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)
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
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
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
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
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
7
Q
Invasion of the CNS
Function:
A
Function: inhibit passage of microbes, antibodies and some antimicrobial drugs
8
Q
Invasion of the CNS
Mechanism:
A
Mechanism: tight junctions (zonula occludens) between endothelial (BBB) and epithelial cells (BCB)
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)
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
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
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
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
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
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
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)
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
18
Q
Carriage Rates
Streptococcus pneumoniae:
A
o Significant carriage in pharynx and mouth
o Small amount of carriage in nose and UG tract
19
Q
Carriage Rates
Neisseria meningitidis
A
o Heavy carriage in pharynx
o Significant carriage in nose, mouth and UG tract
20
Q
Carriage Rates
Haemophilus influenza:
A
o Significant carriage in nose, pharynx and mouth
21
Q
Carriage Rates
Group B Streptococcus:
A
o Heavy carriage in GI tract
o Significant carriage in UG tract
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
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
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)
25
Normal
```
Indicator
WBCs (per uL)
%PMNs
RBCs (per uL)
Glucose (mg/dL)
Protein (mg/dL)
```
```
0-5
0
0-2
45-85
15-45
```
26
Acute Bacterial
```
Indicator
WBCs (per uL)
%PMNs
RBCs (per uL)
Glucose (mg/dL)
Protein (mg/dL)
```
>1,000 (PMNs)
>50
0-10
100
27
Fungal or Viral
```
Indicator
WBCs (per uL)
%PMNs
RBCs (per uL)
Glucose (mg/dL)
Protein (mg/dL)
```
```
100-500 (lymphocytes)
<10
0-2
≤40
50-100
```
28
Acute Bacterial Meningitis
| Basics:
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)
29
Acute Bacterial Meningitis
Symptoms
Common:
Common: high fever, severe/persistent headache, stiff neck, N/V
30
Acute Bacterial Meningitis
Symptoms
Important (may require emergency treatment:
Infants:
Important (may require emergency treatment: changes in behavior (confusion), sleepiness, and difficulty waking up
Infants: irritability, tiredness, poor feeding, fever (hard to diagnose)
31
Acute Bacterial Meningitis
Onset
Acute:
Acute: onset of symptoms within hours or days (bacterial or viral infection)
32
Acute Bacterial Meningitis
Onset
Chronic:
Chronic: symptoms fluctuate over the course of weeks, months or years (viruses)
33
Primary cause of bacterial meningitis in the US:
Streptococcus pneumoniae (pneumococcus):
34
```
Streptococcus pneumoniae (pneumococcus)
Virulence Factors: (6)
```
Adhesins
IgA protease
Pneumolysin
Autolysin
Capsule: over 90 serotypes
Outer wall components (PG, TA)
35
Streptococcus pneumoniae (pneumococcus)
Virulence Factors
Adhesins:
Adhesins: PspA and CpbA (bind carbohydrate on cell surfaces)
36
Streptococcus pneumoniae (pneumococcus)
Virulence Factors
Pneumolysin:
Pneumolysin: cytotoxin released when the bacteria lyses (also inhibits Ab binding to bacteria)
37
```
Streptococcus pneumoniae (pneumococcus)
Virulence Factors
```
Autolysin:
Bacteria able to detect:
_____ to increase survival of cells that don’t lyse
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
38
```
Streptococcus pneumoniae (pneumococcus)
Virulence Factors
# of capsule serotypes:
```
Capsule: over 90 serotypes
39
```
Streptococcus pneumoniae (pneumococcus)
Virulence Factors
```
Outer wall components (PG, TA):
Outer wall components (PG, TA): pro-inflammatory (results in tissue damage)
40
```
Streptococcus pneumoniae (pneumococcus)
Etiology/Pathogenesis
```
Acquisition:
Distribution:
Acquisition: aerosols or direct contact with oral secretions (carried asymptomatically in nasopharynx; carriage rate DECREASES with age)
Distribution: ubiquitous
41
```
Streptococcus pneumoniae (pneumococcus)
Etiology/Pathogenesis
```
Risk Factors: (3)
* Immunosuppression
* Distant foci of infection
* Low levels of circulating Abs to capsular polysaccharide
42
```
Streptococcus pneumoniae (pneumococcus)
Structure:
```
Structure: Gram (+) diplococci (lancet shaped)
43
```
Streptococcus pneumoniae (pneumococcus)
Biochemical Tests
```
Catalase:
Hemolysis:
Optochin:
* Catalase (-)
* Alpha hemolytic
* Optochin sensitive (distinguish from other alpha hemolytic strep)
44
```
Streptococcus pneumoniae (pneumococcus)
Biochemical Tests
```
What distinguishes it from GDS?
Quelling Reaction:
Swelling of the capsule caused by:
• Bile sensitive (distinguish from GDS)
• Quelling Reaction (+)
- Swelling of the capsule caused by contact with serum containing serotype-specific Abs
45
Streptococcus pneumoniae (pneumococcus)
Vaccines
23 Valent:
23 Valent: capsular polysaccharides to 23 serotypes that are responsible for ~90% of infections
• 60-70% efficacy
• Not effective in kids under 2
46
```
Streptococcus pneumoniae (pneumococcus)
Vaccines
7 valent (PCV7):
```
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
47
```
Neisseria menigitidis (meningococcus)
Basics:
```
Basics: second leading cause of acute bacterial meningitis; human specific
48
```
Neisseria menigitidis (meningococcus)
Virulence Factors: (4)
```
o IgA protease
o Pili (Pil proteins): adherence to epithelium
o LOS: similar to LPS (toxic/pro-inflammatory)
o Capsule
49
```
Neisseria menigitidis (meningococcus)
Capsule: several serogroups:
```
```
Capsule: several serogroups
• A: 5%
• B: 50%
• C: 20%
• Y: 10%
• W135: 10%
```
50
```
Neisseria menigitidis (meningococcus)
Acquisition:
```
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
51
```
Neisseria menigitidis (meningococcus)
Distribution:
```
Distribution: ubiquitous (causes sporadic outbreaks and epidemics)
52
```
Neisseria menigitidis (meningococcus)
Risk Factors:
```
Risk Factors: close contact with infected people or areas of outbreak
53
Neisseria menigitidis (meningococcus)
Symptoms:
What reflects associated septicemia?
May lead to:
In ~1/3 of patients:
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
54
```
Neisseria menigitidis (meningococcus)
Vaccines
```
protect against:
Do NOT protect against:
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
55
```
Neisseria menigitidis (meningococcus)
Vaccines
```
55:
11-55:
o Meningococcal polysaccharide vaccine (MPSV4): 55
| o Meningococcal conjugate vaccine (MCV4): 11-55
56
Neisseria menigitidis (meningococcus)
Shape:
Fastidious:
o Shape: Gram (-) cocci (generally diplococci)
| o Fastidious: requires CAP to grow (needs heme from lysed RBCs)
57
Neisseria menigitidis (meningococcus)
Biochemical Tests:
• Oxidase (+)
• Ferments glucose and maltose
.
58
Haemophilus influenza type B (Hib)
| Basics:
Basics: used to be the leading cause of meningitis in ages 5 mo-5 years, but now rare where Hib vaccine used
59
Haemophilus influenza type B (Hib)
| Virulence Factors: (3)
o IgA protease
o LPS
o Capsule: 6 serotypes (A-F; B responsible for most cases of meningitis)
60
Haemophilus influenza type B (Hib)
Acquisition:
Distribution:
Risk Factors:
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
Haemophilus influenza type B (Hib)
Shape:
Aerobe vs anaerobe:
Capsule:
o Shape: Gram (-) pleiomorphic coccobacilli
o Facultative anaerobe
o Capsule: can be encapsulated (typeable) and non-encapsulated (nontypeable)
62
Haemophilus influenza type B (Hib)
Fastidious growth and nutrient requirements:
Factor V:
Factor X:
o Fastidious growth: requires CAP
• Factor V: NAD
• Factor X: hemin
63
Haemophilus influenza type B (Hib)
| Vaccine:
Protective Ab would develop naturally by age 5, but also develops following vaccination
64
College Outbreaks
Cause:
Risk Factors:
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
N. meningitidis
Host:
Clinical Features:
Mortality (% of treated cases):
Sequelae (% of treated cases):
Children and adolescents
Acute onset (6-24 hours) skin rash
7-10
<1
66
H.influenzae
Host:
Clinical Features:
Mortality (% of treated cases):
Sequelae (% of treated cases):
Children <5
Onset less acute (1-2 days)
5
9
67
S.pneumoniae
Host:
Clinical Features:
Mortality (% of treated cases):
Sequelae (% of treated cases):
All ages Esp. <2 and elderly
Acute onset; May follow pneumonia or septicemia in elderly
20-30
15-20
68
N.meningitidis
```
Capsule
IgA Protease
Pili
Endotoxin
OMPs
```
```
+
+
+
+
?
```
69
H.influenzae
```
Capsule
IgA Protease
Pili
Endotoxin
OMPs
```
```
+
+
+
+
+
```
70
S.pneumoniae
```
Capsule
IgA Protease
Pili
Endotoxin
OMPs
```
```
+
+
-
-
-
```
71
Neonatal Infections
Fatal in _____ of cases
Often lead to:
Clinical diagnosis in infant:
- 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
Neonatal Infections
| Causative agents: (4)
- Listeria monocytogenes: G(+) rod
- E.coli K1: G(-) rod
- Group B Streptococcus: G(+) cocci in chains
- Toxoplasma gondii: parasite
73
Mycobacterium tuberculosis
Prevalence:
Pathogenesis is a 2 step process:
Basics: relatively rare
Pathogenesis:
Enter host by droplet inhalation
Dissemination to LNs as lung infection progresses
74
Mycobacterium tuberculosis
| Enter host by droplet inhalation:
Enter host by droplet inhalation: infect lung macrophages, forming a granuloma (primary lesion)
75
Mycobacterium tuberculosis
| Dissemination to LNs as lung infection progresses:
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
Mycobacterium tuberculosis
Acquisition:
Distribution:
Acquisition: aerosol spread or reactivation of latent disease
Distribution: highest in urban and endemic areas
77
```
Mycobacterium tuberculosis
Risk Factors (3)
```
* Previous TB infection
* Immunosuppression
* Travel to endemic areas
78
Encephalitis
Most often caused by:
Can also occur as result of:
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
Encephalitis
Symptoms
Common:
Common: sudden fever, headache, vomiting, abnormal visual sensitivity to light, stiff neck and back, confusion, drowsiness, clumsiness, unsteady gait, irritability
80
Encephalitis
Symptoms
Require Emergency Treatment:
Require Emergency Treatment: LOC, poor responsiveness, seizures, muscle weakness, sudden severe dementia, memory loss, withdrawal from social interaction, impaired judgment
81
Borrelia burgdorferi (Lyme Disease)
Dissemination after initial infection:
Bacteria spread hematogenously within days, causing:
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
Borrelia burgdorferi (Lyme Disease)
Can localize in ________ after several months
Encephalitis is usually aseptic:
• Can localize in CNS, joints and skin after several months
Encephalitis is usually aseptic: due to inflammatory response and not pathogen itself
83
Borrelia burgdorferi (Lyme Disease)
Acquisition:
Distribution:
o Acquisition: tick bite
| o Distribution: most common in NE US (now in Midwest)
84
Borrelia burgdorferi (Lyme Disease)
Symptoms:
Risk Factors:
o Symptoms: initial skin lesion leading to possible arthritis and neurological problems
o Risk Factors: residence/travel to endemic areas
85
Borrelia burgdorferi (Lyme Disease)
Shape:
Aerobic?
o Shape: spirochete (difficult to Gram stain)
| o Microaerophilic
86
Borrelia burgdorferi (Lyme Disease)
Requires _____ to culture:
Diagnosis requires use of:
Difficult to culture: requires BSK-II media
Diagnosis requires use of serological tests: have variable reliability
87
Treponema pallidum (Tertiary Syphilis)
Basics:
Basics: late stage CNS infection that is rare in the US because of ability to easily treat syphilis
88
Treponema pallidum (Tertiary Syphilis)
3 stages of disease:
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
Treponema pallidum (Tertiary Syphilis)
Acquisition:
Symptoms
primary:
secondary:
neurosyphilis:
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
Treponema pallidum (Tertiary Syphilis)
Shape:
Shape: Gram (-) spirochete
Note: Immunological testing is available
91
```
Campylobacter jejuni (Guillain Barre Syndrome)
Virulence Factors
```
Infectious Dose:
What allows for attachment and colonization of gut epithelium:
Low Infectious Dose: as few as 800 organisms required
Chemotaxis, motility and flagella: allows for attachment and colonization of gut epithelium
92
```
Campylobacter jejuni (Guillain Barre Syndrome)
Virulence determinants after colonization: (4)
```
* Iron acquisition
* Host cell invasion
* Toxin production
* Epithelial disruption
.
93
Campylobacter jejuni (Guillain Barre Syndrome)
Acquisition:
Symptoms:
o Acquisition: contaminated food (usually chicken)
| o Symptoms: food poisoning, acute paralysis
94
Campylobacter jejuni (Guillain Barre Syndrome)
Guillan Barre Syndrome:
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
Campylobacter jejuni (Guillain Barre Syndrome)
Shape:
Aerobic?
Motile?
o Shape: Gram (-) curved rods
o Microaerophilic
o Motile: darting motility
96
Polymicrobial Abscesses
| Basics:
Basics: localized suppurative infection within the brain
97
Polymicrobial Abscesses
Leads to:
Symptoms:
• Pathogenesis: leads to space occupying region that compresses normal structures
- Symptoms: headache, drowsiness, confusion, hemiparesis, seizures, speech difficulties, fever, NO stiff neck
98
Polymicrobial Abscesses
Etiology
Gram (+): (5)
o Gram (+): Streptococcus**, Peptostreptococcus, Staphylococcus, Nocardia, Actinomyces
99
Polymicrobial Abscesses
Etiology
Gram (-): (6)
Bacteroides, Prevotella, Fusobacterium, E.coli, Citrobacter koseri, Proteus mirabilis
100
Polymicrobial Abscesses
Most common cause is:
US vs Europe:
Infect synergistically with:
Most common cause is Streptococcus:
o S.anginosus (US)
o S.milleri (Europe)
o Infect synergistically with anaerobic organisms
101
Polymicrobial Abscesses
Brain abscesses in AIDS patients: (2)
o Toxoplasma gondii
| o Cryptococcus
102
Polymicrobial Abscesses
CT scan prior to:
After 4-5 days, abscess surrounded by:
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
Polymicrobial Abscesses
Acquisition:
Treat:
Acquisition: usually normal flora (usually sequelae of local/remote infections; do not arise de novo)
o Treat primary infection
104
Polymicrobial Abscesses
| Risk Factors: (5)
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
FUNGAL INFECTIONS (CHRONIC MENINGOENCEPHALITIS): (3)
* Cryptococcus neoformans
* Coccidiodes imitis (Valley Fever):
* Histoplasma capsulatum (North America Histoplasmosis):
106
POST-INFECTIOUS SYNDROMES: (1)
Campylobacter jejuni (Guillain Barre Syndrome):
107
BACTERIAL ENCEPHALITIS: (2)
* Borrelia burgdorferi (Lyme Disease)
| * Treponema pallidum (Tertiary Syphilis)
108
CHRONIC BACTERIAL MENINGITIS: (1)
Mycobacterium tuberculosis
109
Post-Neonatal Infections:
* Streptococcus pneumoniae (pneumococcus):
* Neisseria menigitidis (meningococcus):
* Haemophilus influenza type B (Hib)
110
Cryptococcus neoformans
| Virulence Factors: (5)
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
Cryptococcus neoformans
Virulence Factors
Latent Infection:
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
Cryptococcus neoformans
Virulence Factors
Capsule:
Capsule: antiphagocytic; prevents complement and Ab deposition
113
Cryptococcus neoformans
Virulence Factors
Melanin:
Melanin: pigment that protects against oxidative defenses of macrophages
114
Cryptococcus neoformans
Virulence Factors
Phospholipase B:
Phospholipase B: degrades host phospholipids and aids in tissue destruction/cellular escape
115
Cryptococcus neoformans
Acquisition:
Distribution:
Risk Factors::
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
Cryptococcus neoformans
Clinical ID
G+/-?
What stains for capsule?
What is a fungal stain?
* Gram (+) yeast
* India Ink (+): stain for capsule
* Calcofluor White (+): fungal stain
117
Cryptococcus neoformans
Clinical ID
Biochemical:
Detection of __________
o Biochemical: urease (+)
| o Detection of capsular Ag in CSF or serum
118
```
Coccidiodes imitis (Valley Fever)
Pathogenesis
```
Formation of spherules in the lungs:
Meningitis:
Symptoms:
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
```
Coccidiodes imitis (Valley Fever)
Pathogenesis
```
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
Coccidiodes imitis (Valley Fever)
Acquisition:
Distribution:
Risk Factors:
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
Coccidiodes imitis (Valley Fever)
Clinical ID:
o Mold at 25 degrees; spherules at 37 degrees
| o Endospores seen in tissues
122
Histoplasma capsulatum (North America Histoplasmosis)
Acquisition:
Distribution:
Acquisition: inhalation of macroconidia from the soil
Distribution: central and southern US (bird and bat guano)
123
Histoplasma capsulatum (North America Histoplasmosis)
Risk Factors:
* Immunosuppresion
* Age (<2, elderly)
* Exposure to large inoculum
124
Histoplasma capsulatum (North America Histoplasmosis)
Majority of infections follow:
Dissemation:
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
CAPSULE: THE UBIQUITOUS VIRULENCE FACTOR
| Present on bacteria and fungi: (6)
- Streptococcus pneumoniae
- Neisseria meningitidis
- Haemophilus influenza
- GBS
- Cryptococcus neoformans
- E.coli K1
126
CAPSULE: THE UBIQUITOUS VIRULENCE FACTOR
Used for identification:
- Serogroups/serotypes
- Quelling reaction
- India ink stain
127
CAPSULE: THE UBIQUITOUS VIRULENCE FACTOR
Functions:
- Prevent complement and Ab deposition
- Antiphagocytic
- Intracellular protection
- Toxic to host cells
128
PARASITIC INFECTIONS: (3)
* Trypanosoma cruzi (Chagas Disease)
* Plasmodium falciparum (Malaria)
* Toxoplasma gondii
129
Trypanosoma cruzi (Chagas Disease)
Acquisition:
Distribution:
- Acquisition: bite from infected Triatome bug
| - Distribution: southern US to southern Argentina
130
Trypanosoma cruzi (Chagas Disease)
Risk Factors:
Symptoms:
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
Plasmodium falciparum (Malaria)
Acquisition:
Site of infection:
Risk Factors:
Acquisition: bite from infected mosquito
Site of infection: liver and RBCs
Risk Factors: age (<10) and exposure to endemic areas
132
Plasmodium falciparum (Malaria)
Symptoms:
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
```
Plasmodium falciparum (Malaria)
Humans:
```
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
```
Plasmodium falciparum (Malaria)
Mosquito:
```
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
Toxoplasma gondii
Primary infection:
Progression:
- Primary infection: flu-like symptoms
| - Progression: can progress to encephalitis and psychotic symptoms (similar to schizophrenia)
