L34- Multi-system Infections IV Flashcards
desribe the following features of Coxsackievirus A, B:
- family
- genome
- structure and size –> relationship with surviving environment
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
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
1- humans 2- lower SES areas, schools / daycares 3- summer 4- neonates 5- intestinal viral shedding for 30 days (or longer), possibly asymptomatic
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)
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
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
1- ICAM-1, CD-55
2- lytic infections
3- cytosol
4- polyprotein
5- 10-15 mins after infecting cells
describe the major protective response to Coxsackievirus A, B and the role of each type
Antibodies:
-Secretory Abs: prevents initial infection in oropharynx and GIT
-Serum Abs: prevents viremic spread to target tissues –> and thus the disease
list the factors that affect the clinical syndromes caused by Coxsackievirus A, B
- viral serotype, tissue tropism
- portal of entry, infecting dose
- age, gender, immune/disease status
- pregnancy
Coxsackievirus A, B:
- (1) incubation period
- (2) are the possible syndromes from A type
- (3) are the possible syndromes from B type
1- 1-35 days
2- herpangina, hand-foot-and-mouth disease
3- pleurodynia, myocardial and pericardial infections
Herpangina:
- (1) pathogen
- (2) is the classic / hallmark finding
- (3) are the other associated symptoms
- (4) treatment
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
Hand-Foot-and-Mouth disease:
- (1) pathogen
- (2) is main finding, (3) is mild but usually present
- (4) progression
1- coxsackievirus A16
2- vesicular exanthema on hands, feet, mouth
3- mild fever
4- self-limiting, subsides in few days
coxsackievirus A16 is the main cause of…..
hand-foot-and-mouth disease
Pleurodynia, aka (1):
- (2) pathogen
- (3) initial symptoms
- (4) other symptoms
- (5) progression
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
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.
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)
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
1- serology
2- culture (not always possible), ELISA, RT-PCR
3- elevated glucose, elevated proteins
4- low glucose, elevated proteins
HHV-4 = (1):
- (2) family
- (3) genome and structure
EBV- epstein-barr virus
- gamma-herpesviridae subfamily
- linear dsDNA, enveloped
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
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
describe the distribution of EBV infections among the US population
- 70% people <30 y/o are infected
- 90% of infected people shed EBV for life (even if totally asymptomatic)
list the many symptoms of EBV infections, mark hallmark symptoms
(Note- more mild in younger patients)
- *cervical lymphadenopathy
- *splenomegaly (avoid trauma to avoid rupture)
- HA, fatigue
- fever, malaise
- inflamed throat
- swollen liver
- rash
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.
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
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.
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)
list the causative associations EBV has (hint- 4)
- lymphoma, immuno-compromised
- African Burkitt’s lymphoma, children
- nasopharyngeal carcinoma, China
- oral hairy leukoplakia, HIV pts - non-cancer
the cellular response typical of infectious mononucleosis caused by EBV is due to….
proliferation of Tc cells responding to EBV Ags expressed on surface of B cells
EBV clinical manifestations:
- (1) most common, as seen in most children
- (2) is the classic triad
- (3) other symptoms
- (4) complications
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
EBV Dx:
- (1) is for quick screening
- (2) is the main test —- (3) is if symptoms resemble EBV, but (2) is negative
1- monospot test (rapid Dx)
2- presence of heterophile Ab (against viral Ag to viral DNA)
3- CMV infection
HHV-5 = (1):
- (2) family
- (3) genome and structure
CMV, cytomegalovirus:
- beta-herpesviridae subfamily
- linear dsDNA, enveloped
______ is the typical histological sign of cells infected with CMV
owl-eye appearance: nucleus with perinuclear clearing (cytomegalic cells)
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
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
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.
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
compare the alternate names of EBV and CMV infections
EBV- heterophile-positive infectious mononucleosis
CMV- heterophile-negative infectious mononucleosis
in terms of clinical features of CMV:
- it is linked with (1) operation failures
- in immuno-compromised it may cause the following: (2)
1- kidney transplant failures
2- (moderately compromised) pneumonia/pneumonitis // (severely compromised - AIDS) retinitis, colitis, oesophagitis
______ is the main risk or clinical relevance of CMV infections, explain
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
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
1- saliva, urine
2- owl-eyes in cytomegalic cells
3- cotton wool retina (ophthalmoscopy)
4- ELISA (EM microscopy is expensive alternative to visualize virus)
