneumoniae. 
N. meningitidis.
H. influenzae, type b
120
Q

vesicular rash

A

HSV
fungi
non-polio enteroviruses.

121
Q

Petechial / Purpuric:

A

S. pneumoniae.
N. meningitidis.
H. influenzae, type b.

122
Q

Bacteria penetration of blood-brain barrier and into CSF leads to:

A

Local release of inflammatory cytokines in CSF

Adhesion of leukocytes to brain endothelium and diapedesis into CSF

Blood-brain barrier is further damaged and becomes permeable

123
Q

Blood-brain barrier is further damaged, becomes permeable, which results in:

A

Exudation of albumin through opened intercellular junctions of meningeal venules.

Brain edema, increased intracranial pressure, cerebral vasculitis, altered cerebral blood flow.

Cranial nerve injury, seizures, hypoxic-ischemic brain damage, brain-stem herniation.

124
Q

Mechanisms responsible for the encephalitic aspects of bacterial meningitis include:

A

metabolic encephalitis caused by endotoxin and TNF-α.
perivascular inflammation.
infarcts (strokes/seizures) caused by occluded blood

125
Q

Encephalopathy is

A

is depressed or altered level of consciousness lasting >24 hours

126
Q

Encephalitis is encephalopathy plus 2 or more of the following

A

fever (>38oC)
seizures
altered mental status,
severe headache

focal neurological findings (e.g., paralysis, cognitive disorders, if focal encephalitis is present),
CSF pleocytosis (> 5 WBC/ml),

electroencephalogram findings compatible with encephalitis,
abnormal results on neuroimaging.

Some manifestations of meningitis may also be present.

127
Q

Arbovirus diffuse encephalitis

A

fever (>38oC), seizures, altered mental status, severe headache.

128
Q

Polio focal encephalitis (Encephalomyelitis)

A

Acute osnet of a flaccid, ascending asymmetrical paralysis due to involvement of motor neuron in brain and spinal column with loss of superficial and deep reflexes, severe muscle aches or spasms, muscle pain, Sensory involvement - Abnormal sensations (but not loss of sensation) in an area, sensitivity to touch and paresthesia

129
Q

Rabies focal encephalitis

A

dumb or furious forms

130
Q

Rabies: Furious form

A

Sensory sensitivity to external stimuli, hyperactivity, agitation, anxiety, insomnia, loss of natural timidity - aggressive sexual behavior, hydrophobia and foaming at the mouth arise from excruciatingly painful, laryngeal spasms → confusion, delirium → coma → death

131
Q

Rabies: Paralytic/Dumb rabies form

A

Signs and symptoms are indistinguishable from viral encephalitis, then the patient manifests with paralysis starting at extremities and spreading to the trunk as areas of the brain are destroyed. Paralysis → to hypoventilation/respiratory paralysis →hypotension/cardiac failure → eventually coma and death.

132
Q

Herpes focal encephalitis with distinctive clinical features due to its remarkable localization:

A

memory defects, psychosis, slurred speech, personality changes from involvement of one temporal lobe - primarily the cerebral cortex with characteristic lesions (inflammation, focal hemorrhage, necrosis.

Treat with acyclovir.

133
Q

Pathology of viral encephalitis:

A

Mononuclear accumulation in meningeal and perivascular spaces.

Fragility of brain blood vessels and the occurrence of perivascular hemorrhages and infarcts allow spillage of RBC, WBC and protein into the Virchow-Robin spaces that communicate with cerebrospinal fluid.

Viral replication in the brain parenchyma causes inflammation and severe CNS dysfunction. Few survive and those who do have serious emotional disorders and learning deficits.

134
Q

During a viral infection in the CNS, viral agents are recognized by at least one of the

A

TLRs on neurons → neuronal death in the brain

(Neurons possess toll-like receptors that can activate a protein called SARM1 in neurons, which induces their death by affecting the function of mitochondria)

135
Q

Focal sites of viral encephalitis:

A

Herpes virus

Polio

136
Q

?? is the most common form of paralytic poliomyelitis; it results from viral invasion of the ???
which do what ??

A

Spinal polio

the motor neurons of the anterior horn cells, or the ventral (front) gray matter section in the spinal column

are responsible movement of the muscles, including those of the trunk, limbs and the intercostal muscles

137
Q

Bulbar polio:

A

white matter pathway that connects the cerebral cortex to the brain stem

The destruction of these nerves weakens the muscles supplied by the cranial nerves, producing symptoms of encephalitis, and causes difficulty breathing, speaking and swallowing

138
Q

Rabies:

A

predominates in the Grey matter.

localizes in the limbic regions (producing focal symptoms).

infects neurons in almost all areas of the brain:
cerebellum, the Purkinjes cells and also cells of the hippocampus, hypothlaamus and pontine nuclei

139
Q

mass lesions s/s

A 
Fever
Headaches (elevated intracranial pressure)

Seizures – Focal or generalized tonic-clonic seizures.

Neurological deficits/focal signs (hemiparesis, visual loss, paraparesis).

Altered mental status (dementia, confusions, stupor)

140
Q

CT scan showing ??

In severe cases ??

A

ring-enhancing (mass) lesion supports the diagnosis.

a mid-line shift, risk of brain stem herniation

141
Q

an encapsulated structure grows in size (becomes visible to the naked eye) creating a

A

mass effect – displaces brain tissue and creates intracranial pressure

142
Q

Etiology – Abscess:

A

Localized collection of purulent infectious agent material and host cell debris in a cavity formed by the disintegration of tissue

143
Q

3 distinct abscess locations:

A

epidural (between vertebrae and dura)
subdural (between dura and arachnoid).
parenchyma (in the brain tissue)

144
Q

Etiology of abscesses:

A

Procaryotic: S. aureus, anaerobic infections, L. monocytogenes.

Fungi agents: Candida albicans

145
Q

Cystic lesions - humans as Intermediate hosts of parasites

A

A helminth (flat worm) produces a tissue cyst as part of its life cycle

146
Q

2 distinct cystic lesion locations:

A

in the ventricles, subarachnoid space or meninges

parenchyma (in the brain tissue).

147
Q

cystic lesion agents

A

Taenia solium (Neurocysticercosis)

Echinococcus granulosus or multilocularis (Cystic Echinococcosis-hydatid cyst).

148
Q

Pseudocyst lesions humans as Intermediate hosts of parasites

A

a pseudocyst is formed in the brain parenchyma as a result of the human immune response to the parasitic/protozoan infection

149
Q

Pseudocyst lesions caused by

A

Toxoplasma gondii (Toxoplasmosis) - protozoan

150
Q

neurotoxins: Floppy (hypotonic)paralysis:

A

Guillain-Barre’ Syndrome – demyelination of PNS - autoimmune disease –primarily molecular mimicry of Ab first raised against Campylobacter jejuni antigens.

Botulism – an exotoxin/neurotoxin inhibits nerves at the neuromuscular junction / PNS – Clostridium botulinum elaborates the exotoxin

151
Q

Botulism toxin acts at the ?? not the ??

A

myoneural/neuromuscular junction (not the CNS, unlike tetanus) paralyzing of the cholinergic nerve fibers at the point of release of acetylcholine

Toxin blocks both cholinergic transmission points in the autonomic system:
Synaptic ganglia
Parasympathetic motor end plates peripherally located in the junction between the nerve cell and muscle cell fibers

152
Q

Botulism: Anticholinergic/inhibition of the parasympathetic with no effect on the ?? results in such symptoms as ??

A

sympathetic nerves

dilated and un-responsive pupils, dry mouth, and constipation

153
Q

Botulism: Progressive neuromuscular blockade of muscles innervated by ?? occurs first, then ??

A

cranial nerves

the trunk (systemic generalized muscle weakness)

finally the extremities (peripheral motor weakness) and diaphragm

154
Q

Later complications of botulism

A

paralytic ileus, severe constipation, and urinary retention

Ocular and cranial muscle weakness occurs first because neuromuscular junctions of these muscles have the lowest threshold for synaptic failure

155
Q

Polio virus does what ??

A

kills neurons

156
Q

Spastic (Rigid, hypertonic) paralysis

A

tetanus (mimics some S/S of meningitis)

exotoxin/neurotoxin inhibits nerves in the spinal column-CNS Clostridium tetani elaborates the exotoxin/neurotoxin.

157
Q

tetanus is transported to inhibitory ??

A

interneurons e.g. Renshaw cells.

Interneurons: small neurons that that are involved in local processing of nerve signals and which generally have inhibitory activities

158
Q

tetanus irreversibly inhibits the release of

A

inhibitory transmitter substances, γ-aminobutyric acid (GABA) and glycine,
(presynaptic blockade of these cells)

does not act on the synapses of Renshaw cells that handle
ACh transmission.

Absence of inhibitory Renshaw cell activity allows LMNs to increase muscle tone and rigidity and permits simultaneous contractions of both agonist and antagonist muscles

159
Q

tetanus toxin is rapidly transported up the spinal column to reach the ??
where it ??

A

brain stem and/or hypothalamus

inhibits interneurons so that normal INHIBITORY feedback of the symp and parasym systems is disrupted and ONLY positive feedback of these systems occurs, resulting in severe disruption of autonomic function in late, severe, general tetanus

160
Q

Lumbar puncture results are

A

clinical clues; not definitive diagnosis

161
Q

Direct smear of CSF (~30% sensitive) that is stained by

A

Gram-stain (variable sensitivity)

A Gram stain of CSF is positive in 60% to 90% of cases, but results vary with the organism as well as with the concentration of bacteria in the CSF

In terms of bacterial concentrations, the CSF Gram stain is positive in up to 97% of cases when there are >10/ml, as opposed to around 25% when there are less than 10/ml

162
Q

Gram-positive agents

A

Listeria monocytogenes
S. pneumoniae
S. agalactiae

163
Q

Gram-negative agents

A

H. influenzae, type b
N. meningitidis
E. coli K1
K. pneumoniae

164
Q

Sensitivity by organism

A 
S pneumoniae, 90%;
H influenzae, 86%; 
N meningitidis, 75%;
Gram-negative bacilli, 50%;
L monocytogenes, less than 50%.
165
Q

other stains

A

acid-fast stain (Mycobacterium).
India ink preparation (Cryptococcus).
Saline wet mount (Naegleria fowleri).

166
Q

Culture and sensitivity of sedimented CSF (~50% sensitive)

A

Order MIC and MBC

CSF cultures are positive in 70% to 85% of cases

167
Q

other parameters

A

PMNs, lymphocytes, or monocytic lineage predominates?

RBC present?

Hypoglycorrhachia (low or normal levels of glucose) present?

Hyperproteinosis (elevated protein levels) or hypoproteinosis

Hyperglobulinorrachia - elevated antibodies in CSF present?

168
Q

14-3-3 chaperone brain protein elevated (normal:

A

cerebrovascular events/acccidents (CVAs),
viral encephalitis,
Creutzfeldt-Jakob disease (prions)

169
Q

Hypoglycorrhachia and Hyperproteinosis are related

A

In a patient with bacteria meningitis, albumin from the brain parenchyma enters the CSF and this protein movement disrupts the protein gradient that normally exists between the CSF and blood

The protein gradient between the blood and CSF is used to co-transport glucose from the blood to the CSF

high protein levels in the CSF stops co-transport of glucose so glucose levels are low in the CSF

This is why a normal CSF glucose level is ~80% of the blood glucose level : important to do simultaneous measurements of blood and CSF glucose*

170
Q

Normal CSF is

A

a clear, colorless fluid
contains β2-transferrin

Not straw-colored like serous fluid

171
Q

in a meningitis pt during Gram-staining of CSF specimens, CSF protein is

A

heat-fixed to the glass slide and stains pale pink, making detection of any Gram-negative bacteria in the CSF difficult.

172
Q

Rapid test:

A

antigen testing/latex agglutination test:

Latex spheres coated with antibody detects presence of capsular Ag in CSF

Very low (@7%) sensitivity except with positive Gram-stain or culture positive specimen

173
Q

antigen testing/latex agglutination test can detect

A

S. pneumoniae,
H. influenzae, type b
N. meningitidis
cryptococcal antigen

174
Q

other tests

A

EIA test of a CSF specimen
*VDRL for syphilis
Procalcitonin: detection for bacterial meningitis

175
Q

PCR – for specific agents:

A

enteroviruses (RT-PCR)
herpes simplex virus
JC virus
HIV (RT-PCR)

176
Q

Skin specimen: vesicular

A

Tzanck or Papanicolaou stained skin biopsy specimen for HSV

177
Q

Skin specimen: purpuric

A

Gram-stained smear of skin biopsy specimen:
S. pneumonia
N. meningitidis.

Culture and sensitivity (MIC, MBC)

178
Q

blood tests:

A

Culture and sensitivity (MIC, MBC) of blood (2 samples from different sites)

positive culture:
most likely if pt is spiking a fever or fever is present!
establishes diagnosis in presence of negative CSF culture in symptomatic pt
40-90%

PCR or RT-PCR of blood for specific viral agents

Ag testing
serology: specific Abs

179
Q

Other bodily fluids (e.g., urine):

A
  • Order Gram-stain*
  • Order culture and sensitivity* (MIC, MBC).

PCR of urine for specific viral agents may also be done.

Latex agglutination for cryptococcal antigen.

Vaginal and Rectal swabs for GBS - Treat if culture positive – Learn.

180
Q

??? diagnostic tests are NOT feasible for CNS infectious diseases, so ???

A

sequential

order all appropriate tests right away – in parallel, NOT sequentially

181
Q

EEG pattern indicative of

A

focal or diffuse problem

182
Q

Neuroimaging: CT-scan or MRI

A

X-ray, CT scan, MRI – indicative of focal or diffuse problem

CT-scan will show contrast/ring-enhancing lesions for mass effect/lesion.

183
Q

ddx

A

meningitis
encephalitis.

Non –Infectious → patient is usually afebrile:

a. (SAH or ICH) subarachnoid or intracerebral hemorrhage: Incidence is 40→50K/y in US, with the rate expected to double in next 50 y, thus hemorrhage is much more common than meningitis and/or encephalitis
b. (CVT) Cerebral venous thrombosis
c. Ischemic stroke.

Mass lesions.
paralysis – floppy vs spastic

184
Q

Bacterial meningitis and viral meningitis have similar presentation, but

A

bacterial meningitis has a high mortality rate and survivors have serious neurological sequelae, viral meningitis doesn’t

so…
TRY to differentiate
and
treat all cases of meningitis as bacterial etiology until proven otherwise

185
Q

For all cases of meningitis and encephalitis - until a definitive diagnosis is made use ??

and if clinical manifestations warrant add ??
until ??

A

combinational antibiotics efficacious for bacterial meningitis (but not necessarily exclusively for bacterial meningitis)

antifungal drugs and/or acyclovir
until diagnostic tests results and/or the patient fails to respond (fails to improve) to treatment over 1→2 days.

186
Q

mportant to initiate combinational antimicrobial therapy within ?? of ?? via what route ?? even before ??

A

30 minutes of tap
via the parenteral route

before the results of culture, Gram-stain, PCR are known because mortality due to bacterial meningitis is high (10%) and long term neurological sequelae (subtle, moderate or serve) occur in many (>50%) survivors

187
Q

For a patient with acute bacterial meningitis, antimicrobial therapy and the host immune response is thwarted by:

A

Acidic pH of CSF, this results in impaired PMN function and many antibiotics are less efficacious at acidic pH.

Elevated CSF proteins (albumin from brain) will bind to and inactivate many antibiotics

188
Q

BIG CLUE TO ETIOLOGY: Normal vs. Disease:

Selection of drugs for therapy should be based on Lab findings

A

type WBC predominating [PMNs vs. Monocytic or lymphocytic lineage]

sugar, protein levels,

Stained smear reveals agent.

Gram-stain findings on spinal fluid, urine, skin lesions.

Latex agglutination tests of CSF, urine, etc.

189
Q

Antimicrobial therapy must be ??

A

able to penetrate subarachnoid space (secreted in tears)

bactericidal: 10X the MBC

empiric, based on age (neonate, infant →middle age, elderly)

Combinational therapy: e.g., penicillin or ceftriaxone and an amino glycoside (empirical)
Switch to best drug when etiologic agent and susceptibility are determined.
MDR is documented

190
Q

S. pneumoniae tx

A

IV cefotaxime (200 mg/kg/d) and continuous infusion vancomycin (60mg/kg/d after a loading dose of 15mg/kg) with adjunctive therapy with dexamethasone (10 mg every 6 hours)

*unless the strain is proven penicillin sensitive

191
Q

For adults younger than 50 years, empiric treatment should consist of

for pts >50 yo add ?? for possible infection with L. monocytogene

A

ceftriaxone or 2 g of cefotaxime plus 1 g of vancomycin plus 10 mg of dexamethasone IV

Ampicillin 2 g IV

192
Q

?? preferred over ?? in neonates

because ??

A

Cefotaxime over ceftriaxone

ceftriaxone may alter bilirubin metabolism in this population

193
Q

Adults with gram-positive cocci on a CSF Gram stain who are receiving adjunctive corticosteroids should be treated with a ??

because ??

A

broad-spectrum cephalosporin plus rifampin (600 mg/d) instead of vancomycin

because of vancomycin’s diminished CNS penetration in the presence of corticosteroids

194
Q

If the etiologic agent is or suspected to be ?? or ?? in a person >17 y-o-age administer dexamethasone when ??

A

S. pneumo
Hib

15→ 30m before or at the same time as antibiotics are administered
NOT after

195
Q

If the agent is S. pneumoniae that is resistant to penicillins or cephalosporins, then ?? is the drug of choice

BUT it must be used in ?? and the administered doses of said drug must be sufficient to ensure that ??

A

vancomycin

combinational therapy

appropriate concentrations are achieved in the CSF in the presence of dexamethasone

196
Q

In children with pneumococcal meningitis, especially if there is a relapse, be aware of ??
what drogas ??

A

tolerance

Vancomycin, penicillin, aminoglycoside, quinolone –*antibiotics are static, not cidal

197
Q

Do not administer dexamethasone to a person who has ?? or who is ??

A

already received antimicrobial therapy

manifesting with septic shock

198
Q

Dexamethasone use in children

A

not associated with and any change in survival or time of hospital discharge

199
Q

Clostridium tetenaii tx

A

metrodianazole

200
Q

Haemophilus influenzae, type b tx

A

ceftriaxone, cefotaxime, cefuroxime or the alternative option is TMP-SMX.

201
Q

Listeria monocytogenes tx

A

ampicillin plus gentamycin or TMP-SMX

202
Q

Mycobacterium leprae tx

A

dapsone plus rifampin or clofazimine

203
Q

Neisseria meningitidis tx

A

ceftriaxone or cefotaxime

204
Q

Streptococcus pneumoniae tx

A

vancomycin + extended spectrum cephalosporin

205
Q

Streptococcus agalactiae tx

A

penicillin G

some abx resistance

206
Q

Toxoplasma gondii tx

A

sulfonamides or clindamycin + pyrimethamine

207
Q

Cryptococcus neoformans tx

A

amphotericin B with 5-fluorocytosine

208
Q

Herpes simplex virus tx

A

acyclovir

209
Q

non polio Enteroviruses tx

A

pleconaril

210
Q

Naegleria fowleri tx

A

Miltefosine

211
Q

tx for GBS

A

all identified carriers and women who deliver pre-term before screening can be done should be offered intrapartum antimicrobial prophylaxis iv

212
Q

Treatment of ?? as well as the protocol for treatment of an asymptomatically infected individual.

A

neurocysticercosis ??

213
Q

Neurocysticercosis tx

A

Niclosamide, Praziquantel, Albendazole

214
Q

obtain nasopharyngeal cultures to screen for carriers for ??

and tx with ??

A

H. influenzae, type b
N. meningitidis

meds for vacc and nonvacc:
rifampin or minocycline/doxycycline to prevent familial spread or spread in closed populations. Must use antimicrobial which will secreted in tears (i.e., present in mucosal surface).

215
Q

Meningococcemia-induced purpura fulminans aka symmetrical peripheral gangrene (SPG) tx

A

Drotecogin alfa (activated, recombinant protein C) antibiotics, fluid resuscitation, inotropic drugs, mechanical ventilation

216
Q

Cryptococcus treatment

for long-term (life-long) suppressive therapy??

A

high dose amphotericin B with 5-fluorocytosine (fluconazole [FLU]) for 2 weeks duration

Fluconazole or Itraconazole

217
Q

Leprosy treatment

treatment of the lepromatous form??
to prevent ??

A

multidrug therapy for up to 2 years and is based on the form of disease (TT, LL, or borderline) manifested.

Thalidomide for treatment of the lepromatous form, to prevent ENL

218
Q

Neurocysticercosis - Must treat both ?? and ??

A

asymptomatic and symptomatic patients

albendazole and/or praziquantel – antihelmenthic drugs

anticonvulsant

corticosteroids (dexamethasone) – to suppress the immune/inflammatory response

219
Q

Toxoplasmosis treatment

A

2→4m combination of sulfonamides or clindamycin +pyrimethamine

220
Q

Focal encephalitis is often caused by ??

treatable ??

A

HSV

IS treatable (but NOT curable) versus focal or diffuse encephalitis caused by other viral agents which are generally untreatable, except supportively

antiviral agents(s): acyclovir, vidarabine/adenosine arabinoside, idoxuridine, trifluridine, famciclovir, valacyclovir

221
Q

Before the introduction of the measles and mumps vaccine

A

viral>bacterial meningitis/ meningoencephalitis
(still most common! but now not caused by measles/mumps)

measles and mumps vaccine has made the most significant reduction in the number of cases of meningitis

222
Q

For bacterial meningitis, ??? originally accounted for majority of community-acquired cases and ??? was responsible for most of cases involving children until ???

then ??? became the nuevo numero uno until ???

and now ??? is the number one and ??? account for the majority of of community-acquired cases of bacterial meningits

A

children younger than 5 yrs
Hib
conjugated Hib vaccine

S. pneumoniae
pneumococcal vaccine

N. meningitidis
adults

*case rate hasn’t changed much over time

223
Q

Vaccines exist for CNS diseases caused by ??

A 
S. pneumoniae
H. influenzae, type b
N. meningitidis
polio
rabies
botulism
tetanus
measles
mumps
224
Q

Immunization with polysaccharide conjugate vaccines (T dependent antigen) does what ??

A

decrease carriage rate and disease incidence of disease

is recommended for children younger than 2 yrs

225
Q

S. pneumoniae T dependent antigen vaccine

A

7/13 valent conjugated vaccine (PCV-7/13)

up to 5-y-o-age

prevents:
pneumococcal OM
meningitis
bacteremia

226
Q

N. meningitidis T dependent antigen vaccine

A

Quadrivalent (groups A, C, Y, and W-135) polysaccharide diphtheria toxoid (CRM197) conjugate vaccine

Menactra (MCV4; Sanofi-Pasteur) for all persons aged 11→ 18-y-o-age and for persons aged 2→55 years at increased risk for meningococcal disease.

Menveo (Novartis Pharmaceuticals, Inc) in people 11 to 55-y-o-age

227
Q

H. flu T dependent antigen vaccine

A

(Hib) Conjugated vaccine

228
Q

N. meningitidis group B vaccines (T dependent antigen vaccine)

A

4CMenB (Bexsero; composed of 3 recombinant proteins) and Trumenba (composed of 2 recombinant proteins)

229
Q

Immunization with polysaccharide (Type II, T-independent antigen)vaccines

A

No decrease in carriage rate due to no class switching

decrease incidence of disease.

not recommended for children younger than 2 yrs

230
Q

Type II, T-independent antigen vaccines

A

S. pneumoniae 23 valent (pnu-immune pnuemovax) (NOT prevenar: 7-valent, T-dependent)

N. meningitidis: Tetravalent/quadrivalent polysaccharide vaccine for Groups A, C, Y, W-135 ([MPSV4]; Menomune®, manufactured by Sanofi Pasteur, Inc.)

H. influenzae, type b (Hib). Pure polysaccharide vaccine

231
Q

Immunoglobulin preps exist for ??

A

Rabies
Tetanus
Botulism

232
Q

post-exposure prophylaxis to prevent rabies

A

rabies vaccine
IG
wound care
tetanus immunization

233
Q

things to review ??

A

protocol for pre-exposure rabies vaccination followed by post-exposure prophylaxis with the rabies vaccine

polio vaccination protocol and why we administer e-IPOL and not the live attenuated vaccine, that is superior to e-IPOL

protocols for tetanus and botulism

234
Q

If carriage of H. influenzae, type b and/or N. meningitidis is detected by nasopharyngeal cultures do what ??

A

eliminate the immune carrier state by chemoprophylaxis of both vaccinated and non-vaccinated individuals

Treat to prevent spread via:
familial spread

spread in closed populations:
daycare settings
college campuses

235
Q

If carriage of H. influenzae, type b and/or N. meningitidis is detected by nasopharyngeal cultures: chemoprophylaxis ??

A

Ciprofloxacin, ceftriaxone, rifampin, or azithromycin

**if fluoroquinolone-resistant N. meningitidis is detected in the area do NOT administer ciprofloxacin

236
Q

polio vaccine: IPV

A

Inactivated (killed) polio vaccine (IPV)

AKA Salk vaccine, AKA IPOL

Enhanced potency vaccine (e-IPV)-used in US

237
Q

Oral polio vaccine

A

aka Sabin

A live attenuated virus which replicates in oropharynx and intestinal tract but cannot infect neuronal cells, less transimisable than wt virus

cheaper than e-IPV
may put others/unvaccinated ppl at risk

During viral replication in vaccinated children, the attenuated virus mutates back to the virulent/wt virus , but only causes extremely rare cases of vaccine-associated paralytic polio/poliomyelitis (VAPP) in the US (8→10 cases/year)
VAPP
cVDPV

238
Q

current vaccine recommendation

A

4 doses e-IPV (IPOL) ONLY to eliminate any chance of vaccine-associated paralytic polio and in doing so, assure parents and thus obtain better vaccination compliance

in the past: e-IPV for first 2 doses (2, 6 months) and OPV for last 2 doses (6 → 12 m, 12 → 16 m)

239
Q

Rabies management

A

Pre-exposure prophylaxis (vaccine) (animal-exposed pops) or postexposure treatment for rabies (vaccine + immunoglobulin)

*prevention is mainstay of controlling human rabies

240
Q

purpose of rabies pre-exposure management and prophylaxis??

A

to prime immune system for an anamnestic response when booster is administered; this anamnestic response:

  1. eliminates the need for passive immunization.
  2. reduces number of doses of rabies vaccine needed for postexposure treatment (3 doses i.m., 3 days apart).
241
Q

rabies pre and post-exposure ppx site

A

3 doses i.m. in deltoid muscle in adult or anterolateral zone of thigh in children

*NEVER done done as a gluteal injections → neuropathy, lower Ab titers

242
Q

People provided pre-exposure vaccination, were bitten by a rapid dog and then ?? died!

A

failed to receive appropriate post-exposure prophylaxis

243
Q

Must do both ?? unless pre-exposure prophylaxis is done (Rabies)

also give ??? unless pt is appropriately immunized

A

Vaccination + antirabies serum (Human antirabies immune globulin (HRIG))

tetanus ppx

244
Q

Human antirabies immune globulin (HRIG)

site ??

A

HyperRab™ S/D
Imogam® Rabies-HT

Half of the dose i.m., in gluteal region.

Half of the dose should be injected in and around the wound site

245
Q

rabies vaccine

when to admit post-ppx?

A

Human diploid cell strain rabies vaccine (HDCV)

purified chick embryo cell
vaccine (PCECV, RabAvert®)

*all are killed

on 5 days: 0, 3, 7, 14, 28→30.

246
Q

prevention of tetanus

A

Primary immunization with DTaP at 2, 4, 6 and 15 months-of-ages

Boosters (dTaP) administered at:

  • 4→ 6-y-o-age.
  • every 10 years thereafter.
247
Q

Prevention of Neonatal tetanus is accomplished by either of…

A

Vaccination of pregnant women (2 doses of tetanus toxoid [TT2+]).

clean delivery and chord care procedures.

measles
mumps (vaccination?)

248
Q

meningitis presentation

A

fever, lethargy, irritability, meningimus

249
Q

encephalitis presentation

A

fever, altered mental status (cognitive disorders, focal changes)

250
Q

meningoencephalitis presentation

A

fever, lethargy, irritability, meningimus, altered mental status

251
Q

Mass lesions presentation

A

fever, headache, seizures

252
Q

Transverse myelitis presentation

A

fever, motor and sensory loss at the same level

253
Q

Poliomyelitis presentation

A

fever, asymmetric motor deficit and no sensory loss

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