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MNI (immuno path) > L34- Multi-system Infections IV > Flashcards

L34- Multi-system Infections IV Flashcards

1
Q

desribe the following features of Coxsackievirus A, B:

  • family
  • genome
  • structure and size –> relationship with surviving environment
A

Picornaviridae family: (+)ssRNA

  • naked (non-enveloped), icosahedral capsid
  • relatively small (25-30nm)

-Since Naked: survives wide range pH (3-9), detergents, mild sewage treatment, heat

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2
Q

Coxsackievirus A, B:

  • (1) reservoirs
  • (2) common areas / locations it is usually found / spread
  • (3) common season of transmission
  • (4) are the most susceptible to severe infection
  • (5) unique feature of viral shedding
A 
1- humans
2- lower SES areas, schools / daycares
3- summer
4- neonates
5- intestinal viral shedding for 30 days (or longer), possibly asymptomatic
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3
Q

Coxsackievirus A, B:

  • (1) route of transmission
  • viral replication initially starts in (2) and continues in (3) –> leading to (4)
  • viruses then infect (5) leading to (6)
A

1- fecal-oral transmission
2- mucosa and lymphoid tissue of tonsils and pharynx
3- M cells and lymphocytes in Peyer’s patches + enterocytes in intestinal mucosa
4- 1st viremia (+ shedding)

5- RES cells (LNs, spleen, liver)
6- 2nd viremia

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4
Q

Coxsackievirus A, B:

  • after the 2nd viremia, viruses bind to (1) receptors, causing a (2) type infection in those cells
  • replication occurs in the (cytosol/nucleus) and (4) is synthesized to form viral proteins in a (5) timeframe
A

1- ICAM-1, CD-55
2- lytic infections

3- cytosol
4- polyprotein
5- 10-15 mins after infecting cells

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5
Q

describe the major protective response to Coxsackievirus A, B and the role of each type

A

Antibodies:
-Secretory Abs: prevents initial infection in oropharynx and GIT

-Serum Abs: prevents viremic spread to target tissues –> and thus the disease

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6
Q

list the factors that affect the clinical syndromes caused by Coxsackievirus A, B

A
  • viral serotype, tissue tropism
  • portal of entry, infecting dose
  • age, gender, immune/disease status
  • pregnancy
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7
Q

Coxsackievirus A, B:

  • (1) incubation period
  • (2) are the possible syndromes from A type
  • (3) are the possible syndromes from B type
A

1- 1-35 days

2- herpangina, hand-foot-and-mouth disease

3- pleurodynia, myocardial and pericardial infections

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8
Q

Herpangina:

  • (1) pathogen
  • (2) is the classic / hallmark finding
  • (3) are the other associated symptoms
  • (4) treatment
A

1- coxsackievirus A

2- vesicular ulcerated lesions around soft palate, uvula (uncommonly hard palate)

3- fever, sore throat, dysphagia –> anorexia, vomiting

4- self-limiting, Sx management

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9
Q

Hand-Foot-and-Mouth disease:

  • (1) pathogen
  • (2) is main finding, (3) is mild but usually present
  • (4) progression
A

1- coxsackievirus A16
2- vesicular exanthema on hands, feet, mouth
3- mild fever
4- self-limiting, subsides in few days

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10
Q

coxsackievirus A16 is the main cause of…..

A

hand-foot-and-mouth disease

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11
Q

Pleurodynia, aka (1):

  • (2) pathogen
  • (3) initial symptoms
  • (4) other symptoms
  • (5) progression
A

1- Bornholm disease, ‘devil’s grip’
2- coxsackievirus B

3- sudden onset fever, unilateral lower thoracic pleuritic chest pain (excruciating)
4- abdominal pain, vomiting, malaise, muscle tenderness

5- last 4 days —> may relapse after asymptomatic period

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12
Q

In addition to pleurodynia, coxsackievirus B virus is also known to cause (1), mostly affecting (2) people- age. (3) symptoms will most always present, and (4) symptoms may also appear. (5) is the main progression that treatment tries to prevent.

A

1- myocardial and pericardial infections
2- elderly, young children, neonate (life threatening)

3- febrile illness, sudden unexplained heart failure
4- cyanosis, tachycardia, cardiomegaly, hepatomegaly
5- infection associated mortality (high in these patients)

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13
Q

Coxsackievirus A, B diagnosis:

  • mainly by (1) method
  • (2) are alternatives

-(3) is results from CSF sample (aseptic meningitis), compared to (4) results from bacterial meningitis

A

1- serology
2- culture (not always possible), ELISA, RT-PCR

3- elevated glucose, elevated proteins
4- low glucose, elevated proteins

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14
Q

HHV-4 = (1):

  • (2) family
  • (3) genome and structure
A

EBV- epstein-barr virus

  • gamma-herpesviridae subfamily
  • linear dsDNA, enveloped
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15
Q

EBV:

  • (1) is most common route of transmission
  • (2) is the most common clinical manifestation
  • (3) may occur after (2)
  • (4) are the dangerous complications that develop from previous EBV infection
  • (5) incubation time
A

1- saliva (blood, semen, transfusions, transplants are others)

2- infectious mononucleosis (Mono)

3- latent infection — can be reactivated later in life

4- B cell lymphomas, hairy oral leukoplakia

5- up to 2 mos

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16
Q

describe the distribution of EBV infections among the US population

A
  • 70% people <30 y/o are infected

- 90% of infected people shed EBV for life (even if totally asymptomatic)

17
Q

list the many symptoms of EBV infections, mark hallmark symptoms

A

(Note- more mild in younger patients)

  • *cervical lymphadenopathy
  • *splenomegaly (avoid trauma to avoid rupture)
  • HA, fatigue
  • fever, malaise
  • inflamed throat
  • swollen liver
  • rash
18
Q

EBV enters cell via (1) process and then travels to (2). It then employs (3) to allow expression of (4) in order to transcribe and replicate viral DNA, occurring in (cytoplasm/nucleus). (6) are the final products of viral DNA transcription.

A 
1- fusion and capsid release
2- nucleus
3- α-proteins: early gene expression
4- β-proteins (via early genes) --> DNA replication 
5- nucleus
6- γ-proteins: structural proteins
19
Q

EBV binds (1) receptor on tonsillar B cells, where (1) usually binds (2). (3) is the result of this interaction and (4) are employed to control (3), and yield the Mono symptoms.

A

1- CD21 receptor (B cells)
2- C3d complement
3- B cell growth
4- CD8+ cytotoxic T cells control B cell overgrowth (Abs have limited role in controlling infection)

20
Q

list the causative associations EBV has (hint- 4)

A
  • lymphoma, immuno-compromised
  • African Burkitt’s lymphoma, children
  • nasopharyngeal carcinoma, China
  • oral hairy leukoplakia, HIV pts - non-cancer
21
Q

the cellular response typical of infectious mononucleosis caused by EBV is due to….

A

proliferation of Tc cells responding to EBV Ags expressed on surface of B cells

22
Q

EBV clinical manifestations:

  • (1) most common, as seen in most children
  • (2) is the classic triad
  • (3) other symptoms
  • (4) complications
A

1- asymptomatic / subclinical disease

2- lymphadenopathy, splenomegaly, exudative pharyngitis

3- fever, malaise, fatigue, hepatosplenomegaly (rash after ampicillin Tx)

4- Neurological disorders (eg. Guillain-Barre), laryngeal obstructions, **ruptured spleen

23
Q

EBV Dx:

  • (1) is for quick screening
  • (2) is the main test —- (3) is if symptoms resemble EBV, but (2) is negative
A

1- monospot test (rapid Dx)

2- presence of heterophile Ab (against viral Ag to viral DNA)
3- CMV infection

24
Q

HHV-5 = (1):

  • (2) family
  • (3) genome and structure
A

CMV, cytomegalovirus:

  • beta-herpesviridae subfamily
  • linear dsDNA, enveloped
25
Q

______ is the typical histological sign of cells infected with CMV

A

owl-eye appearance: nucleus with perinuclear clearing (cytomegalic cells)

26
Q

CMV:

  • (1) discuss distribution in developed countries
  • (2) route of transmission
  • (3) incubation period
  • (4) is typical clinical manifestation
  • (5) is unique result of infection in terms of timeline
A

1- 40-100% adults have CMV Abs
2- contact with infected: urine, saliva, breast milk, tears (semen, genital secretions)

3- 4-8 wks
4- subclinical — asymptomatic shedding
5- lifelong infections

27
Q

CMV will infect and replicate in (1) cells initially before persisting in (2) cells. Viral replication is usually (rapid and short / slow and long) and infection can spread via (4). (5) is unique characteristic in terms of viral shedding.

A

1- epithelial cells of respiratory tract, salivary glands, kidneys
2- lymphocytes

3- slow and long
4- spreads from cell to cell
5- shedding in pharynx / urine can last mos-yrs after primary infection

28
Q

compare the alternate names of EBV and CMV infections

A

EBV- heterophile-positive infectious mononucleosis

CMV- heterophile-negative infectious mononucleosis

29
Q

in terms of clinical features of CMV:

  • it is linked with (1) operation failures
  • in immuno-compromised it may cause the following: (2)
A

1- kidney transplant failures

2- (moderately compromised) pneumonia/pneumonitis // (severely compromised - AIDS) retinitis, colitis, oesophagitis

30
Q

______ is the main risk or clinical relevance of CMV infections, explain

A

Most prevalent viral cause of congenital disease:

  • small size, thrombocytopenia, microencephaly, intercerebral calcification, jaundice, hepatosplenomegaly, rash
  • ***vision or hearing loss with mental retardation

NOTE- worse if mother had primary infection during pregnancy

31
Q

CMV Dx:

  • samples are taken from (1)
  • (2) is the main sign in infected cells
  • (3) is a useful clinical sign
  • (4) is the standard test of diagnosis
A

1- saliva, urine
2- owl-eyes in cytomegalic cells
3- cotton wool retina (ophthalmoscopy)
4- ELISA (EM microscopy is expensive alternative to visualize virus)

MNI (immuno path) (14 decks)

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