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Micro Exam 3 > Neely: CNS Infections- Bacterial, Fungal and Parasitic > Flashcards

Neely: CNS Infections- Bacterial, Fungal and Parasitic Flashcards

1
Q

CNS Architecture

CNS:
Should be _______
Protection:

A

CNS: brain and spinal cord

Should be sterile: no normal flora

Protection: skull and vertebral column (protect from mechanical pressure and act as barriers to infection)

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2
Q

CNS Architecture
Main routes of infection:
most common route of infection:

A

Main routes of infection: blood vessels and nerves that traverse the walls of the skull and vertebral column
o Blood Borne Invasion: most common route of infection

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3
Q

Types of Infections
Meningitis:
Encephalitis:

A

• Types of Infections: all lead to inflammation

  • Meningitis: inflammation of the meninges
  • Encephalitis: inflammation of the brain tissue
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4
Q

Types of Infections
Abscesses:
Meningoencephalitis:
Encephalomyelitis:

A

Abscesses: suppurative infection of the brain tissue

Meningoencephalitis: inflammation of the brain and meninges

Encephalomyelitis: inflammation of the spinal cord

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5
Q

Blood borne invasion occurs across the _____ (encephalitis and abscesses) or the ______

A

Blood borne invasion occurs across the BBB (encephalitis and abscesses) or the BCB

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6
Q

BBB:
BCB:

A

Blood Brain Barrier (BBB): tightly joined endothelial cells surrounded by glial processes

Blood-CSF Barrier (BCB): endothelium with fenestrations and tightly joined choroid plexus epithelial cells

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7
Q

Invasion of the CNS

Function:

A

Function: inhibit passage of microbes, antibodies and some antimicrobial drugs

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8
Q

Invasion of the CNS

Mechanism:

A

Mechanism: tight junctions (zonula occludens) between endothelial (BBB) and epithelial cells (BCB)

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9
Q

Invasion of the CNS

Microbes may traverse these barriers: (3)

A

o Infect cells that compromise the barrier
o Passive transport across in intracellular vacuoles
o Carried across by white blood cells (ie. macrophages)

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10
Q

Mechanisms of Bacterial Infection of the CNS

Mucosal Colonization:

A

Mucosal Colonization: many CNS infection causing bacteria are members of normal mucosal flora; infection usually requires immunocompromised or overgrowth of microbe

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11
Q

Mechanisms of Bacterial Infection of the CNS

Invasion of the bloodstream:

A

Invasion of the bloodstream: with survival and multiplication, leading to high levels of bacteremia

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12
Q

Mechanisms of Bacterial Infection of the CNS

Survival and multiplication:

A

Survival and multiplication: must occur in the meninges and/or brain parenchyma

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13
Q

Mechanisms of Bacterial Infection of the CNS

Bacterial products are proinflammatory (LPS, TA, PG):

A

Bacterial products are proinflammatory (LPS, TA, PG): cause edema and increased pressure via recruitment of WBC and release of pro-inflammatory cytokines

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14
Q

Mechanisms of Bacterial Infection of the CNS

Cytokine action:

A

Cytokine action: recruit more WBCs and promote edema (increasing intracranial pressure), which leads to increased permeability of the BBB

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15
Q

Mechanisms of Bacterial Infection of the CNS

Increased permeability leads to diapedesis:

A

Increased permeability leads to diapedesis: infiltration of neutrophils and lymphocytes into the CNS

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16
Q

Mechanisms of Bacterial Infection of the CNS

Neuronal injury and edema:

A

Neuronal injury and edema: due to production of more cytokines by WBC (can lead to neuronal death)

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17
Q

Acquisition of Bacterial CNS Pathogens

Many bacterial are normal mucosal flora:

A

Many bacterial are normal mucosal flora: as mentioned above, CNS infection with these microbes usually requires immunocompromise or overgrowth

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18
Q

Carriage Rates

Streptococcus pneumoniae:

A

o Significant carriage in pharynx and mouth

o Small amount of carriage in nose and UG tract

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19
Q

Carriage Rates

Neisseria meningitidis

A

o Heavy carriage in pharynx

o Significant carriage in nose, mouth and UG tract

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20
Q

Carriage Rates

Haemophilus influenza:

A

o Significant carriage in nose, pharynx and mouth

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21
Q

Carriage Rates

Group B Streptococcus:

A

o Heavy carriage in GI tract

o Significant carriage in UG tract

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22
Q

Carriage Rates

E.coli K1:

A

o Heavy carriage in GI tract
o Significant carriage in mouth and UG tract
o Small amount of carriage in nose and pharynx

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23
Q

Quantification of CSF Inflamation

Response to Viruses/Fungal Infections: (3)

A

o Increase in lymphocytes (mostly T cells)
o Increase in monocytes
o Slight increase in protein

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24
Q

Quantification of CSF Inflamation

Response to Bacteria: rapid and dramatic (3)

A

o Increase in PMNs
o Increase in proteins (CSF visibly turbid; due to cytokine release and release of protein by bacteria)
o Decrease in glucose (because bacteria are using it as food source)

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25
Q

Normal

Indicator
WBCs (per uL)
%PMNs
RBCs (per uL)
Glucose (mg/dL)
Protein (mg/dL)
A 
0-5
0
0-2
45-85
15-45
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26
Q

Acute Bacterial

Indicator
WBCs (per uL)
%PMNs
RBCs (per uL)
Glucose (mg/dL)
Protein (mg/dL)
A

> 1,000 (PMNs)
50
0-10
100

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27
Q

Fungal or Viral

Indicator
WBCs (per uL)
%PMNs
RBCs (per uL)
Glucose (mg/dL)
Protein (mg/dL)
A 
100-500 (lymphocytes)
<10
0-2
≤40
50-100
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28
Q

Acute Bacterial Meningitis

Basics:

A

Basics: may be caused by viral or bacterial infection, or by disease that can cause inflammation of tissues without infection (viral are most common cause)

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29
Q

Acute Bacterial Meningitis
Symptoms

Common:

A

Common: high fever, severe/persistent headache, stiff neck, N/V

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30
Q

Acute Bacterial Meningitis
Symptoms

Important (may require emergency treatment:
Infants:

A

Important (may require emergency treatment: changes in behavior (confusion), sleepiness, and difficulty waking up

Infants: irritability, tiredness, poor feeding, fever (hard to diagnose)

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31
Q

Acute Bacterial Meningitis
Onset

Acute:

A

Acute: onset of symptoms within hours or days (bacterial or viral infection)

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32
Q

Acute Bacterial Meningitis
Onset

Chronic:

A

Chronic: symptoms fluctuate over the course of weeks, months or years (viruses)

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33
Q

Primary cause of bacterial meningitis in the US:

A

Streptococcus pneumoniae (pneumococcus):

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34
Q 
Streptococcus pneumoniae (pneumococcus)
Virulence Factors: (6)
A

Adhesins

IgA protease

Pneumolysin

Autolysin

Capsule: over 90 serotypes

Outer wall components (PG, TA)

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35
Q

Streptococcus pneumoniae (pneumococcus)
Virulence Factors
Adhesins:

A

Adhesins: PspA and CpbA (bind carbohydrate on cell surfaces)

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36
Q

Streptococcus pneumoniae (pneumococcus)
Virulence Factors
Pneumolysin:

A

Pneumolysin: cytotoxin released when the bacteria lyses (also inhibits Ab binding to bacteria)

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37
Q 
Streptococcus pneumoniae (pneumococcus)
Virulence Factors

Autolysin:
Bacteria able to detect:
_____ to increase survival of cells that don’t lyse

A

Autolysin: release causes bacteria to release intracellular contents (including pneumolysin)
• Bacteria able to detect number of bacteria present and turn on these genes if necessary
• Lyse (die) to increase survival of cells that don’t lyse

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38
Q 
Streptococcus pneumoniae (pneumococcus)
Virulence Factors
# of capsule serotypes:
A

Capsule: over 90 serotypes

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39
Q 
Streptococcus pneumoniae (pneumococcus)
Virulence Factors

Outer wall components (PG, TA):

A

Outer wall components (PG, TA): pro-inflammatory (results in tissue damage)

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40
Q 
Streptococcus pneumoniae (pneumococcus)
Etiology/Pathogenesis

Acquisition:
Distribution:

A

Acquisition: aerosols or direct contact with oral secretions (carried asymptomatically in nasopharynx; carriage rate DECREASES with age)

Distribution: ubiquitous

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41
Q 
Streptococcus pneumoniae (pneumococcus)
Etiology/Pathogenesis

Risk Factors: (3)

A
  • Immunosuppression
  • Distant foci of infection
  • Low levels of circulating Abs to capsular polysaccharide
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42
Q 
Streptococcus pneumoniae (pneumococcus)
Structure:
A

Structure: Gram (+) diplococci (lancet shaped)

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43
Q 
Streptococcus pneumoniae (pneumococcus)
Biochemical Tests

Catalase:
Hemolysis:
Optochin:

A
  • Catalase (-)
  • Alpha hemolytic
  • Optochin sensitive (distinguish from other alpha hemolytic strep)
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44
Q 
Streptococcus pneumoniae (pneumococcus)
Biochemical Tests

What distinguishes it from GDS?
Quelling Reaction:
Swelling of the capsule caused by:

A

• Bile sensitive (distinguish from GDS)
• Quelling Reaction (+)
- Swelling of the capsule caused by contact with serum containing serotype-specific Abs

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45
Q

Streptococcus pneumoniae (pneumococcus)
Vaccines
23 Valent:

A

23 Valent: capsular polysaccharides to 23 serotypes that are responsible for ~90% of infections
• 60-70% efficacy
• Not effective in kids under 2

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46
Q 
Streptococcus pneumoniae (pneumococcus)
Vaccines
7 valent (PCV7):
A

o 7 valent (PCV7): 7 capsular polysaccharides that cause disease most commonly in children, immunocompromised and elderly patients
• 100% effective for serotypes it protects against
• Conjugated to diphtheria proteins

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47
Q 
Neisseria menigitidis (meningococcus)
Basics:
A

Basics: second leading cause of acute bacterial meningitis; human specific

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48
Q 
Neisseria menigitidis (meningococcus)
Virulence Factors: (4)
A

o IgA protease
o Pili (Pil proteins): adherence to epithelium
o LOS: similar to LPS (toxic/pro-inflammatory)
o Capsule

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49
Q 
Neisseria menigitidis (meningococcus)
Capsule: several serogroups:
A 
Capsule: several serogroups
•	A: 5%
•	B: 50%
•	C: 20%
•	Y: 10%
•	W135: 10%
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50
Q 
Neisseria menigitidis (meningococcus)
Acquisition:
A

Acquisition: aerosols or direct contact with oral secretions (carried asymptomatically in nasopharynx; carriage rate INCREASES with age)
• Invasion of blood and CNS is rare and poorly understood

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51
Q 
Neisseria menigitidis (meningococcus)
Distribution:
A

Distribution: ubiquitous (causes sporadic outbreaks and epidemics)

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52
Q 
Neisseria menigitidis (meningococcus)
Risk Factors:
A

Risk Factors: close contact with infected people or areas of outbreak

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53
Q

Neisseria menigitidis (meningococcus)

Symptoms:
What reflects associated septicemia?
May lead to:
In ~1/3 of patients:

A

Symptoms: same as previously mentioned, PLUS
• Hemorrhagic rash with petechiae (reflects associated septicemia)
• May lead to eccymosis and necrosis of fingertips and toes that could require amputation
• In ~1/3 of patients the rash is fulminating with complications due to DIC, endotoxemia, shock and renal failure

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54
Q 
Neisseria menigitidis (meningococcus)
Vaccines

protect against:
Do NOT protect against:

A

Basics: protect against groups A, C, Y and W135

Do NOT protect against B (which causes the majority of disease) because of sialic acid that can lead to autoimmunity

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55
Q 
Neisseria menigitidis (meningococcus)
Vaccines

55:
11-55:

A

o Meningococcal polysaccharide vaccine (MPSV4): 55

o Meningococcal conjugate vaccine (MCV4): 11-55

56
Q

Neisseria menigitidis (meningococcus)
Shape:
Fastidious:

A

o Shape: Gram (-) cocci (generally diplococci)

o Fastidious: requires CAP to grow (needs heme from lysed RBCs)

57
Q

Neisseria menigitidis (meningococcus)

Biochemical Tests:

A

• Oxidase (+)
• Ferments glucose and maltose
.

58
Q

Haemophilus influenza type B (Hib)

Basics:

A

Basics: used to be the leading cause of meningitis in ages 5 mo-5 years, but now rare where Hib vaccine used

59
Q

Haemophilus influenza type B (Hib)

Virulence Factors: (3)

A

o IgA protease
o LPS
o Capsule: 6 serotypes (A-F; B responsible for most cases of meningitis)

60
Q

Haemophilus influenza type B (Hib)

Acquisition:
Distribution:
Risk Factors:

A

o Acquisition: aerosols or direct contact with oral secretions (carried asymptomatically in nasopharynx)
o Distribution: ubiquitous
o Risk Factors: close contact with infected people or areas of outbreak

61
Q

Haemophilus influenza type B (Hib)

Shape:
Aerobe vs anaerobe:
Capsule:

A

o Shape: Gram (-) pleiomorphic coccobacilli
o Facultative anaerobe
o Capsule: can be encapsulated (typeable) and non-encapsulated (nontypeable)

62
Q

Haemophilus influenza type B (Hib)

Fastidious growth and nutrient requirements:
Factor V:
Factor X:

A

o Fastidious growth: requires CAP
• Factor V: NAD
• Factor X: hemin

63
Q

Haemophilus influenza type B (Hib)

Vaccine:

A

Protective Ab would develop naturally by age 5, but also develops following vaccination

64
Q

College Outbreaks

Cause:
Risk Factors:

A

Cause: meningococcus and pneumococcus

Risk Factors: lifestyle changes (poor eating habits, alcohol use, smoking, pulmonary infections) result in change in immune function and microbiota composition

65
Q

N. meningitidis

Host:
Clinical Features:
Mortality (% of treated cases):
Sequelae (% of treated cases):

A

Children and adolescents
Acute onset (6-24 hours) skin rash
7-10
<1

66
Q

H.influenzae

Host:
Clinical Features:
Mortality (% of treated cases):
Sequelae (% of treated cases):

A

Children <5
Onset less acute (1-2 days)
5
9

67
Q

S.pneumoniae

Host:
Clinical Features:
Mortality (% of treated cases):
Sequelae (% of treated cases):

A

All ages Esp. <2 and elderly

Acute onset; May follow pneumonia or septicemia in elderly

20-30

15-20

68
Q

N.meningitidis

Capsule
IgA Protease
Pili
Endotoxin
OMPs
A 
\+
\+
\+
\+
?
69
Q

H.influenzae

Capsule
IgA Protease
Pili
Endotoxin
OMPs
A 
\+
\+
\+
\+
\+
70
Q

S.pneumoniae

Capsule
IgA Protease
Pili
Endotoxin
OMPs
A 
\+
\+
-
-
-
71
Q

Neonatal Infections

Fatal in _____ of cases
Often lead to:
Clinical diagnosis in infant:

A
  • Fatal in 1/3 of cases
  • Often lead to permanent sequelae (cerebral palsy, epilepsy, mental retardation, hydrocephalus)
  • Clinical diagnosis in infant is difficult (non-specific signs such as fever, poor feeding, V/D, respiratory distress)
72
Q

Neonatal Infections

Causative agents: (4)

A
  • Listeria monocytogenes: G(+) rod
  • E.coli K1: G(-) rod
  • Group B Streptococcus: G(+) cocci in chains
  • Toxoplasma gondii: parasite
73
Q

Mycobacterium tuberculosis

Prevalence:
Pathogenesis is a 2 step process:

A

Basics: relatively rare

Pathogenesis:
Enter host by droplet inhalation
Dissemination to LNs as lung infection progresses

74
Q

Mycobacterium tuberculosis

Enter host by droplet inhalation:

A

Enter host by droplet inhalation: infect lung macrophages, forming a granuloma (primary lesion)

75
Q

Mycobacterium tuberculosis

Dissemination to LNs as lung infection progresses:

A

Dissemination to LNs as lung infection progresses: results in a short, but significant bacteremia, which can lead to dissemination to CNS
• Tubercle forms at meninges (initial CNS lesion)
• Caseating exudate → meningitis → blockage of CSF fluid → nerve/blood vessel damage

76
Q

Mycobacterium tuberculosis

Acquisition:
Distribution:

A

Acquisition: aerosol spread or reactivation of latent disease

Distribution: highest in urban and endemic areas

77
Q 
Mycobacterium tuberculosis
Risk Factors (3)
A
  • Previous TB infection
  • Immunosuppression
  • Travel to endemic areas
78
Q

Encephalitis

Most often caused by:
Can also occur as result of:

A

Most often caused by viral infection of the brain

Can also occur as result of fungal infection of the brain OR dissemination of a systemic bacterial infection

79
Q

Encephalitis
Symptoms
Common:

A

Common: sudden fever, headache, vomiting, abnormal visual sensitivity to light, stiff neck and back, confusion, drowsiness, clumsiness, unsteady gait, irritability

80
Q

Encephalitis
Symptoms
Require Emergency Treatment:

A

Require Emergency Treatment: LOC, poor responsiveness, seizures, muscle weakness, sudden severe dementia, memory loss, withdrawal from social interaction, impaired judgment

81
Q

Borrelia burgdorferi (Lyme Disease)

Dissemination after initial infection:
Bacteria spread hematogenously within days, causing:

A

Dissemination after initial infection: inflammatory response and characteristic skin lesion at site of insect bite
• Bacteria spread hematogenously within days, causing systemic inflammatory response

82
Q

Borrelia burgdorferi (Lyme Disease)

Can localize in ________ after several months
Encephalitis is usually aseptic:

A

• Can localize in CNS, joints and skin after several months

Encephalitis is usually aseptic: due to inflammatory response and not pathogen itself

83
Q

Borrelia burgdorferi (Lyme Disease)

Acquisition:
Distribution:

A

o Acquisition: tick bite

o Distribution: most common in NE US (now in Midwest)

84
Q

Borrelia burgdorferi (Lyme Disease)

Symptoms:
Risk Factors:

A

o Symptoms: initial skin lesion leading to possible arthritis and neurological problems
o Risk Factors: residence/travel to endemic areas

85
Q

Borrelia burgdorferi (Lyme Disease)

Shape:
Aerobic?

A

o Shape: spirochete (difficult to Gram stain)

o Microaerophilic

86
Q

Borrelia burgdorferi (Lyme Disease)

Requires _____ to culture:
Diagnosis requires use of:

A

Difficult to culture: requires BSK-II media

Diagnosis requires use of serological tests: have variable reliability

87
Q

Treponema pallidum (Tertiary Syphilis)

Basics:

A

Basics: late stage CNS infection that is rare in the US because of ability to easily treat syphilis

88
Q

Treponema pallidum (Tertiary Syphilis)

3 stages of disease:

A

Primary: multiplication of bacteria at site of entry, producing localized infection

Secondary: follows asymptomatic period; dissemination of bacteria to other tissues (ie. CNS)

Tertiary: can occur after 20-30 years

89
Q

Treponema pallidum (Tertiary Syphilis)

Acquisition:

Symptoms
primary:
secondary:
neurosyphilis:

A

o Acquisition: STI
o Symptoms:
• Initial genital chancre (primary)
• If untreated, leads to skin rash (secondary)
• If untreated, lead to dissemination to CNS (neurosyphilis)
➢ Difficulty controlling muscle movements, paralysis, numbness, gradual blindness, dementia

90
Q

Treponema pallidum (Tertiary Syphilis)

Shape:

A

Shape: Gram (-) spirochete

Note: Immunological testing is available

91
Q 
Campylobacter jejuni (Guillain Barre Syndrome)
Virulence Factors

Infectious Dose:
What allows for attachment and colonization of gut epithelium:

A

Low Infectious Dose: as few as 800 organisms required

Chemotaxis, motility and flagella: allows for attachment and colonization of gut epithelium

92
Q 
Campylobacter jejuni (Guillain Barre Syndrome)
Virulence determinants after colonization: (4)
A
  • Iron acquisition
  • Host cell invasion
  • Toxin production
  • Epithelial disruption

.

93
Q

Campylobacter jejuni (Guillain Barre Syndrome)

Acquisition:
Symptoms:

A

o Acquisition: contaminated food (usually chicken)

o Symptoms: food poisoning, acute paralysis

94
Q

Campylobacter jejuni (Guillain Barre Syndrome)

Guillan Barre Syndrome:

A

Guillan Barre Syndrome: occurs in 1/100 infections
• Demyelinating disorder characterized by immunologic attack on peripheral nerve myelin
• Due to cross reactivity between microbial LPS and human gangliosides

95
Q

Campylobacter jejuni (Guillain Barre Syndrome)

Shape:
Aerobic?
Motile?

A

o Shape: Gram (-) curved rods
o Microaerophilic
o Motile: darting motility

96
Q

Polymicrobial Abscesses

Basics:

A

Basics: localized suppurative infection within the brain

97
Q

Polymicrobial Abscesses

Leads to:
Symptoms:

A

• Pathogenesis: leads to space occupying region that compresses normal structures
- Symptoms: headache, drowsiness, confusion, hemiparesis, seizures, speech difficulties, fever, NO stiff neck

98
Q

Polymicrobial Abscesses
Etiology

Gram (+): (5)

A

o Gram (+): Streptococcus**, Peptostreptococcus, Staphylococcus, Nocardia, Actinomyces

99
Q

Polymicrobial Abscesses
Etiology

Gram (-): (6)

A

Bacteroides, Prevotella, Fusobacterium, E.coli, Citrobacter koseri, Proteus mirabilis

100
Q

Polymicrobial Abscesses

Most common cause is:
US vs Europe:
Infect synergistically with:

A

Most common cause is Streptococcus:
o S.anginosus (US)
o S.milleri (Europe)
o Infect synergistically with anaerobic organisms

101
Q

Polymicrobial Abscesses

Brain abscesses in AIDS patients: (2)

A

o Toxoplasma gondii

o Cryptococcus

102
Q

Polymicrobial Abscesses

CT scan prior to:
After 4-5 days, abscess surrounded by:

A

CT scan: prior to lumbar puncture (due to risk of brain herniation)
o After 4-5 days, abscess surrounded by fibrous capsule that results in ring-enhancing appearance on CT with contrast

103
Q

Polymicrobial Abscesses
Acquisition:
Treat:

A

Acquisition: usually normal flora (usually sequelae of local/remote infections; do not arise de novo)
o Treat primary infection

104
Q

Polymicrobial Abscesses

Risk Factors: (5)

A

o Immunocompromise
o Head injury (skull fracture)
o Congenital heart disease in kids
o Distal infection (infections of heart, lungs, kidneys etc.)
o Local infection (otitis media, dental abscess, sinusitis)

105
Q

FUNGAL INFECTIONS (CHRONIC MENINGOENCEPHALITIS): (3)

A
  • Cryptococcus neoformans
  • Coccidiodes imitis (Valley Fever):
  • Histoplasma capsulatum (North America Histoplasmosis):
106
Q

POST-INFECTIOUS SYNDROMES: (1)

A

Campylobacter jejuni (Guillain Barre Syndrome):

107
Q

BACTERIAL ENCEPHALITIS: (2)

A
  • Borrelia burgdorferi (Lyme Disease)

* Treponema pallidum (Tertiary Syphilis)

108
Q

CHRONIC BACTERIAL MENINGITIS: (1)

A

Mycobacterium tuberculosis

109
Q

Post-Neonatal Infections:

A
  • Streptococcus pneumoniae (pneumococcus):
  • Neisseria menigitidis (meningococcus):
  • Haemophilus influenza type B (Hib)
110
Q

Cryptococcus neoformans

Virulence Factors: (5)

A

o Latent Infection: most primary pulmonary infections usually asymptomatic and lead to latent infection that can be reactivated in immunocompromised patients (may remain localized or disseminate through the body to CNS)
o Capsule: antiphagocytic; prevents complement and Ab deposition
o Melanin: pigment that protects against oxidative defenses of macrophages
o Phospholipase B: degrades host phospholipids and aids in tissue destruction/cellular escape
o Urease

111
Q

Cryptococcus neoformans
Virulence Factors
Latent Infection:

A

Latent Infection: most primary pulmonary infections usually asymptomatic and lead to latent infection that can be reactivated in immunocompromised patients (may remain localized or disseminate through the body to CNS)

112
Q

Cryptococcus neoformans
Virulence Factors
Capsule:

A

Capsule: antiphagocytic; prevents complement and Ab deposition

113
Q

Cryptococcus neoformans
Virulence Factors
Melanin:

A

Melanin: pigment that protects against oxidative defenses of macrophages

114
Q

Cryptococcus neoformans
Virulence Factors
Phospholipase B:

A

Phospholipase B: degrades host phospholipids and aids in tissue destruction/cellular escape

115
Q

Cryptococcus neoformans

Acquisition:
Distribution:
Risk Factors::

A

o Acquisition: inhalation
o Distribution: pigeon excreta and rotting wood are natural reservoirs
o Risk Factors: immunosuppression (common cause of meningitis in HIV+ patients)

116
Q

Cryptococcus neoformans
Clinical ID

G+/-?
What stains for capsule?
What is a fungal stain?

A
  • Gram (+) yeast
  • India Ink (+): stain for capsule
  • Calcofluor White (+): fungal stain
117
Q

Cryptococcus neoformans
Clinical ID

Biochemical:
Detection of __________

A

o Biochemical: urease (+)

o Detection of capsular Ag in CSF or serum

118
Q 
Coccidiodes imitis (Valley Fever)
Pathogenesis

Formation of spherules in the lungs:
Meningitis:
Symptoms:

A

Formation of spherules in the lungs: from arthroconidia

Meningitis: fatal if not treated

Symptoms: initial flu-like symptoms, then possible spread to CNS (1% of cases)

119
Q 
Coccidiodes imitis (Valley Fever)
Pathogenesis
A

Acute Respiratory Infection: 7-21 days after exposure (resolves rapidly under most conditions)
• May lead to chronic pulmonary condition
• May disseminate to meninges, bones, joints, subcutaneous and cutaneous tissues

120
Q

Coccidiodes imitis (Valley Fever)

Acquisition:
Distribution:
Risk Factors:

A

Acquisition: inhalation (no person to person spread)

Distribution: endemic to SW US

Risk Factors: outbreaks occur in dust storms, earthquakes, and earth excavations (due to dispersion of arthroconidia)

121
Q

Coccidiodes imitis (Valley Fever)

Clinical ID:

A

o Mold at 25 degrees; spherules at 37 degrees

o Endospores seen in tissues

122
Q

Histoplasma capsulatum (North America Histoplasmosis)

Acquisition:
Distribution:

A

Acquisition: inhalation of macroconidia from the soil

Distribution: central and southern US (bird and bat guano)

123
Q

Histoplasma capsulatum (North America Histoplasmosis)

Risk Factors:

A
  • Immunosuppresion
  • Age (<2, elderly)
  • Exposure to large inoculum
124
Q

Histoplasma capsulatum (North America Histoplasmosis)

Majority of infections follow:
Dissemation:

A

o Majority of infections follow subclinical and benign course: in normal hosts
o Dissemation: typically amongst imunosuppressed; can lead to chronic meningitis or encephalitis, which can be potentially fatal

125
Q

CAPSULE: THE UBIQUITOUS VIRULENCE FACTOR

Present on bacteria and fungi: (6)

A
  • Streptococcus pneumoniae
  • Neisseria meningitidis
  • Haemophilus influenza
  • GBS
  • Cryptococcus neoformans
  • E.coli K1
126
Q

CAPSULE: THE UBIQUITOUS VIRULENCE FACTOR

Used for identification:

A
  • Serogroups/serotypes
  • Quelling reaction
  • India ink stain
127
Q

CAPSULE: THE UBIQUITOUS VIRULENCE FACTOR
Functions:

A
  • Prevent complement and Ab deposition
  • Antiphagocytic
  • Intracellular protection
  • Toxic to host cells
128
Q

PARASITIC INFECTIONS: (3)

A
  • Trypanosoma cruzi (Chagas Disease)
  • Plasmodium falciparum (Malaria)
  • Toxoplasma gondii
129
Q

Trypanosoma cruzi (Chagas Disease)

Acquisition:
Distribution:

A
  • Acquisition: bite from infected Triatome bug

- Distribution: southern US to southern Argentina

130
Q

Trypanosoma cruzi (Chagas Disease)

Risk Factors:
Symptoms:

A

Risk Factors: infants and travel to endemic areas

Symptoms: initial sore where bite occurred; fever, acute encephalitis; possible chronic disease affected heart, colon or CNS

131
Q

Plasmodium falciparum (Malaria)

Acquisition:
Site of infection:
Risk Factors:

A

Acquisition: bite from infected mosquito

Site of infection: liver and RBCs

Risk Factors: age (<10) and exposure to endemic areas

132
Q

Plasmodium falciparum (Malaria)

Symptoms:

A

Symptoms: acute
o Widespread disease of the brain accompanied by recurrent episodes of malarial fever (fever, chills, anemia)
o If cerebral malaria (CM) not treated, it is fatal in 24-72 hours

133
Q 
Plasmodium falciparum (Malaria)
Humans:
A

o Humans: sporozoites injected by mosquito; grow and multiply in liver cells first, then in RBCs
• RBCs: growth destroys cell, releasing merozoites (daughter cells) that continue the cycle by invading other RBCs)

134
Q 
Plasmodium falciparum (Malaria)
Mosquito:
A

o Mosquito: gametocytes are picked up by mosquito when they bite humans, undergo a different cycle
• Sporozoites: found in mosquito’s salivary glands after 10-18 days; inject into humans when they bite them
• Therefore, mosquito carries disease form human to human (vector): does not suffer from infection with parasite

135
Q

Toxoplasma gondii

Primary infection:
Progression:

A
  • Primary infection: flu-like symptoms

- Progression: can progress to encephalitis and psychotic symptoms (similar to schizophrenia)

Micro Exam 3 (11 decks)

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