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CNS > Microbiology > Flashcards

Microbiology Flashcards

1
Q

what are the pathogens that cause meningitis?

A
  1. neisseria meningitidis
  2. group B strept
  3. S.pneumonia
  4. H.influenza
  5. listeria monocytogenes
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2
Q 
neisseria meningitidis;
gram?
shape?
is it motile,spore forming,acid fast?
capsule or not?
what is the ideal growing culture?
virulence factor ? 
usually collected in?
trans?
can infect?
what group can cause wide spread epedemics?
A
  • negative
  • diplococci pairs wt opposing sides flattened , KIDNEY-BEAN appearance
  • NON all three
  • capsulated wt 13 serotypes ;A B C W135 Y
  • grow in an aerobic CO2 +enriched medium
  • pilli ,OMP ,LOS
  • PMNs
  • respiratory droplets (usually quiescent in nasopharyngeal flora
  • blood and CNS , and may cause rapid shock and die within 24 hr
  • group A
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3
Q 
pathogenesis of N. meningitidis ;
carrier state?
cause ?
v factor impo.?
capsule impo?
how it inter cells ?
A
  • carrier state has protective Ab
  • cause bacteremia endotoxemia and meninitis
  • pili +OMP attach to non ciliated naso. cells
  • LOS +sialic acid interfers wt C3
  • LOS +peptidoglycan trigger cytokine release
  • OM blebs (LOS )contain endotoxin ;cause endotoxic shock
  • scavenge iron and resist phagocytosis &C
  • attachment to microvilli ,enter as vesicles , to sub mucosa to bloodstream (vs gonococcus which remains localized in phagosomes .)
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4
Q

immunity of N. meningitidis;
age?and why?
what about group B?

A
  • anticapsular Ab is protective
  • carrier and infected have Ab
  • deficiency in terminal C increase the risk
  • mainly in 6-24 m , because the IgG2 response is deficient ,and the T-independant response to capsular is poor
  • not immunogenic due to similarity to sialic acid of m.o. to neural cell adhesion mol
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5
Q

clinical of N. menin.

A

-acute purulent meningitis ,

skin petechie –>ecchymosis or DIC

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6
Q

diagnosis of N.menin.

A

-gram smear ;CSF
culture ;blood /chocolate agar
skin lesion samples
speciation;biochemical /immunological tests

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7
Q

ttt, of N.menin.

A

penicillin ,if R

give cephalosporin 3rd generation ;ceftriaxone /cefotaxime

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8
Q

prevention of N, menin.

A

-rifampin or ciprofloxacin (prophylaxis )

-MCV4 (meningococcal conjugate quadravalent); A C Y W135 :
IT stimulates Tcell dependent R

  • conjugation wt diphtheria toxoid vaccine
  • given from 9 m and boostered at 11-16 yrs
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9
Q 
group B strept"streptococcus agalactiae" ;
gram?
shape?
b-hemolytic?
capsule or not?
virulence factor?
cause?
age?
found in?
A
  • positive
  • short chains diplococcic
  • b-hemolytic
  • capsular wt 9 types(type 3 most common
  • pili ans surface proteins
  • meningitis and sepsis
  • first days of life & late in 1-3 months(mainly menin.)
  • found in lower GIT and vagina in 10-40%
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10
Q

lancefield group A

s pnuumonia relation wt tests?

A
  • the 1st is positive bacitracin and PYR

- the 2nd is positive optochin and bile solubility

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11
Q

clinical of B strept

A

-newborn wt fever ,lethargy, poor feeding, respiratory distress
high mortality rate

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12
Q

pathogenesis /immunity of B strept

A
  • capsule sialic acid binds factor H
  • C3b disrupted
  • trans-placental IgG is protective
  • anticapsular Ab is protective
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13
Q

diagnosis of B strept ;

A

-CSF ;gram smear
-culturing
lancefield grouping

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14
Q

ttt of B strept

A

penicillin (not beta lactamase )

-early :aminoglcoside is added

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15
Q

prevention of B strept ;

A

if a carrier pregnant ;give IV penicillin intra partum (during labor)
-vaccine during pregnancy 3rd tri.

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16
Q 
H.influenza ;
gram?
shape?
capsule or not?how many serotypes ?
virulence factor ?
requirement for growth?
trans?
A
  • negative
  • coccobacili
  • capsulated wt 6 serotypes a-f

-type b(Hib) capsule contains PRP
+ OMP (HMW1&2) +LPS,LOS

  • require factor X and NAD (factor V )
  • respiratory droplets
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17
Q

what is satellite phenomenon ?

A

occurs. when one bacterial species produces growth factors required by. a second species when these , ex; staph aureus provides NAD which is required by H.influenza

18
Q 
pathogenesis of H.inf.;
what is NTHi?
which form is invasive?
meningitis most common in?
pili for?
invasion inside or btwn cells?
impo. of capsule?
A

• Nasopharyngeal colonization is common
(20% to 80% ; mostly non-capsulated “NTHi”
= nontypeable Haemophilus influenzae)

  • Only capsulated m.o. are invasive
  • Meningitis: Children < 2 years , 6-18 m because Ab is absent and Tcell independent R to PRP is poor
  • Pili/ adhesins attach to epithelial cells
  • Invasion goes between cells
  • Capsule prevents phagocytosis and enter blood stream
19
Q

immunity of H.inf;

A

-anti capsular Ab is bactericidal and protective

-

20
Q

causes of H.inf.

A

–acute purulent meningitis
-preceded by URT inf. ;(pharyngitis ,otitis media,sinusitis)
• Started as vague malaise, lethargy, irritability and fever
- mortality 3-6% even wt ttt , rapid within 1 day
-1/3 of survival ends wt significant neurologic sequelae

21
Q

diagnosis /ttt of H.inf.

A
  • Gram staining: CSF
  • Culture
  • Rapid diagnostic kits for Hib
  1. 3rd G cephalosporin
    If susceptibility test is available change to:
  2. Ampicillin
    -BUT 5% to 50% of strains are resistant due to production of beta-lactamases.
    *dont start wt ampicillin
22
Q

prevention of H.inf.
vaccine ?
prophylaxis?

A

• Conjugated Hib vaccine;
- Conjugation to Diphtherial Toxoid or
outer membrane protein of N. meningitidis
- Given from 2 months of age

  • 99% reduction in incidence
  • Reduction in colonization rate
  • Stimulate T cell-dependent response

• Rifampin prophylaxis: Unimmunized close contacts

23
Q 
strept. pneumoniae;
gram?
shape?
hemolysis?
capsule? /serotypes?
virulence factor?
A

• Gram positive
- oval, diplococcic (end to end)

  • alpha-hemolytic aerobically
  • Capsule has > 90 serotypes

1• Choline-binding proteins attaches to cells
2• Pneumolysin forms pores after release by
action of autolysins (present in cell wall)
3• Polysaccharide capsule ;block C3b

24
Q

causes of S.pneum.

A

• Acute purulent meningitis

• Following pneumococcal pneumonia/otitis media
or without antecedent infection, or trauma

• Sequelae are slightly higher than other

25
Q

diagnosis of S.pneum.

tests? 3

A
  1. Gram staining: CSF
  2. Culture
    • Optochin sensitivity test (sensitive) &/or
      - Bile solubility test (soluble): Differentiate
      it from viridans streptococci
  • Quellung test capsule “swelling test” : Conducted with anti-capsular antibody
    (usually not done routinely )
26
Q

ttt of S.pneum.

A
  1. 3rd G Cephalosporin
    (Ceftriaxone,Cefotaxime):
    - If MIC > 0.06 µg/mL: High doses +Vancomycin unless the MIC < 0.05µg/mL
  2. Penicillin
    - Resistant strains (10%-40%)
    - Due to altered transpeptidation
27
Q

prevention of S.pneum.

vaccine ? 2 valent

A
  1. 13-valent pneumococcal conjugate vaccine(PCV):
    - Is T-cell dependent vaccine
    - Stimulate TH2 response
    - Given from 2 months of age and on.
    - Immunocompromised < 5 years of age.
  2. 23-valent pneumococcal polysaccharide
    vaccine (PPV): “Added Protection”
    - Is T-cell independent vaccine
    - Used for > 2 years of age
28
Q 
listeria monocytogenes ;
gram?
hemolysis?
catalase?
growing temp.?
at what temp. tumbling motility occur?
virulence?
A

• Gram positive rods; resemble Corynebacterium
(diphtheroids)

• Beta-hemolytic colonies

  • Catalase positive (D/D S. pyogenes : -ve)

• Grow at temperature below Zero Celsius (due to RNA Helicase); important in frozen food
- Below 30 Celsius in fluid: Tumbling Motility
(D/D Corynebacteria: non-motile)

• Virulence: Internalin (attachment/ invasion) &Listeriolysin-O (LLO; pore-forming cytotoxin +to escape from phagosomes to cytosol )

29
Q 
pathogenesis of Listeria;
site of growing?
cross placenta?
tail?
common in?
A
  • Grow in non-immune macrophages
  • Invasion: Surface protein and internalin
  • Can also cross placental-blood barrier
  • (comet tail) from Actin polymerization
  • Common: < 1 month and > 60 Years
30
Q

causes of listeria?

A

-it has tropism to CNS including brain parenchyma(encephalitis)
or Meningitis; Bacteremia (occult)

  • Not distinguished clinically from other bacterial meningitis
  • Does NOT have high mortality rate
31
Q

immunity to listeria ?

A
  • Both innate and adaptive immunity
  • Toll-like receptors recognize peptidoglycan
  • Specific CD4+, CD8+ cells generation
  • Increased in AIDS & immuncompromised
32
Q

diagnosis /ttt of listeria?

A

• CSF: Gram staining
• Culture on blood agar: Beta-hemolytic
G+ Rods

ttt;
• Ampicillin
- Ampicillin+gentamicin :Fulminating cases
• Cotrimoxazole

  • ** No vaccine is available
  • check the table on slide 49 lec 1 (very impo.)
33
Q

What are the viruses that cause meningitis?

A

Coxsackieviruses ,Echoviruses ,Enteroviruses
Arboviruses
Rabies virus

34
Q

Coxsackieviruses, echoviruses and enteriviruses ;
What do they affect?
Manifestaions?
What is the most sensitive test?

Route of transmission of enteroviruses/resistant to what/what does it cause?

A

- Most sensitive/specific test: RT-PCR/ CSF

• Affect meninges and cerebellum (do not
affect motor neurons)

• Aseptic meningitis: Enterovirus (frequently)

  • Mild
  • Self-limiting (5-14days) - May be accompanied by encephalitis
35
Q 
Arboviruses (arthropod-born zoonotic viruses);
Transmitted by?
Genera? 
Virion structure? 
Virion structure of flavivirus? 
Virion s of bunyavirus? 
Pathogenesis? 
Cause ? 
Immunity? 
Ttt and prevention ?
A

Immunity

-transmitted by blood- sucking insects such as mosquitos,tick, and sandflies (Phlebotomus)

  • # 1. Togaviruses; mainly Alphavirus
    1. Flaviviruses
    2. Bunyaviruses
    3. Reoviruses (e.g. Rotavirus)

**check the virion structure in slides

Pathogenesis
• Human infection by biting with infected arthropod –>Viremia: Replication in RES/endothelium
• Cell necrosis, inflammation –>Fever
• Cross brain-blood barrier or along neural pathway:
1. Aseptic meningitis
2. Encephalitis (neuronal dysfunction)
• CNS: Meningeal and perivascular mononuclear
cell infiltrates, degeneration of neurons

1 • Antibody response; appears after 3 days:
- Hemagglutination Inhibition Antibody (HI)
- Neutralizing Antibody (Most specific)
- IgM (for 2 months)
2 • Humoral & cellular immunity: Specific & Permanent

#Treatment and Prevention
  • Treatment: Supportive only
  • Prevention:
       - Protection from bites
       - Vector control
36
Q 
Rabies virus ;
Shape? 
Shape of envelop ?what does it elicit? 
Transmitted by?
Virus G protein binds to? 
Pathogenesis? 
Two epizootic forms? 
What pathognomonic about it? 
IP? 
How many clinical stages does it pass?*check the table in slide
A

pathogenesis:1• Negative sense RNA virus internalized and replicate in the cytoplasm Then G protein-containing lipoprotein envelop acquired from plasma membrane

  • Enveloped ssRNA, bullet- shaped virus
  • Knob-like envelope glycoproteins elicit neutralizing and hemagglutination antibodies

• Virus travel from biting site (dog bite) to CNS
• Virus G protein binds to acetylcholine or neural
cell adhesion molecule (NCAM) receptor on cells

2• Replicates initially in muscles at the site of entry and then enters peripheral nervous system
3• Spread to CNS and replicates exclusively in
the gray matter
4• Passes centrifugally along autonomic nerves to reach tissues, including salivary glands, adrenal medulla, kidneys, and lungs
5• Presence of the virus in salivary glands (of animals) facilitates further transmission

  1. Urban: Unimmunized dogs and cats
  2. Sylvatic: Wild bats, foxes, raccons ,skunks, wolves

•pathognomonic: Negri (inclusion) bodies found in neurons:

  • I.P. = 10 days to 1 year (average 20-90 days)
  • Immunization early I.P. aborts infection

• Rabies passes through 4 clinical stages

• Encephalitis common, sometimes with
ascending paralysis
• Almost uniformly fatal once symptoms start

37
Q

Diagnosis of rabies ;
By 2 methods : from patient and from brain of animal ;
First:Patient CSF? IF? PCR? Serum Ab?
What is the best diagnostic test?

Second: brain of an animal ;
Detection by?

A

First: Patient
• CSF: Minimal or no abnormalities; sometimes
lymphocytic pleocytosis
• Immuno-fluorescent (DFA) stain: Nape of neck biopsy (BEST DIAGNOSTIC TEST)
• PCR: For viral antigens in CSF or saliva
• Serum antibodies: Detected late in disease

#Second: Brain of animal (e.g. dog)

  1. Detection of virus by:
    - Immunofluorescent (IF)
    - Animal inoculation (die in 3-10 days; suckling mice intra-cerebral inoculation)
  2. Negri bodies found histologically in the brain tissue in 80% of cases.
  3. EM microscopy detect Negri bodies and rhabdovirus (= rod) particles in brain tissue.
38
Q

ttt of rabies ;
Vaccination? 3

PEP ttt ,how?

A 
#1- rabies vaccination;
- Induces neutralizing Ab &amp; cytotoxic T cells
2• Pre-exposure vaccination
- To high risk individuals
- Day 0, 3, and 21 or 28
3• Post-exposure
- Animal Negative: No treatment
- Animal positive : Treatment
## (PEP)/Treatment;
• Washing the wound (soap &amp; water)
• Passive immunization: Anti-rabies with hyperimmune globulin
• Active immunization with anti-rabies
vaccine: Days: 0, 3, 7, and 14
• Previously immunized: Vaccine on day
0 and 3; hyperimmune globulin not given
39
Q 
Cryptococcus neogormans ; 
Type of pathogen? 
Capsulated?
When the colonies appear? 
Transmitted by? 
Common in? 
Pathogenesis ? 
Clinically?
A

Pathogenesis

  • Genus of yeast
  • Capsulated ; complex polysaccharide polymer (GXM)
  • Colonies appear in 2-3 days at 25 or 37o C
  • Associated with soil and bird droppings
  • Yeasts and basidiospores inhaled
  • Common in immunocompromised (AIDS)
  • Capsule: Anti-phagocytic
  • Circulating GXM: Interferes with immune function
  • Melanin: Oxidative protection in macrophages
  • Cross blood-brain barrier in macrophages
    (Trojan horse) plus Laccase action
    Colonies appear in 2-3 days at 25 or 37o C
  • Urease, and Laccase (induces melanin pigment production from Acetylcholine)
40
Q

clinical manifestations of cryptococcus neogorman
/Diagnosis ;
What CSF shows?

A

Clinical:
• Meningitis: Slow, insidious onset, with non-specific findings
• Intermittent headache, irritability, dizziness
-difficulty with complex cerebral functions, and
behavior changes (D/D psychosis)
• Seizures, cranial nerve signs, papilledema

 • CSF:
 - Increased pressure
 - Lymphocyte pleocytosis (> 100 cells)
- Decreased glucose
- Capsule stain (Indian Ink); 50% +ve
- Use > 30 ml of CSF for culture (because of very scanty organisms/ml)
- GXM polysacchare in CSF or serum (S/S; antigen titer- 
prognostic if rising) 
- PCR (improves the diagnosis)
41
Q

ttt of cryptococcus neogormans?

A

• Fluconazole

  • 75% respond properly
  • Relapses: Significant %, require repeated courses of therapy
  • 50% of the cured : Have residual neurologic damage.

CNS (4 decks)

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