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Y2B4 - Central Nervous System πŸ“™ > Microbiology 🦠 > Flashcards

Microbiology 🦠 Flashcards

1
Q

what is meningitis?

A

Inflammation of the meninges.

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2
Q

what are the types of meningitis?

A

Three different types of meningitis exist based on manifestations & etiology:

  1. Acute bacterial meningitis
  2. Chronic meningitis
  3. Aseptic (viral) meningitis
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3
Q

what causes acute bacterial meningitis?

A
  • bacterial infection
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4
Q

what is acute bacterial meningitis associated with?

A

Marked acute inflammatory bacterial exudate

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5
Q

what do the causes of acute bacterial meningitis Depend on?

A

The common causes depend on age, immune status, and whether infection is community acquired or nosocomial.

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6
Q

what causes chronic meningitis?

A

slow-growing agents (Mycobacteria or fungi).

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7
Q

examples of chronic meningitis

A

Mycobacterium tuberculosis: the most common cause.

Cryptococcus neoformans: the most common cause of chronic meningitis in AIDS patients

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8
Q

what is the most common type of meningitis?

A

Aseptic (viral) meningitis

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9
Q

what causes aseptic meningitis?

A

result from a viral infection.

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10
Q

examples of viral causes of aseptic meningitis

A

Echoviruses and Coxsackieviruses A & B are the most common.

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11
Q

clinical picture of meningitis

A
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12
Q

and what is considered as a fourth type of meningitis?

A

Neonatal meningitis

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13
Q

diagnosis of neonatal meningitis

A
  • based on the age of the infant, manifestations and laboratory tests
  • these indicate whether the infant has aseptic viral meningitis or acute bacterial meningitis
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14
Q

what are the causes of neonatal Meningitis?

A
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15
Q

what is the most common cause of neonatal viral meningitis?

A

enteroviruses

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16
Q

what is the most common cause of neonatal bacterial meningitis?

A

streptococcus agalactiae & Escherichia Coli

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17
Q

what species of bacteria cause acute bacterial meningitis?

A

More than 50 species of bacteria can cause acute bacterial meningitis. However, five species cause ~90% of cases:

  • Streptococcus agalactiae
  • Haemophilus influenzae
  • Streptococcus pneumonia
  • Neisseria meningitidis
  • Listeria monocytogenes
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18
Q

what are the types of acute bacterial meningitis?

A

Community-acquired and nosocomial

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19
Q

which bacteria Cause Neonatal meningitis?

A
  1. Streptococcus agalactiae (Group B streptocci) Most common
  2. Escherichia coli strain K1
  3. Listeria monocytogenes
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20
Q

Which bacteria cause community acquired acute bacterial meningitis in children older than one month??

A
  1. Haemophilus influenza type b Most common
  2. Streptococcus pneumoniae
  3. Neisseria meningitidis
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21
Q

which bacteria cause acute bacterial meningitis in adults?

A
  1. Streptococcus pneumoniae (most common)
  2. Neisseria meningitidis
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22
Q

which bacteria cause nosocomial acute bacterial meningitis in children older than one month?

A
  • Gram-negative bacilli (especially Escherichia coli)
  • Staphylococcus aureus (following endocarditis)
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23
Q

what was the leading cause of bacterial meningitis before 1990s?

A
  • H. influenzae was the leading cause of bacterial meningitis, but an effective childhood vaccine reduced number of cases by >90%.
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24
Q

what are the more prevalent causes of bacterial meningitis nowdays?

A
  • Today, S. pneumoniae & N. meningitidis are the more prevalent causes of bacterial meningitis.
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25
Q

what is acute purulent meningitis caused by?

A

encapsulated pathogen

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26
Q

morphology of Neisseria Meningitidies (Meningococcus)

A
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27
Q

Culture of Neisseria Meningitidies (Meningococcus)

A
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28
Q

Virulence factor of Neisseria Meningitidies (Meningococcus)

A

Polysaccharide capsule: the most important virulence factor
- Anti-phagocytic.
- 12 different capsular antigens exist, but serogroups A, B, C, W135, and Y are responsible for most cases of the disease.

Pili (fimbriae): fine hair-like projections important for initial attachment to host cells.

Endotoxin or lipooligosaccharide (LOS): mediates damage to body tissues and is responsible for inflammation, fever, vasodilation, shock, and widespread blood clotting.

Outer membrane proteins: facilitate adherence to host cells & blocks host serum bactericidal IgG action against the organism.

IgA protease: cleaves IgA on mucosal Surfaces.

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29
Q

what is Neisseria Meningitidies (Meningococcus) associated with?

A
  • Epidemic forms of meningitis
  • Neisseria meningitidis is also known as meningococcus.
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30
Q

what does Neisseria Meningitidies (Meningococcus) cause?

A

It causes the most serious form of acute meningitis (can kill within 6 hours of the initial symptoms, allowing little time for treatment, with mortality rate of ~100% in untreated patients).

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31
Q

where is Neisseria Meningitidies (Meningococcus) common?

A

common in crowded living environments e.g., day care facilities, college dormitories & military training camps.

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32
Q

reservoir of infection by Neisseria Meningitidies (Meningococcus)

A

humans (case or carrier).

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33
Q

Mode of transmission of Neisseria Meningitidies (Meningococcus)

A

inhalation of infected droplets.

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34
Q

portal of entry of Neisseria Meningitidies (Meningococcus)

A

upper respiratory tract (nasopharynx).

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35
Q

risk factors of infection by Neisseria Meningitidies (Meningococcus)

A
  1. Prolonged contact with a carrier.
  2. Recent viral upper respiratory tract infection.
  3. Complement deficiency.
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36
Q

pathogenesis of infection by Neisseria Meningitidies (Meningococcus)

A
  • Upon reaching the nasopharynx, meningococci use pili to adhere to mucosa.
  • In many people, this result in simple asymptomatic colonization.
  • In more vulnerable people, meningococci are engulfed by epithelial cells of the mucosa & penetrate into the nearby blood vessels.
  • Damage to epithelium causes pharyngitis & the pathogen continues its way to meninges utilizing the previously mentioned virulence factors to maintain infection & produce symptoms of meningitis.
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37
Q

complications of Neisseria Meningitidies (Meningococcus)

A
  • The most serious complications are due to meningococcemia, which can accompany meningitis or occur on its own.
  • Meningococcemia has a sudden onset, fever >40Β°C, chills, delirium, severe widespread ecchymosis (areas of bleeding under the skin larger than petechiae), shock.
  • The pathogen releases endotoxin in blood β†’ potent stimulation of WBCs β†’ release cytokines β†’ damage to blood vessels β†’ vascular collapse, hemorrhage, petechiae on trunk & appendages.
  • Generalized intravascular clotting, cardiac failure & death can occur within a few hours.
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38
Q

treatment of Neisseria Meningitidies (Meningococcus)

A
  • Penicillin is the drug of choice because of its anti meningococcal activity and good CSF penetration.
  • Resistance mediated by both Ξ²- lactamase and altered penicillin- binding proteins (PBPs) has been reported but is still extremely rare.
  • Third generation cephalosporins such as cefotaxime are effective alternatives to penicillin.
  • Chloramphenicol or third-generation cephalosporin is used in persons allergic to penicillin .
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39
Q

prevention of infection by Neisseria Meningitidies (Meningococcus)

A
  • Capsular pilysaccharide vaccines (Quadri-valent vaccines)
  • Chemoprophylaxis
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40
Q

what does capsular polysaccharide vaccines contain? and do they not?

A
  • Containing A, C,Y, and W-135 polysaccharides
  • Doesn’t contain group B capsule
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41
Q

Characters of Group B Capsule

A
  • Weakly antigenic (similar to human glycoproteins), and it can cause hypersensitivity reactions as a result of molecular mimicry.
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42
Q

Why are pure polysaccharide vaccines ineffective in young children?

A
  • ineffective in young children, Because immune responses are underdeveloped in the first year of life
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43
Q

Is routine immunization recommended in children?

A

No

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44
Q

What groups of people should take Capsular polysaccharide vaccination of N. menegitides?

A
  • Pilgrims on Hajj or Umrah
  • Military populations
  • Those with predisposing factors such as complement deficiencies or asplenia (removal of spleen)
  • Individuals at age 11-12 years
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45
Q

Chemoprophylaxis of N. menegitides

A
  • Rifampicin is the drug of choice for chemoprophylaxis, but ciprofloxacin has also been effective.
  • Penicillin is not effective, probably because of inadequate penetration of the uninflamed CSF .
  • Close contact with meningococcal meningitis case is indication for chemoprophylaxis.
  • Sulfonamides was used until the development and spread of sulfonamide resistance in the 1960s so not used now
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46
Q

Laboratory diagnosis of N. menegitides

A
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47
Q

Types of clostridium bacteria and what they cause

A

a) Clostridium tetani: cause tetanus.

b) Clostridium botulinum: cause botulism.

c) Clostridium perfringens: cause gas gangrene.

d) Clostridium difficile: cause pseudomembranous colitis.

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48
Q

Morphology of C.Tetani

A
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49
Q

Culture of C.Tetani

A
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50
Q

Morphology of C.Botulinum

A
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51
Q

Culture of C.Botulinum

A
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52
Q

virulence factors of C.Tetani

A

Tetanolysin:

  • A hemolysin that has NO role in pathogenesis.

Tetanospasmin:

  • A neurotoxin responsible for the symptoms of tetanus by blocking the release of inhibitory neurotransmitters (GABA at AHCs) β†’ generalized muscular spasms.
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53
Q

Virulence factors of C.Botulinum

A

Botulinum toxin

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54
Q

MOI of C.Tetani

A

Infection occurs by:
1. Wounding.
2. Tetanus neonatorum.
3. Surgical tetanus.
4. Post abortive tetanus.
5. Idiopathic

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55
Q

Pathogenesis of C.Tetani

A
  • Tetanus results from contamination of injured host tissue with C. tetani spores that germinate and produce tetanospasmin which reaches the CNS along neural axons
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56
Q

C/P of C.Tetani

A
  • Spasms, rigidity of the voluntary muscles and convulsions (trismus, lock jaw) and death occurs due to respiratory failure.
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57
Q

Control & Prevention of C.Tetani

A
  • Tetanus toxoid is used for immunization, as part of DPT vaccine.
  • Three injections are given in the first year (2,4,6) of life, and a booster is given about a year later, and again on the entrance into elementary school.
  • Booster doses are recommended only every 10 years.
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58
Q

Treatment of C.Tetani

A
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59
Q

Diagnosis of C.Tetani

A
  1. Patient should be treated on a clinical basis before the toxin reaches neural tissue.
  2. Sample: tissues from wounds
  3. Direct film stained by Gram stain: show the morphology.
  4. Anaerobic culture on blood agar at 37Β°C: Colonies produce complete haemolysis on blood agar.
  5. Isolation of C.tetani must be confirmed by production of toxin and its neutralization by specific antitoxin.
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60
Q

Is C.Tetani invasive?

A
  • Not invasive –> infection is localized & toxin reaches the CNS along neural axons
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61
Q

where is C.Tetani found?

A
  • Found in soil, intestinal tracts, feces of human & various animals
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62
Q

Characters of C.Tetani spores

A
  • Extremely hard & Resistant to heat, various antiseptics & boiling for minutes
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63
Q

Is tetanospasmin heat liable?

A

Destroyed at 56 degrees in 5 minutes

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64
Q

what is tetanospasmin converted into?

A

Rapidly converted to toxoid in the presence of formalin

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65
Q

Virulence factor of C.Botulinum

A

Botulinum toxin

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66
Q

Characters of Botulinum toxin

A
  • Neurotoxin acts specifically on cholinergic nerves.
  • It acts by preventing the release of acetyl choline at the synapses and at the neuromuscular junctions
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67
Q

what are types of botulism?

A
  • Food borne poisoning
  • Wound botulism
  • Infant botulism (the most common)
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68
Q

what causes food-borne botulism?

A
  • botulinum toxin is ingested with food (specially home canned) in which spores have germinated and the organism has grown.
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69
Q

Characters of wound botulism

A

A rare disease, results from C. botulinum growing in necrotic tissue of wound.

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70
Q

what causes infant botulism?

A
  • By toxins produced by C. botulinum present in the intestine.
  • Honey contaminated with C. botulinum spores.
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71
Q

Incubation period of C. botulinum

A
  • Clinical symptoms of botulism begin 18-36 hours after toxin ingestion.
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72
Q

Mechanism of pathology of C.Botulinum

A
  • The toxin binds to neuromuscular junctions of parasympathetic nerves and interferes with acetylcholine release at motor end plate of cranial nerves, causing flaccid muscle paralysis.
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73
Q

what are the neurological features of C.Botulinum?

A
  • Blurred vision, inability to swallow, difficulty in speech, descending weakness of skeletal muscles, respiratory paralysis and death
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74
Q

Diagnosis of C.Botulinum

A
  • Based on clinical presentation
  • Demonstartion of toxin in food, patient feces, serum or vomitus
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75
Q

Treatment of C.Botulinum

A

Antitoxin therapy should be administereted early

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76
Q

Survival of spores of C.Botulinum

A

Can survive boiling (100 dergrees at 1 atm) for more than 1 hour

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77
Q

what kills the spores of C.Botulinum?

A

by autoclave

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78
Q

Where could the spores of C.Botulinum be found?

A
  • widely distributed in soil and intestinal tract of birds, mammals, and fish
  • Present in vegetables and meat or fish
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79
Q

Sample for diagnosis of bacterial meningitis

A

blood samples aswell

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80
Q

what is CSF examined for? (In diagnosis of bacterial meningitis)

A
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81
Q

Compare between CSF in cases of Acute bacterial meningitis, Aseptic (Viral) meningitis & Mycobacterial meningitis in terms of:

  • Pressure
  • Clarity
  • Protein
  • Glucose
  • CSF:Serumd glucose ratio
  • WBCS
  • WBC differtial
  • Gram stain & Culture
A
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82
Q

Should empiric therapy be initiated in cases of bacterial meningitis?

A

Yes

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83
Q

Direct film in cases of bacterial meningitis

A
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84
Q

Culture in cases of bacterial meningitis

A
85
Q

identification of cultured colonies (In cases of bacterial meningitis)

A
86
Q

what are other techniques for diagnosis of bacterial meningitis?

A
87
Q

Characters of PCR (diagnosis of bacterial meningitis)

A
88
Q

Characters of latex agglutination (diagnosis of bacterial meningitis)

A
89
Q

what do serological tests detect (diagnosis of bacterial meningitis)?

A
90
Q

Sample taken in case of carries (diagnosis of bacterial meningitis)

A

Nasopharyngeal swab

91
Q

Definition of viral meningitis

A
  • Viral meningitis, also known as aseptic meningitis, it is a type of meningitis (inflammation of the membranes covering the brain and spinal cord)due to a viral infection.
92
Q

EHMMI St. Wn

Causative agents of viral meningitis

A

βœ“ Enteroviruses: Echovirus, Poliovirus, Coxsackie A virus

βœ“ Herpes: Herpes simplex virus type 1 (HSV-1 / HHV-1) or type 2 (HSV-2 / HHV-2), Varicella zoster (VZV / HHV-3); also causes chickenpox and shingles (herpes zoster), Epstein–Barr virus (EBV / HHV-4), Cytomegalovirus (CMV / HHV-5).

βœ“ Measles, Mumps, influenza

βœ“ Human immunodeficiency virus (HIV)

βœ“ Lymphocytic choriomeningitis virus (LCMV)

βœ“ St. Louis encephalitis virus, West Nile virus

93
Q

Signs and symptoms of viral meningitis

A
  • Fever
  • headaches
  • Neck stiffness
  • Nausea, vomiting, photophobia (light sensitivity), muscle aches and malaise
  • Increased cranial pressure
94
Q

what causes fever in viral meningitis?

A
  • Fever is the result of cytokines released that affect the thermoregulatory neurons of the hypothalam
95
Q

what causes headache in viral meningitis?

A

(cytokines and increased intracranial pressure stimulate nociceptors in the brain).

96
Q

what causes neck stiffness in viral meningitis?

A
  • Neck stiffness is the result of inflamed meninges stretching due to flexion of the spine
97
Q

what causes Nausea, vomiting, photophobia (light sensitivity), muscle aches and malaise in viral meningitis?

A

meningeal irritation.

98
Q

what is the difference in symptoms between viral and bacterial meningitis?

A

symptoms are often less severe in viral meningitis and do not progress as quickly.

99
Q

what happens in severe infections of viral meningitis?

A
  • people may experience concomitant encephalitis (meningo-encephalitis), which is suggested by symptoms such as altered mental status, seizures or focal neurologic deficits .
100
Q

what are the types of infection by viral meningitis?

A

Primary infection: meningitis is a primary disease caused by these viruses: Poliomyelitis, ECHO, Coxsakie viruses

Secondary infection: meningitis is a complication of these viruses: chicken pox, Mumps, measles viruse

101
Q

Structure of Herpes viruses

A

Virion: Icosahedral.
Genome: Double stranded DNA, linear.
Envelope: with glycoprotein spikes.

102
Q

Classification of Herpes viruses

A

1. Alpha herpesvirinae: Herpes simplex virus and Varicella – Zoster virus.

2. Beta herpesvirnae: Cytomegalovirus, Human herpes viruses (HHV) types 6 and 7.

3. Gamma herpesvirinae: Epstein-Barr virus and Human herpes virus 8.

103
Q

Transmission of Herpes viruses

A
  • HSV-1 is transmitted primarily in saliva, (Mainly orofacial lesions).
  • HSV-2 is transmitted by sexual contact. (Genital lesions).
104
Q

pathogenesis of Herpes viruses

A
  • Multiplies locally in the mucous membrane or a braded skin causing vesicular lesion, However, both types can infect oral or genital mucosa depending on the regions of contact
105
Q

symptoms of primary infection by HSV-1

A
  • Acute gingivostomatitis, Herpes labials (cold sores)
  • Keratoconjunctivitis
  • Herpetic whitlow
  • Encephalitis and disseminated infections, such as esophagitis and pneumonia in immunocompromised patients.
106
Q

what is herpetic whitlow?

A

is a pustular lesion of the skin of finger or hand of medical personnel.

107
Q

Symptomds of primary infection by HSV-2

A
  • Genital herpes
  • Neonatal infection
  • Aseptic meningitis
108
Q

what is genital herpes?

A
  • vesiculo-ulcerative lesions on external genitalia as well as the cervix
109
Q

what causes neonatal infection by HSV-2?

A

Originates chiefly from contact with vesicular lesions within the birth canal

110
Q

Symptoms of neonatal infection by HSV-2

A
  • Neonatal herpes varies from a severe generalized disease often involving the CNS, through milder local lesion to asymptomatic infection.
111
Q

Latency of HSV

A
  • After primary infection, the virus travels via the nerves from the site of infection to the related ganglia as following:
  • HSV-1β†’ Trigeminal ganglia
  • HSV-2β†’ Sacral ganglia
112
Q

what reactivates HSV virus?

A
  • in response to various stimuli as common colds, hormonal changes, and sunlight
113
Q

what happens when HSV virus is reactivated?

A
  1. Reactivation of HSV-1 may lead to: Cold sores and Keratitis.
  2. Reactivation of HSV-2 can occur more frequently, and is often asymptomatic with viral shedding
114
Q

Diagnosis of HSV

A
115
Q

Treatment of HSV

A
  • Acyclovir is the treatment of choice; it shortens the duration of the lesion and decreases shedding
  • No drug treatment prevents recurrences and drugs have no effect on the latent state.
116
Q

Symptoms of primary infection by VZV

A
  • Varicella (chicken pox)
  • Neonatal Varicella
117
Q

IP of chicken pox

A
  • 14-21 days
118
Q

transmission of chicken pox

A

by droplets and by direct contact with
the lesions

119
Q

Clinical findings in chicken pox

A
  • febrile illness with a characteristic vesicular rash which starts on the trunk and spreads to the limbs and face.
120
Q

Vesicles pattern in chicken pox

A

Vesicles appear in successive waves so that the lesions of different stages are present together.

121
Q

Complications of varicella (Chicken pox)

A
  • Complications of Varicella are rare as meningitis, encephalitis and pneumonia.
122
Q

Types of infection by neonatal varicella

A
  • Early in pregnancy
  • Near the time of birth
123
Q

Neonatal varicella early in pregnancy

A

fetal infection is uncommon, but can result in multiple developmental abnormalities (limbs Scarring, damage to the lens, retina and brain and microphthalmia)

124
Q

Neonatal varicella near the time of birth

A
  • Fetal infection is more common and may exhibit typical varicella at birth or shortly there after
  • The severity of the disease depends on whether the mother has begun to produce anti-VZV, IgG by the time of delivery or not.
125
Q

Latency of VZV

A
  • Trigeminal and dorsal root ganglia being most common sites of latency.
126
Q

what happens in case of reactivation of VZV?

A

Zoster or shingles

127
Q

what is zoster?

A
  • a sporadic disease of adults or immunosuppressed patients.
128
Q

Symptoms of zoster

A
  • Painful vesicles along the course of a sensory nerve of the head or the trunk (a belt of roses from hell).
  • The pain can last for weeks, and post-zoster neuralgia may exist.
  • In immunocompromised, disseminated infection as pneumonia can occur.
129
Q

Diagnosis of VZV

A
  • Mainly clinically. But, laboratory diagnosis can be done as on the same line used for HSV.
  • A rise in antibody titer can be used to diagnose varicella, but is less useful in diagnosis of zoster, since antibody is already present.
130
Q

Treatment of VZV

A
  • No antiviral therapy is necessary for chicken pox in normal
  • Systemic disease in immunocompromised patients can be treated with acyclovir
131
Q

Prevention of VZV

A
  • Varicella-Zoster immunoglobulin (VZIG)
  • VZV vaccine
132
Q

Use of VZIG

A
  • Can be used to prevent varicella and disseminated zoster in immunocompromised people exposed to the virus.
133
Q

what is VZV vaccine?

A

a live attenuated vaccine

134
Q

VZV vaccine plan

A

one dose is recommended for children 1 to 12 years of age

135
Q

Significance of VZV vaccine

A
  • Prevents varicella,
  • Zoster still occurs in those previously infected because the vaccine does not eliminate the latent state.
136
Q

Compare between Chicken pox (Varicella) & Shingles (Zoster) in terms of:

  • Def
  • Age of the patient
  • Transmission
  • Type of infection
  • Symptoms
  • Rash
  • Compliaction
A
137
Q

Transmission of Cytomegalovirus (CMV)

A
  • Early in life, transmitted trans placentally, within birth canal and commonly in breast milk.
  • Later in life it is transmitted via saliva (most common route), sexually, by blood transfusion and organ transplants.
138
Q

Clinical syndromes of Cytomegalovirus (CMV)

A
  • Primary infection
  • Latency
  • Reactivation
139
Q

Primary infection of Cytomegalovirus (CMV)

A
  • In healthy individuals
  • In immuno-deficient patients
  • Congenital infection
140
Q

Primary infection of Cytomegalovirus (CMV) in healthy individuals

A
  • Asymptomatic infection: may be associated with intermittent shedding in saliva and urine.
  • Infectious mononucleosis-like syndrome: clinically similar to EBV infection. However, they are heterophile antibodies negative.
141
Q

Primary infection of Cytomegalovirus (CMV) in Immuno-deficient patients

A
  • hepatitis and pneumonia are common. In AIDS patients, diarrhea and retinitis may also occur.
142
Q

Primary infection of Cytomegalovirus (CMV) in congenital infections

A
  • In-utero it causes abortion or still-birth. The disease is characterized by congenital mental retardation, microcephaly, blindness and deafness.
  • Perinatal infection from the birth canal or from the milk usually subclinical infection.
143
Q

what is the most common intrauterine viral infection?

A

CMV

144
Q

Latency of CMV

A

Latency is established in monocytes, macrophages and kidney.

145
Q

what happens when CMV is reactivated?

A
  • Repeated episodes of asymptomatic virus shedding over prolonged periods of times.
146
Q

Diagnosis of CMV

A
  • Virus isolation in cell culture, CPE in the form of typical swollen and translucent cells with intra nuclear inclusion bodies.
  • Fluorescent antibody and histological staining of inclusion bodies in giant cells in urine and in tissue. The inclusion bodies are intranuclear and have an oval-owls eye shape.
  • PCR for detection of CMV nucleic acid in tissues or body fluids e.g. CSF.
  • Serological diagnosis.
147
Q

Treatment of CMV

A
  • Ganciclovir is effective for treatment of retinitis and pneumonia in AIDS patients
148
Q

Transmission of EBV

A
  • By intimate contact with infected saliva.
149
Q

Pathogenesis of EBV

A
  • Viral replication occur in the oropharyngeal epithelium
  • following which some of the progeny virus infect B lymphocytes β€”> polyclonal B cell proliferation and non specific ↑ of IgM (heterophil antibodies that aggregate sheep and horse RBCs), IgG and IgA.
  • Infected B cells are rejected by cytotoxic T cells which change in morphology and appear as atypical T lymphocytes in the peripheral blood.
150
Q

Clinical syndromes of EBV

A
  • Primary infection
  • Latency
  • Reactivation
151
Q

Primary infection by EBV

A
  • Infectious mononucleosis (IM)
  • malignancies
152
Q

what is Infectious mononucleosis (IM) charachterized by?

A
  • Characterized by fever, headache, malaise, pharyngitis, lymphadenopathy and increased levels of liver enzymes in the blood. It lasts several weeks and complete recovery may take much longer.
153
Q

what are malegnancies related to EBV?

A

Burkitt’s lymphoma:
- It is a unique malignancy of the jaw in African children.

Nasopharyngheal carcinoma:
- common among Chinese

Oral hairy leukoplakia:
- benign lesion of the tongue

154
Q

Latency of EBV

A

remains latent in B cells

155
Q

What happens when EBV is reactivated?

A
  • reactivation results in initiation of the viral lytic cycle.
156
Q

Diagnosis of EBV

A
  • Blood smear to detect lymphocytosis and 30% abnormal lymphocytes are seen.
  • DNA hybridization for Detection of EBV in patient’s peripheral lymphocytes
  • Detection of heterophile antibodies which agglutinate sheep erythrocytes (paul-Bunnel test). It is nonspecific test.
  • Detection of EBV specific Abs to viral capsid antigen or EBV nuclear antigen by ELISA.
  • Virus isolation from saliva (difficult and not readily available)
157
Q

Treatment of EBV

A
  • No drug available to treat EBV
  • EBV vaccine is being developed
158
Q

Transmissiom of Mumps

A
  • Spread by person to person via respiratory droplets and saliva, direct contact, or fomites.
159
Q

Incubation period of Mumps

A
  • has a relatively long incubation of (21 days )
160
Q

Clinicl manifestations of Mumps

A
  • It causes a febrile illness and inflammation of the salivary glands, classically the parotid and submandibular glands. The swelling may be asynchronous, and lasts about 1 week.
161
Q

Complications of Mumps

A

Aseptic meningitis: fairly common complication. In about half of the mumps meningitis cases, parotitis will not be apparent.

Mumps meningoencephalitis: is rarer but a more serious development.

Orchitis: can occur, more often after puberty, unilateral or bilateral, but is rarely followed by infertility, Other glandular tissue is very occasionally involved e.g.. pancreatitis, oophoritis or thyroiditis.

162
Q

Diagnosis of Mumps

A
  • Isolation of the virus from saliva, CSF or urine by culture on monkey kidney cells.
  • Serologically: Confirmed Diagnosis by positive IgM antibodies by using CF, HI,ELISA
163
Q

Transmission of Measles

A
  • Measles is one of the most infectious diseases known.
  • Transmission is by respiratory droplets. After infecting the cells lining the upper respiratory tract, the virus enters the blood and spreads to the skin.
  • The virus can also infect via the eye and multiply in the conjunctivae.
164
Q

IP of Measles

A

10-12 day.

165
Q

Clinical manifestations of Measles

A
  • Prodromal phase is characterized by fever, dry cough, sore throat, conjunctivitis, and Koplik’s spots (raised red spots with white centers in the mouth). After few days, the characteristic red, maculopapular rash starts on the head and then spreads to body.
166
Q

Complications of Measles

A
  • Bronchopneumonia and otitis media (with or without secondary bacterial infections).
  • Encephalitis occurs in ~1:2000 cases.
  • Subacute sclerosing pan- encephalitis: It is a chronic infection in which the virus multiplies in the brain resulting in neurodegenerative disease.
167
Q

Diagnosis of Measles

A
  • Easy to diagnose clinically.
  • Laboratory diagnosis is rarely needed.
168
Q

Prevention of Mumps & Measles

A
  • Trivalent live attenuated vaccine (MMR) is usually given by subcutaneus injection. It is given at 12 – 15 months age. A single dose of the MMR vaccine gives around 90% protection against measles and mumps and 95-99% against rubella.
169
Q

Diagnosis of viral meningitis

A
170
Q

Treatment of viral meningitis

A
171
Q

Definition of Encephalitis

A
  • Inflammation of the brain parenchyma, associated with clinical evidence of brain dysfunction usually a result of viral infection.
172
Q

Definition of Meningitis

A

Inflammation of the meninges

173
Q

Definition of Meningoencephalitis

A
  • Inflammation of the meninges and brain parenchyma.
174
Q

What are the causes of Encephalitis?

A
175
Q

what are the types of viral encephalitis?

A
  • Primary Encephalitis
  • Secondary Encephalitis
176
Q

Definition of Primary viral Encephalitis

A
  • direct viral infection of the brain & spinal cord
177
Q

Causes of Primary viral Encephalitis

A

1- Eastern equine encephalitis virus

2- Western equine encephalitis virus (Rare in Egypt due to cross immunity with West Nile Fever Virus)

3- Rabies virus

4- La Crosse encephalitis virus

178
Q

Definition of Secondary Viral Encephalitis

A

A Viral infection first occurs elsewhere in the body then travels to the brain.

179
Q

Causes of Secondary Viral Encephalitis

A
  • Measles
  • rubella
  • Varicella zoster Virus.

NB: May results from a faulty immune system reaction to an infection elsewhere in the body (post-infection encephalitis).

180
Q

Family of Polio virus

A
  • Picornaviridae
181
Q

Morphology of Polio virus

A
  • single-stranded small RNA virus
  • icosahedral capsid
  • nonenveloped
182
Q

Mode of infection by Polio virus

A
  • Ingestion of contaminated food and drink by faces
183
Q

Pathogenesis of Polio virus

A
  • inflammation within the grey matter of the brain stem
184
Q

Family of Mumps and measles

A
  • Paramyxoviridae
185
Q

Morphology of Mumps and measles

A
  • One piece of single stranded RNA
  • A helical nucleocapsid
  • An outer lipoprotein envelope
186
Q

Mode of infection by Mumps & Measles

A

respiratory route

187
Q

Pathogenesis of Mumps

A

Mumps meningoencephalitis

188
Q

Pathogenesis of Measles

A

The acute post-infectious encephalitis, measles inclusion-body encephalitis and subacute sclerosing panencephalitis

189
Q

What does Rhabdo mean in Greek?

A

rod-shaped

190
Q

Morphology of Rhabdovirses

A
191
Q

Mode of transmission of Rhabdoviruses

A
  • by bite of an infected rabid animal (Rabies virus in dog’s saliva, Zoonotic infection).
192
Q

What are hosts of Rhabdoviruses?

A

foxes,dogs,cats,bats,camels.

193
Q

Pathogenesis of Rhabdoviruses

A
  • The virus enters from wound or abrasion of skin (site of the bite) directly into blood.
  • Primary replication of the rabies virus occurs locally in muscle & connective tissue (no symptoms
  • Virus then infects peripheral nerves {PNS} then travels along neuronal axons to CNS
194
Q

Symptoms of infection by Rhabdoviruses

A
  • produce photophobia, hydrophobia, severe and fatal encephalitis.
  • Few cases escape these severe consequences.
195
Q

IP of Rhabdoviruses

A
  • varies from 3-8 weeks to 1 year depending on size & site of inoculation (head/face/neck vs. hands or feet).
196
Q

Diagnosis of Rhabdoviruses

A
  • Specimen: infected tissue (brain).

1) Detection of viral antigens or nucleic acid: IF & PCR.

2) Histopathological diagnosis: by detection of Negri bodies in the brain or spinal cord.

3) Isolation of the virus: infected tissue is inoculated into a suckling mice result in encephalitis & death.

197
Q

Treatmet & Vaccination of Rhabdoviruses

A
  • In veterinary medicine: rabies vaccines are used as a preventive measure.
  • Vaccination of humans mainly after exposure to a rabid animal (not to prevent infection
    but to moderate the severity of the disease).
  • In the case of severe exposure: vaccination is often accompanied by injection of rabies
    immunoglobulin (IG)
198
Q

what are human vaccines of Rhabdoviruses?

A
  • Nerve Tissue vaccine
  • Duck embryo vaccine
  • HDC vaccine
199
Q

Nerve tissue vaccine

A
  • Infected sheep, goat, or mouse brains ➱ Post vaccination encephalitis
200
Q

Duck embryo vaccine

A

Growing the virus in embryonated duck eggs ➱ 21 injections

201
Q

HDC vaccine

A

Diploid human fibroblasts (effective & safe but expensive) ➱ 6 injections

202
Q

what is the type of candida?

A

opportunistic

203
Q

Morphology of candida

A

Yeast like fungi: budding cells &form chains of broad- spectrum pseudo-hyphae.

204
Q

Mode of infection by candida

A
  • usually endogenous but cross infection can occur
205
Q

Pathogenesis of candida

A
  • Candida has a predilection for the microcirculation, classically resulting in multiple cerebral micro-abscesses
206
Q

Type of Cryptococcus

A

opportunistic

207
Q

Mode of infection by Cryptococcus

A
  • Inhalation of spores (organisms found in soil and often associated with pigeon droppings or trees)
208
Q

Pathogenesis of Cryptococcus

A

Fulminant meningoencephalitis occurs commonly in the setting of advanced immunosuppression (frequently associated with advanced HIV disease)

209
Q

Morphology of cryptococcus

A

Encapsulated yeast:

  • oval or round single cells reproduce by asexual budding

Y2B4 - Central Nervous System πŸ“™ (8 decks)

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