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Unit 3 > Microbio > Flashcards

Microbio Flashcards

1
Q

Classic symptoms of meningitis

A

headache

fever

stiffneck

photophobia

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2
Q

Neisseria meningitidis

A
  • Gram (-) diplococci
  • facultative intracellular
  • encapsulated (nonencapsulated strain are nonpathogenic)
    • antibodies raised against the capsule are protective
  • Oxidase (+), catalase (+)
  • Ferments glucose and maltose, not sucrose or lactose
  • Growth inhibited by trace metals and fatty acids:
    • can grow on chocolate agar not blood agar
  • associated with a petechial rash
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3
Q

Neisseria meningitidis - what is the biggest contributing virulence factor to its pathogenesis? and why?

A

Encapsulated – polysaccaride capsule allows the bacteria to escape phagocytosis and to circulate in bloodstream and reach the meninges

Strains that are not encapsulated, are NOT pathogenic

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4
Q

Gram stain - Neisseria meningitidis

A

Gram (-) diplococci

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5
Q

Neisseria meningitidis - what sugars can it ferment?

A

Glucose and maltose

Cannot ferment sucrose or lactose

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6
Q

Neisseria meningitidis – growth characteristics (laboratory)

A

Inhibited by trace metals and fatty acids –> can’t grow on blood agar

Culture needs to be done on chocolate agar or Thayer-martin

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7
Q

Neisseria meningitidis - how is it transmitted?

A

Airborne droplets

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8
Q

Neisseria meningitidis - reservoir (where does it colonize?)

A

Nasopharynx

asymptomatic carrier is common in prisons, dorms, military, and family of index case

Problem is when there is the blip in the mucosa that allows the bug to enter the blood stream.

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9
Q

Neisseria meningitidis - pathogenesis

A
  1. Colonization of nasopharynx (only reservoir) –> asymptomatic carrier
  2. Transmission via airborne droplets
  3. Infection often resolves w/o symptoms
    • IgG-enhanced complement and neutrophils defend and leave a lifelong immunity to infecting strains
  4. Danger comes when there is a blip in the mucosa and allows the bug to have access to the blood stream in which it can travel to the meninges
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10
Q

Neisseria meningitidis - who are most susceptible to this and why?

A
  1. young teenagers (before full nasopharynx maturity) – most common cause in 2-18yr old range
    • Most people develop natural immunity by age 20
  2. non immunized/exposed mothers
    • Immune mothers passively immunize newborns
  3. Immunocompromised
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11
Q

Meningococcemia

A

condition when Neisseria meningitidis enters the bloodstream

Fever and hourly-spreading petechial skin rash

Rarely, but may be present for weeks before symptoms become alarming

Complications:

  • Waterhouse–Friderichsen syndrome
  • high fever
  • shock
  • DIC
  • thrombocytopenia
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12
Q

Meningococcemia - favorite colonization sites (where are the symptoms located?)

A

Joints – septic arthritis

meninges – meningitis

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13
Q

Neisseria meningitidis - virulence factors

A
  1. IgA protease - cleaves IgA and reduces defense of mucus membrane
  2. Polysaccharid capsule – resists phagocytosis
  3. endotoxin LOS – causes fever, shock (less immunogenic than LPS)
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14
Q

How to culture Neisseria meningitidis (lab)?

A

Thayer-Martin medium (requires the presence of antibiotics)

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15
Q

Neisseria meningitidis - how is it normally cleared from the system?

A

Complement mediated cascade specifically through the recruitment of the C5-C9 complexes that can punch a hole to through the cell wall.

Ab to capsule is protective –> vaccine

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16
Q

Meningococcemia - complications

A
  • Waterhouse–Friderichsen syndrome (hemorrhagic adrenalitis)
  • high fever
  • shock
  • DIC
  • thrombocytopenia
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17
Q

Waterhouse–Friderichsen syndrome

A

aka Waterhouse–Friderichsen syndrome

defined as adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection: Typically the pathogen is Neisseria meningitidis.

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18
Q

How can you distinguish between N. meningitidis and N. gonnorrhoeae?

A

Only N. meningitidis can ferment maltose.

Only N. meningitidis is encapsulated.

Also IF staining.

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19
Q

Neisseria meningitidis - treatment

A

Penicillin G unless allergic or local history of drug resistance

Alternates: Ceftriaxone, cefotaxime, cefuroxime; CAM if severely allergic to penicillin

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20
Q

Neisseria meningitidis - prevention

A

Close contacts of index cases –> get prophylactic rifampin, ceftriaxone or ciprofloxacin

Vacinnations recommended for travelers

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21
Q

Group B Strep

A

S. agalactiae

Normal GI and vaginal flora – transmits to neonate shortly before and/or during delivery

Gram (+) cocci

ß-hemolytic

Virulence factors

  • Encapsulated
  • polysaccharide toxin
  • pilus-like attachment

serotype-specific antibody mediated immunity

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22
Q

Streptococcus agalactiae

A

Group B strep

Normal GI and vaginal flora – transmits to neonate shortly before and/or during delivery

Gram (+) cocci

ß-hemolytic

Virulence factors

  • Encapsulated
  • polysaccharide toxin
  • pilus-like attachment

serotype-specific antibody mediated immunity

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23
Q

Group B strep - virulence factors

A
  • Encapsulated
  • polysaccharide toxin
  • pilus-like attachment
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24
Q

Group B strep - Gram stain?

A

S. galactiae

Gram (+) cocci

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25
Q

Group B strep - major risk groups

A

Neonates (normal vaginal flora makes it easy to transfer during delivery)

Geriatric population w/ predispositions (major health conditions such as diabetes, malignancy and CHF)

Either way, GBS is an opportunistic pathogen

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26
Q

Group B strep - Examination

A

Pain, fever and other symptoms specific to site

Meningitis (spinal tap positive for Gram + cocci in pairs or short chains)

Cellulitis, abscess

possible endocarditis (echo to confirm)

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27
Q

Group B strep - laboratory

A
  1. CAMP test
    • CAMP factor is secreted by Group B strep (and Listeria)
    • CAMP enhances the activity of ß-hemolysin which is secreted from S. aureus.
    • If streaked on a blood agar plate with both bacteria, there should be enhanced hemolysis in areas of overlap (darker)
  2. Hippurase/Hippurate Test
    • Hippurase is produced by GBS, Gardnerella vaginalis, Campylobacter jejuni, Listeria monocytogenes
    • Less specific
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28
Q

CAMP test - what is it? and what is it testing for?

A

CAMP is a chemical produced by Group B strep (and Listeria). It interacts with ß-hemolysin to enhance its activity (ß-hemolysin is a chemical produced by S aureus).

The test is used to identify Group B strep (or Listeria)

If you streak on a blood agar, Group B strep with S. aureus, the areas where there is overlap will result in enhanced hemolysis (darker color)

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29
Q

Hippurase/Hippurate Test - what is it and what is it testing for?

A

Hippurase is produced by GBS, Gardnerella vaginalis, Campylobacter jejuni, Listeria monocytogenes

Less specific than CAMP test, but still can be used to identify the above organisms.

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30
Q

Group B step - treatment

A

Penicillin or amoxicillin

if allergic – vancomycin

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31
Q

Pneumococcus

A

Strep pneumoniae

  • Gram(+)
  • Catalase(-)
  • alpha-hemolytic
  • facultative anaerobe
  • In culture - forms diplococci in chains
  • Pathogenic strains are encapsulated

This is the most common cause of community-acquired pneumonia, bacterial meningitis, bacteremia and otitis media.

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32
Q

Strep pneumoniae

A

Gram(+)

Catalase(-)

alpha-hemolytic

facultative anaerobe

In culture - forms diplococci in chains

Pathogenic strains are encapsulated

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33
Q

Pneumococcus - pathogenesis

A

Easily colonizes upper respiratory tract using adhesion virulence factors

Infections peak in Fall and Winter when carriers congregate more closely

Normally contained by innate immunity in healthy adults and children.

Infection raises a strong inflammatory response, which underlies most of the clinical disease symptoms

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34
Q

Pneumococcus - virulence factors

A

Major factor: capsule

Also has IgA protease, teichoic acid (play a roll in cell shape)

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35
Q

Pneumococcus - types of disease spread (2)

A

Direct extension: sinuses, bronchi, eustachian tubes

Hematogenous spread: blood, joint fluid, peritoneum, CSF

Capsule protects bacterium against phagocytosis and classic complement unless anti-capsule IgG is already present (protective)

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36
Q

Pneumococcus - vaccine (what is the mechanism? how does it create protection?

A

It creates IgG targeted toward the capsule of S. pneumoniae which is protective

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37
Q

Pneumococcus - clinical findings (of noninvasive disease)

A

Sinusitis, otitis media, bronchitis, pneumonia

  • pneumonia causes significant morbidity and mortality (10-20%)
  • lobar consolidation

Patient looks ill & anxious

38
Q

Pneumococcus - clinical findings (invasive disease)

A

Meningitis, septic arthritis, pericarditis, endocarditis, osteomyelitis

Meningitis develops over hours or days, neurologic signs often prominent

  • mental status changes
    • lethargy
    • delirium
    • Brudzinski +
    • Cranial nerve palsies
    • focal neurologic deficits

Biomodal distribution: patients either younger than 5 (immune system not fully developed) or older than 65 (those starting to lose their immune system to immuno-senescence)

39
Q

Pneumococcus - laboratory

A

Noninvasive disease - can be treated based on exam, optional Gram stain (spread is contained and often will clear on its own)

Invasive Disease:

  • gram stain and culture appropriate samples
  • antibiotic sensitivity testing
  • urine antigen testing available for those (children) who don’t produce enough sputum
  • spinal tap
40
Q

bacterial meningitis spinal tap findings

A
  1. elevated opening pressure
  2. elevated WBC count and neutrophil level
  3. elevated protein
  4. decreased glucose (bacteria actively eating it)
  5. highly elevated lactic acid (bacteria actively fermenting it)
  6. Gram stain and culture positive unless antibiotic treatment began >4hrs prior to tap
41
Q

Pneumococcus - treatment (noninvasive disease)

A

amoxicillin or cephalosporin.

doxycycline for adults only

vancomycin also another option

42
Q

Pneumococcus - treatment (invasive disease)

A

vancomycin + Ceftriaxome/cefotaxime

start treatment immediately as they can spread throughout the brain (not limited to just meninges)

43
Q

Pneumococcal antibiotic resistance - what are the majority of mutations and what is affected?

A

Mutations that change the bacterial cell wall sites to which the antibiotics bind –> lowers binding affinity (but binding is NOT blocked)

An increase in dose can sometimes overcome resistance to this pathogen

MIC = minimum inhibitory concentration - describes this effect in terms of the dosage necessary to kill the patient’s isolated bacteria.

44
Q

MIC (minimum inhibitory concentration)

A

Describes this effect in antibiotic resistance in pneumococcus in terms of the dosage necessary to kill the patient’s isolated bacteria.

45
Q

Which septic meningitis(es) may steroids be used? and why?

A

Pneumococcal – used to help reduce the inflammatory response. Needs to be withdrawn before the end of antibiotics in order to ensure the full clearance of the bug.

Can’t use it in other cases such as Neisseria meningitidis because it depletes/decreases the complement response too much such that your body can’t clear it anymore.

46
Q

Pneumococcus - prevention

A

Prevnar 7 (7 most common serotypes) until 2000

Added another 6 serotypes == Prevnar13 vaccination (original 7 + new 6 serotypes)

47
Q

Replacement disease

A

The idea that vaccination against the most common serotypes will make more prominent other diseases that were either very minimal or hidden behind the larger cases.

Ie, Prevnar7 hit the most common serotypes of pneumococcus but then additional strains came to prominence because the most common ones were dying out.

48
Q

Routes of viral entry into CNS

A
  1. Hematogenous
  2. olfactory (very short distance between your nose and brain)
  3. neuronal (traveling through neurons)
49
Q

Meningitis

A

inflammation of the lining of the brain (meninges)

Aseptic meningitis is NOT caused by bacteria

50
Q

Meningoencephalitis (meaning)

A

Widespread infection of the meninges and brain

51
Q

Aseptic (sterile) meningitis

A

Causes: viruses, fungi, TB, infections near the CNS

Symptoms

  • mental status remains normal (lining is infected, not the brain – distinguishes from encephalitis)
  • headache, fever, and chills, stiff neck, malaise, sore throat, N&V, abdominal pain, rash, muscle pain, confusion, photophobia
    • fever = from generalized infection
    • a lot of the other symptoms from generation of interferons
52
Q

Aseptic meningitis - main symptoms

A

Fever (from generalized infection)

Headache

Stiff neck

53
Q

Most common viruses that cause aseptic meningitis (3)

A

Enterovirus ~80%

HSV ~9%

Arbovirus ~10%

Other ~1% (Rabies, etc…)

54
Q

Brudzinski’s Sign

A

aka Brudzinski’s neck sign

The neck is so stiff that the knees flex (guarding) when the neck is flexed

Indicative for meningitis

55
Q

Encephalitis (meaning)

A

Inflammation of the brain tissues

Causes:

  • exposure to many types of viruses –> influx of immune cells in brain
  • cerebral edema destorys neurons (from inflammation)
  • Intracerebral hemorrhage – distinguishing feature from meningitis

Symptoms

  • mental status is altered (Due to increased intracranial pressure) – distinguishing feature from meningitis
  • Fever, headache, vomiting, photophobia, stiff neck and back, confusion, sleepiness, irritability, stumbling
56
Q

How to distinguish encephalitis from meningitis?

A

Encephalitis:

  • Intracerebral hemorrhage – distinguishing feature from meningitis
  • mental status is altered – distinguishing feature from meningitis

Meningitis

  • mental status normal

Common findings:

  • headache, stiff neck, fever
57
Q

Pathogenesis of viral CNS disease

A

Death of neurons - cytolytic viruses can directly kill tissues

Host factors

  • age - infants and elderly most susceptible
  • immune status
  • genetics (innate differences in resistance to infections)
  • activity (exercise may increase dissemination into CNS)
58
Q

Acute disseminated encephalomyelitis (ADEM)

A

–Postinfectious encephalitis follows viral infection by 1-2 weeks

–Associated with measles, mumps, VZV, influenza, parainfluenza viruses

–Autoimmune disorder

59
Q

Herpesviruses - mechanism of infection

A
60
Q

Which lobe is primarily infected in herpessimplex encephalitis?

A

Unilateral temporal lobe (associated with hearing, vision, language recognition and new memories)

61
Q

Herpesviruses

A
  • HSV-2 >> HSV-1 primary infections often cause meningitis
  • Recurrent HSV-1 infections can also cause encephalitis
  • Other herpesviruses: VZV, CMV, EBV meningitis occur more often in immunocompromised patients

Tends to have an affinity to affect temporal lobes.

Also has an affinity to cause hemorrhage

62
Q

Meningitis associated with HSVs - complications

A

Tend to be associated with temporal lobe

Tend to cause hemorrhage

63
Q

Herpesviruses - main viruses that cause encephalitis/meningitis

A

HSV-1, HSV-2, VZV

64
Q

Herpesviruses - treatment

A

Acyclovir

65
Q

HSV-1 - reactivation “in situ”

A

reactivation of HSV-1 without the recurring sore. the reactivation when directly to the brain

66
Q

HSV-1 encephalitis

A

Most common cause of sporadic viral encephalitis (10-20% of all cases)

Routes of infection

  • Primary HSV-1 in oropharynx –> trigeminal nerve –> CNS
  • Recurrent HSV-1 –> trigeminal nerve –> CNS
  • Reactivation “in situ” HSV-1 –> CNS

Signs and symptoms: altered mental states, focal cranial nerve deficits, hemiparesis, slurred speech, stumbling, seizures, fever

Diagnosis:

  • Gold standard = PCR of CSF for HSV or other viruses
  • Brain imaging: MRI shows predominantly unlateral temporal lobe abnormalities
67
Q

Routes of infection of HSV1

A
  1. Primary HSV-1 in oropharynx –> trigeminal nerve –> CNS
  2. Recurrent HSV-1 –> trigeminal nerve –> CNS
  3. Reactivation “in situ” HSV-1 –> CNS
68
Q

HSV1 signs and symptoms

A
  1. altered mental states
  2. focal cranial nerve deficits
  3. hemiparesis
  4. slurred speech
  5. stumbling
  6. seizures
  7. fever
69
Q

HSV-1 encephalitis - diagnosis

A

Gold standard = PCR of CSF for HSV or other viruses

Brain imaging: MRI shows predominantly unlateral temporal lobe abnormalities

70
Q

Neutropic viruses (loves neurons)

A

HSV-1, HSV-2, VZV, Rabies

71
Q

Rabies virus - disease mechanism

A
  1. Transmitted by saliva through bite or by aerosols (in caves populated by infected bats)
  2. Replicates in muscle at bite site
  3. Incubation period of weeks to months, depending on inoculum and distance of bite from CNS
  4. Infects peripheral nerves and travels to brain
  5. replication in brain causes hydrophobia, seizures, hallucinations, paralysis, coma and death

Postexposure immunization can prevent disease due to long incubation period

72
Q

Rabies - how and why is it preventable?

A

Disease takes a while to progress from site of infection into the CNS. Once it reaches spinal cord, it progresses very quickly, but until then, it has a long incubation period. Anytime during the incubation period, you can vaccinate/immunize against the virus and protect yourself from those symptoms

73
Q

Picornaviruses

A
  1. Poliovirus (nearly irradicated)
  2. Coxsackie
  3. Echovirus
  4. Enterovirus
  5. Parechoviruses
  6. Rhinoviruses (has no CNS symptoms)

At risk:

  • young children
  • older adults
74
Q

Enteroviruses

A

Transmission: fecal-oral (primary transmission route is via water)

Disease more common in summer (warm season = more exposure to water)

No real treatment other than supportive care

75
Q

Picornavirus dissemination

A
76
Q

Arboviruses

A

Mosquito/tick born viruses (Arthropod Born viruses)

Family: Togaviridae

Subfamilies: alphavirus, flavivirus

77
Q

Togavirus dissemination

A

Different viruses have different affinities for organs. Once a sufficient quantity has accumulated in any organ, it will begin dissemination into the CNS

78
Q

Togaviruses: alphaviruses

A

alphavirus is a subdivision of togaviruses (all under the classification of arbovirus)

Includes:

  • VEE
  • EEE
  • WEE
  • Chikungunya virus
  • Rubella
79
Q

Togaviruses: flaviviruses

A

flaviviruses is a subdivision of togaviruses (all under the classification of arbovirus)

Includes:

  • JE (Japanese encephalitis)
  • WNV (west nile virus)
  • SLE (St. Louis encephalitis)

More common in summer

80
Q

West Nile Virus incidence

A

Neuroinvasive cases as of 2015

81
Q

WNV meningoencephalitis

A

Occurs in 1% of WNV infections

Higher risk populations: cancer, diabetes, hypertension and kidney disease

Prognosis:

  • recovery over weeks or months
  • some of the neurologic effects may be permanent

Mortality ~10%

82
Q

Fungal meningitis - what types of patients are these infections seen most commonly seen in?

A

immune-compromised patients (such as HIV/AIDS), but may affect anyone

83
Q

CSF cell changes in meningitis

A

bacterial infection –> increase in neutrophils

viral infection –> increase in lymphocytes

parasitic infection –> increase in eosinophils

84
Q

CSF - how to distinguish between viral and bacterial meningitis?

A

Bacterial

  • increase in neutrophils (innate immunity to bacteria)
  • increase in lactic acid (fermentation)
  • decrease in glucose (metabolism)
  • C-reactive protein (CRP) – acute phase reactant that is markedly increased w/o bacterial meningitis
  • procalcitonin levels in blood

Viral

  • No change in neutrophils
  • increase in lymphocytes
85
Q

Progressive Multifocal Leukoencephalopathy (PML

A

Viral encephalitis caused by JC polyomavirus (mimics symptoms of MS based on its pathophys.)

Virus preferentially infects oligodendrocytes –> demyelination (is its principal effect)

Disease occurs in immunosuppressed people

86
Q

Fungal meningoencephalitis

A

3 patterns

  1. Chronic meningitis
  2. vasculitis
  3. parenchymal invasion

Mucor and Aspergillus associated with vasculitis

Candida and Cryptococcus associated with brain invasion

Mucor associated with diabetics

87
Q

Fungal meningoencephalitis - what fungi are associated with vasculitis (being able to penetrate the vessels)?

A

Mucor and Aspergillus

88
Q

What fungi are associated with brain invasion?

A

Candida and Cryptococcus

89
Q

Kernig Sign

A

One of the physically demonstrable symptoms of meningitis is Kernig’s sign. Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees

90
Q

Where does herpesvirus like to reside?

A

Ganglion of trigeminal nerve

Unit 3 (5 decks)

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