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viruses topics Flashcards

1
Q

III.11 Adenovirus characteristics

A
  • dsDNA (L)
  • Icosahedral capsid
  • Non-enveloped
  • Surface Fibers (toxic Ag’s): attachment to rec. & agglutination of RBCs
  • 57 serotypes (# 14 most severe), differentiated by hemagglutinin inhibition
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2
Q

III.11 Adenovirus Transmission

A
  • Occurs worldwide
  • Naked virus: resistant to drying, detergents, GI secretions

• Fecooral, Aerosol, fingers, close contact
(Crowded places: daycare, military camps, sports clubs)

• Mostly asymptomatic infections (enhanced spread)

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3
Q

III.11 Adenovirus Pathogenesis

A

Pentons of the icosahedral capsid contains fibers that acts as hemagglutinin (toxic to cells)

  • In permissive cells: replication –> production –> cell lysis
  • In non-permissive cells: can be chronic or oncogenic (transformation occurs but not in humans)
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4
Q

III.11 Adenovirus Clinical

A

a) Respiratory diseases:
-Tonsillitis: #1 cause
-Acute febrile pharyngitis: in infants and young children (Sore throat, fever, myalgia, cough)
-Pharyngoconjunctival fever (7-14y children)
-Pneumonia: possible complication of the above
-Pertussis-like synd.
-Acute respiratory disease: Fever, cough, myalgia, fatigue,
cervical lymphadenomegaly

b) Gastroenteric infection:
- Gastroenteritis: Watery diarrhea in infants and children

c) Eye infection:
- conjunctivitis: Mild, either following RTI or develops alone
- ->Watery, itchy, Painful, Photosensitivity, heals rapidly. (1 eye or both)
- ->highly contagious, spread by: coughing, sneezing, Swimming pools
- ->Irritation of the eye –> other infections

d) UTI:
- Acute hemorrhagic cystitis: with dysuria, hematuria

e) Immunosuppressed patients: Disseminated infections (Pneumonia, Hepatitis)
* Reactivation can occur in case of immunosuppressed patients

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5
Q

III.11 Adenovirus Ddx

A

• mostly not identified
• In some cases it can be important to rule out other pathogens (to prevent unnecessary Abx)
• Immunoassays: IF, ELISA
• PCR
• Rapid test: for diarrhoea causing viruses
-Cultivation on HeLA, epithelial cell culture –> strong CPE

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6
Q

III.11 Adenovirus treatment

A

-No approved treatment
(just Symptomatic therapy and fluid replacement)

  • Riba.virin: for disseminated infections
  • Live vaccine: pills for military
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7
Q

III.12 Herepesvirus : HSV1 and HSV2 characteristics

A
  • Alpha-Herpesvirinae (Ubiquitous viruses, frequent infections)
  • Herpes Simplex Viruses
  • dsDNA (L)
  • Icosahedral capsid
  • Enveloped: Sensitive to acid, detergents etc.
  • Produce Virokins: cytokin-like proteins for pathogenesis –> suppress immun. resp.
  • Infections can be: Lytic, latent-recurrent, persistent, immortalising
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8
Q

III.12 Herepesvirus : HSV1 and HSV2 Transmission

A
  • Close contact
  • Saliva
  • Vaginal secretions
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9
Q

III.12 Herepesvirus : HSV1 and HSV2 Pathogenesis

A

• 80% HSV1 (+)
• 20% HSV2 (+)
- Primary (acute) infection of mucosus membranes: The virus targets Mucoepithelial cells
- Lifelong latent infection in DRG of innervating neurons
- Recurrent infection: by stress, trauma, sunlight, fever, immunosupp.

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10
Q

III.12 Herepesvirus : HSV1 clinical

A

a) Primer Herpetic Gingivo-ostomatitis:
- Childhood disease (1st HSV1 exposure)
- Multiple painful oral lesions: prodrome -> macule -> vesicle -> ulcer -> scar -> healing
- Symp.: pharyngitis, fever, Local lymphadenopathy

b) Herpes Labialis (cold sores):
- Recurrent infc. of lips with HSV1
- Less severe & shorter than primer infc.
- Course: prodrome –> vesicles –> ulcer –> crust –> heals (without scar)

c) Herpetic keratitis:
- Recurrent Ulceration of cornea (possible blindness)
- UV light Detection: Eyedrops containg fluorescent labelled Ab’s vs. HSV

d) Herpetic Whitlow (gladiatorum):
- Infection of fingers and body (Former injury needed)
- at risk: Nurses, dentists, wrestlers

e) Herpes Encephalitis:
- HSV1
- Location: temporal lobe (high mortality)
- -> Haemorrhagia, seizures, other CNS complications

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11
Q

III.12 Herepesvirus : HSV2 clinical

A

a) Genital herpes:
- Primer & recurrent infc. by HSV2 (rarely HSV1)
- Location: Glans, vulva, vagina, cervix, perianal, rectum
- Primer infc. accompanied by fever, myalgia, Lyphadenomegaly
* Meningitis may develop – not severe)
* Virus shed also possible in the asymp. periods

b) Neonatal herpes:
- From the mother’s genital herpes
- transmission: during vaginal delivery or ascending infc. (rarely) during pregnancy
- Lead to: Stillbirth, generalised infc. , skin vesicles, Encephalitis, internal organ affection, high mortality
- Prevention: cesarean section

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12
Q

III.12 Herepesvirus : HSV1 and HSV2 ddx

A
  • Clinical symp’s
  • Direct examination of sample:
  • micro for CPE (Cultivation: Scraping the base of lesions –> cultivation on HeLA –> CPE to find inclusion bodies, rounded cells, syncytia, Lysis)
  • IF Ag’s detection
  • PCR
  • Virus isolation: from vesicles (not crusted lesions) –> Aspiration or swab sample onto cell cultures
  • Serology: ONLY for primer infections & epidemiology
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13
Q

III.12 Herepesvirus : HSV1 and HSV2 treatment

A

• Nucleoside analogues: A.cyclovir, vala.cyclovir, pen.cyclovir (inhibition of DNA synthesis)
–> local or systemic -depends on severity-

  • Can’t eliminate the latent viruses
  • Resistance may develop
  • Prevention: avoid close contact
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14
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus characteristics

A
  • α-herpesvirus
  • Human herpes virus 3
  • dsDNA (L)
  • Icosahedral capsid
  • Enveloped
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15
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus transmission

A

by inhalation of resp. droplets (or contact with vesicules)

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16
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus Pathogenesis

A
  • Virus replicates in the resp. tract –> spread via bloodstream to RES (no symp. yet) –> secondary viraemia after 2 w. skin symptoms –> Primer infection: chickenpox (dermal vesiculopapular rash)
  • Establish latent infection in neurones of DRG or cranial nerve ganglia –> Reactivates in old or imunocompromissed –> herpes zoster Shingles (May disseminate)
  • Life-long infection
  • Cell-mediated immunity important in control
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17
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus Clinical

A
  • Highly contagious before and during symp.
  • 90% get infected during life with VZV
  • 10-20% experiences herpes zoster reactivation

Clinical picture:
• Primary infection: Chickenpox (Varicella)
- Classic childhood disease (2 w incubation)
- Fever, maculo-papular itchy rash all over the body (scalp, mucosa)
- Vesicles on erythematous base –> pustule –> crust –> healing
- Asynchronous rash: Any given time all stages present!
- Scratching –> secondary bacterial inf. –> scars
**Chikenpox is more severe in adults
**Interstitial pneumonia may develop, possibly lethal

• Secondary inf.: Zoster (Shingles)

  • Recurrent infc.
  • Belt-like distribution in a dermatome: trunk or face
  • symp: Severe pain, vesicles, pos-herpetic neuralgia for months
  • Disseminated infection in immunocompromissed

***Herpes Zoster ophthalmicus: Vision loss when CNV/I is affected

***Congenital varicella synd: Limb Hypoplesia, cutaneous dermal scarring, blindness

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18
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus ddx

A
  • CPE on cell culture: rarely used
  • PCR
  • Serology: ELISA for detection of antibodies

***Tzanck smear –> Will show multinucleated giant cells, Cowdry bodies

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19
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus treatment

A
  • Only for complications and immunocompromised

* A.cyclovir, fam.cyclovir, vala.cyclovir (large dose)

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20
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus Vaccine

A
  • Passive: Immunoglobulin (VZIg) for immunocompromised

* Active: Live attenuated vaccine: for children, 15 and 18 m (recommended)

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21
Q

III.14 - Herpesvirus - Epstein-Barr Virus (HHV-4) characteristics

A
  • Human herpes virus 4
  • gamma-herpesvirus
  • large dsDNA (L)
  • Icosahedral capsid
  • Enveloped
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22
Q

III.14 - Herpesvirus - Epstein-Barr Virus (HHV-4) transmission

A
  • Spread with and respiratory secretions (90% of population is seropositive)
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23
Q

III.14 - Herpesvirus - Epstein-Barr Virus (HHV-4) pathogenesis

A
  • initially infects oral epithel cells –> spread to B cells, latent infection (Trophism to B-lymphocytes)
  • Possible immortalisation of infected cells
  • Binds CDRI and produce LMP1 (latent membrane protein 1) –>
    a) NFKB activation and B-cell proliferation ( Heterophil antibody production –> IgM to Paul-Bunnell Ag)
    b) Bcl2 ⊣ apoptosis
  • -> This causes production of atypical CD8+ T-cells – Downey cells against it

***Asymptomatic virus shedding possible throughout life

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24
Q

III.14 - Herpesvirus - Epstein-Barr Virus (HHV-4) clinical

A

a) Infectious mononucleosis: “Kissing disease”
• 70% of population get infected by age 30
• Milder or no symptoms in children
• Spread with saliva & contaminated items
• T cell response against infected B cells –> symp:
- Lymphadenomegaly
- HepatoSplenomegaly
- Exudative pharyngitis & tonsillitis: white plaques on tonsils (DD from S.pyogenes!)
- generalised: Fever, malaise, fatigue
- Complications (rarely): spleen rupture, meningo-encephalitis, Guillan-Barré…
- Lymphocytosis with atypical lymptocytes (Downey cells): Presence of atypical lymphocytes used to distinguish from CLL.
- Fatigue may last for months after infection
- Chronic infection: cyclic recurrent infection, chronic fatigue

• If patient with mononucleosis got ampicillin treatment (for „sore throat”) –> rash may develop (misdiagnosed often as penicillin allergy)

b) Burkitt’s lymphoma:
- Epidemic in children in malarial regions of Africa
- Sporadic/non-African type: affects ileocecal region
- Immunodeficient type: associated with AIDS
- Monoclonal B cell lymphoma of lymph nodes (maxilla and mandible)
- -> Due to translocation of c-myc oncogene which becomes active promotor (t(8;14)).
- EBV inf. → immortalisation (malaria could be cofactor)

c) Nasopharyngeal carcinoma:
- Epidemic in Asia (adults)
- Tumor contains EBV DNA
- Exact role of virus is unknown

d) Lymphoproliferative diseases:
- in immunocompromised
- In lack of T cell immunity (eg. after transplantation, AIDS)
- Polyclonal leukaemia-like B cell proliferation or lymphoma

e) Hairy oral leukoplakia:
- EBV infection of oral epithelial cells –> non-precancerous hyper-proliferation
- Opportunistic (AIDS patients)

f) Hodgkin’s (B-cell) lymphoma – Dx by presence of Reed-Sternberg cells

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25
Q

III.14 - Herpesvirus - Epstein-Barr Virus (HHV-4) ddx

A

• Blood smear:

  • Mononuclear lymphocytosis
  • Atypical lymphocytes (Downey cells)

• Heterophil Ab’s: (Heterophiles Ab’s are produced due to B-cell induction by EBV)
– Paul-Bunnell reaction: Monospot test –> IgM agglutination of sheep RBC’s (Paul-Bunnel Ag’s)
– Monospot test, ELISA

  • Other serological methods to detect Ab’s
  • PCR, DNA probes
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26
Q

III.14 - Herpesvirus - Epstein-Barr Virus (HHV-4) treatment

A
  • No treatment or vaccine available

- Lifelong immunity after infection

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27
Q

III.15 - Herpes - Cytomegalovirus (HHV-5) characteristics

A
  • HHV-5
  • beta-herpesvirus
  • dsDNA (L)
  • Icosahedral capsid
  • Enveloped
  • Latency in monocytes, macrophages, T-cells
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28
Q

III.15 - Herpes - Cytomegalovirus (HHV-5) Transmission

A

Spead: secretions

  • orally
  • sexually
  • blood transfusion
  • transplant
  • in utero / at birth (TORCH)
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29
Q

III.15 - Herpes - Cytomegalovirus (HHV-5) Pathogenesis

A
  • Common pathogen
  • Immune status of host: determines the Severity & form of the disease
  • Trophism to lymphocytes but can infect other cells (salivary glands by binding to the integrin rec.)
  • Carries mRNA in the virion
  • Lifelong latent infection: established in mononuclear leukocytes (B-cells, T-cells, macrophages)
  • reactivation may develop by immunosuppression.
  • Cellular immunity important for control
  • May cause asymptomatic shedding
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30
Q

III.15 - Herpes - Cytomegalovirus (HHV-5) clinical

A

• In immunocompetent adults and children:

  • Mainly asymp.
  • Mononucleosis-like disease may develop (less severe than EBV)
  • Pharyngitis, lymphadenopathy, hepatitis
  • Heterophiles Ab’s (–)

• Infection of immunocompromised patients:

  • in Organ transplant, cytostatic therapy, AIDS…
  • Reactivation of latent infection or new infection from blood transfusion or transplanted organ
  • -> Pneumonia (possibly lethal)
  • -> Retinitis, encephalitis,
  • -> Colitis, oesophagitis – diarrhoea, weight loss, anorexia
  • -> Failure of transplants

• Congenital infection:

  • Most frequent viral congenital infection!
  • 10% of infected babies will show symp.
  • Cytomegalic inclusion disease:
  • -> Small size
  • -> Thrombocytopenia
  • -> Microcephaly, Intra-cerebral calcification, Hearing loss, mental retardation
  • -> HepatoSplenomegaly & Jaundice

• Perinatal infection:

  • Neonates acquire CMV during birth from: cervix, vagina, or from maternal milk or blood transfusion
  • No syms in healthy full-term babies
  • Premature babies: pneumonia, hepatitis
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31
Q

III.15 - Herpes - Cytomegalovirus (HHV-5) ddx

A

• Histology: stain with Pap or H&E
- cytomegalic basophilic cell, owl’s eye, inclusion bodies

  • ELISA, PCR – detection of virus
  • Cultivation: fibroblast culture (slow)
  • Serologic detection of Ab’s
  • Congenital: detection of virus from urine during 1st w of life
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32
Q

III.15 - Herpes - Cytomegalovirus (HHV-5) treatment

A
  • Gan.cyclovir, Valgan.cyclovir, Cido.fovir

* No vaccine

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33
Q

III.16 Herpesvirus - HHV6 characteristics

A
  • dsDNA
  • Icosahedral capsid
  • Enveloped
  • beta-herpesvirus
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34
Q

III.16 Herpesvirus - HHV6 Transmission

A
  • salvia
  • Common (most people get infected during childhood)
  • Asymptomatic, or mild febrile viral disease
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35
Q

III.16 Herpesvirus - HHV6 Pathogenesis

A
  • Replicate in salivary glands, shed and transmitted through saliva.
  • Can also infect lymphocytes (mainly CD4+ T-cells) in peripheral blood
  • Can lead to immunosuppression by decreasing the CD4+ T-cells
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36
Q

III.16 Herpesvirus - HHV6 clinical

A

• Childhood disease: Exanthema subitum = Roseola infantum

  • High fever, 39C, for 3-5 days
  • maculopapular rash develops (After the fever subsizes) but spares the face
  • Latent infection (possible reactivation)
  • Role in degenerative neurologic diseases
  • Mononucleosis-like disease in adults
  • Immunocompromised: reactivation
  • -> Encephalitis
  • -> Pneumonitis
  • -> Rejection of transplant
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37
Q

III.16 Herpesvirus - HHV6 ddx

A

Clinical picture

PRC, serology – Virus isolation from lymphocytes

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38
Q

III.16 Herpesvirus - HHV6 treatment

A
  • Self-limited
  • Gan.cyclovir
  • no vaccine
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39
Q

III.16 Herpesvirus - HHV 7 clinical

A
  • Common (most children get infected)
  • Infect T cells
  • May cause asymptomatic infection
  • Cause some cases of exanthema subitum (less frequently than HHV6)
  • Possible complications:
  • -> meningitis, encephalitis, otitis…
  • -> Latent, persistent infection may develop
  • -> may have a Role in pityriasis Rosea
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40
Q

III.16 Herpesvirus - HHV8 characteristics

A
  • gamma-herpesvirus
  • dsDNA
  • Icosahedral capsid
  • Enveloped
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41
Q

III.16 Herpesvirus - HHV8 transmission

A
  • Saliva

- sexual contact

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42
Q

III.16 Herpesvirus - HHV8 pathogenesis

A

• Opportunistic infection in AIDS patients
→ Kaposi’s sarcoma: Brownish skin tumor (rarely visceral manifestation) by activating VEGF

  • Infects mainly B-cells (like EBV), but also epithelial cells, monocytes etc.
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43
Q

III.16 Herpesvirus - HHV8 clinical

A

a) Kaposi sarcoma
- Malignant tumor of the endothelial cells
- Most commonly affects the skin, lymph nodes, mucosa, and viscera
- Develops mostly in AIDS patients

b) Primary effusion (B-cell) lymphoma
- Large B-cell lymphoma located in body cavities
- Characterized by pleural, peritoneal, pericardial fluid lymphomatous effusions

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44
Q

III.16 Herpesvirus - HHV8 ddx

A
  • Clinical
  • Serology
  • PCR
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45
Q

III.16 Herpesvirus - HHV8 treatment

A
  • Treat HIV

- chemotherapy

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46
Q

III. 17 Parvovirus characteristics

A
  • ssDNA
  • Icosahedral capsid (smallest virus)
  • non-enveloped
  • Parvovirus B19 ~ only one to cause human disease

• Dependoviruses: Adeno-associated viruses (AAV)

  • Need other viruses for replication
  • Don’t cause illness
  • Potential use in gene replacement therapy
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47
Q

III. 17 Parvovirus transmission

A
  • Respiratory droplets
  • TORCH

• Pathogenesis:

  • Replication in cells of erythroid line: bone marrow, fetal liver, RBCs
  • 65% of population infected by 40y
  • Generally in winter and spring
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48
Q

III. 17 Parvovirus clinical

A

a) Erythema Infectiosum: “fifth disease”
- childhood infection
- Biphasic course:
1. Starts with: mild, flu-like syms, fever, headache –> Infective stage: Blocks RBC production for few days (no complication in healthy)
2. Late phase: after 1-2 w (imm. resp.): Maculopapular rash on the cheeks ,,slapped face”
- -> Spread to arms and legs

• Infection of adults:

  • Polyarthritis with/without rash (on Hands, wrists, knees, ankles)
  • For weeks - months

• Aplastic crisis:

  • Hosts with chronic anaemia (sickle)
  • Life-threatening Reticulocytopenia

• Hydrops fetalis

  • Infection of seronegative pregnant woman
  • Transplacental inf. of the fetus –> anaemia, heart failure
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49
Q

III. 17 Parvovirus ddx

A
  • Clinical

- serology: Pregnants: Detection of specific IgM

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50
Q

III. 17 Parvovirus treatment

A

self-limiting

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51
Q

III. 18 Papilloma Virus characteristics

A
  • dsDNA (C)
  • Icosahedral capsid (small)
  • non-enveloped

HPV:

  • 100 serotypes
  • Cutaneous and mucosal infections
  • Spread to the skin basal layer through microscopic wounds
  • Multiplication → koilocytes, wart / papilloma
  • Spread with desqammation of the upper layer of the skin
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52
Q

III. 18 Papilloma Virus Transmission

A

Spread with desqammation of the upper layer of the skin

  • Contact – directly or by objects
  • Sexual – most frequent STD!
  • During birth

(Infects the basal cell layer of the skin (stem cells) and mature as the cell matures up to the surface
The virus persists in basal layer and stays hidden from immune system)

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53
Q

III. 18 Polymoavirus characteristics

A
  • dsDNA (C)
  • Icosahedral capsid
  • naked

**similar to papilloma*

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54
Q

III. 18 Papilloma Virus ddx

A

Clinical – for cutaneous warts

PCR – to distinguish serotype

HPV don’t grow on cell cultures - difficult to study

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55
Q

III. 18 Papilloma Virus prevention

A

Vaccine against to most important serotypes for girls before

the begining of sexual life

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56
Q

III. 18 Polymoavirus Transmission

A
  • Respiratory droplets, saliva

- most people infected asymptomatically

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57
Q

III. 18 Polymoavirus Pathogenesis

A

Reactivation in immunocompromised – AIDS, transplantation:
- Infects tonsils & lymphocytes –> spreads by blood to kidney.
(secondary viremia occurs: become latent in immunocompetent or reactive in immunosuppressed)

1) BK virus (from first patient): latency in kidney
- Nephropathy (ureter stenosis) and hemorrhagic cystitis (hematuria) in bone marrow transplanted patients (DDX; Adenovirus)

2) JC (John Cumingham) virus: latency in kidney, B-cells, monocytes ++
- -> progressive multifocal Leuko-encephalopathy (PML) –> oligodendrocytes –> CNS demyelination –> Multifocal brain lesions in white matter
- Speech, vision, mentation defects, paralysis, death in AIDS patients (DDX; Toxoplasma)

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58
Q

III. 18 Polymoavirus ddx

A

MRI/CT

PCR of CSF

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59
Q

III. 18 Polymoavirus treatment

A

none

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60
Q

III. 18 Papilloma Virus clinical

A

• Skin warts: “verruca”

  • Low risk serotypes (1-4)
  • Very frequent
  • benign skin disease (Hyperkeratosis)
  • Self-limited, may resolve spontaneously
  • Usually affect hand and feet
  • Thrombosed vessels in the lesion: black dots
  • **Th: surgical removal, cryotherapy, chemical solutions

• Benign head and neck tumors: (6,11)

a) Oral, conjunctival papillomas:
- Frequent, papillary, cauliflower-like
b) Laryngeal papilloma:
- May obstruct the airway
* **Th: surgical removal

• genital warts: “Condyloma Accuminatum”

  • Low risk serotypes; 6-11
  • Genital & perianal region

• Cervical dysplasia and neoplasia:
- High risk serotypes; 16, 18, 31, 33, 45 (associated with cervix cancer)
- Genital HPV infection (STD)
- Soft cervical warts
- Koilocytes: detected on Papanicolaou smear
• After years of infection wart may transform into dysplasia –> neoplasia (CIN) –> carcinoma!
E6 ⊣ p53
E7 ⊣ Retinoblastoma
***th: surgical removal

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61
Q

III.19 Poxvirus characteristics

A
  • dsDNA (L)
  • Complex structure (Biggest virus!)
  • Enveloped
  • replicates in cytoplasm

• Vaccinia and canary pox viruses can be used as gene delivery vectors in hybrid vaccines:
Infection with a recombinant apathogenic virus expressing antigens of other microbe
- Variola virus ~ Smallpox
- Cow pox virus ~ Share antigenic determinant with variola virus (Jenner)
- Vaccinia virus ~ Vaccination of smallpox

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62
Q

III.19 Poxvirus transmission

A

• Spread: resp.droplets, lymph nodes affected, viraemia
• Smallpox (Variola)
- Variola major and minor
- Once huge epidemics, now eradicated (since 1980)
• Importance: Possible bioterrorism agent

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63
Q

III.19 Poxvirus clinical

A

1) Smallpox (Variola – minor or major depending on immune status)
–> Virus enters the upper resp.T. –> 5-7 days of incubation –> lymphatics –> viremia –> second viremia –> infects all dermal tissues & internal organs “pocks”:
• Fever, headache, vomiting, diarrhea, bleeding (2-4 days)
• Heamorrhage of small vessels, rash, vesicules (Stages of skin signs: macule, paule, vesicule, pustule). All vesicules at the same stage (DD from chickenpox!)
• Spleen, liver, bone marrow, other organs…
***Therapy: cidofovir

2) Molluscum contagiosum virus
• Nodular, wart-like skin lesion (Benign epithelial tumor)
• Spread by direct contact or objects
• Fingers, trunk, genitals
• Treated by liquid nitrogen
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64
Q

III.19 Poxvirus ddx

A

Smallpox Variola:
• Clinical signs
• Cultivation on cell cultures
• PCR

Molluscum contagiosum:
• clinical
• biopsy

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65
Q

III.19 Poxvirus vaccine

A

• Vaccine contained Live attenuated vaccinia (cowpox) virus (side effects)
• (From XVIII.century – Jenner)
• Eradicated by immunization, vaccination stoped in 1980:
- No animal reservoir
- single serotype
- no asymptomatic infection or carriage
- inexpensive vaccine

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66
Q

III.20 Arenavirus characteristics

A
  • arena: sand in latin
  • from BunyaVirales order (big family)
  • ssRNA (Ambisense, has both positive and negative sense sections)
  • Helical
  • Enveloped with projections
  • Natural host; rodents
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67
Q

III.20 Arenavirus transmission

A

Zoonotic, rodents

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68
Q

III.20 Arenavirus -Lymphocytic choriomeningitis virus (LCMV)

A

reservoir: mouse
spread: bite or bodily fluids

Infection:

  • often asymptomatic
  • symptomatic: Fever –> asymp. period –> aseptic meningitis (headache, fever, stiff neck)
  • Rarely: encephalitis

D: Ig from serum or CSF

Treatment: not available

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69
Q

III.20 Arenavirus - Machupovirus

A
  • Machupo virus: Bolivian hemorrhagic fever (BHF)
  • Reservoir: mouse
  • symp: Fever, headache, bleeding, CNS symp. (High mortality)

Diagnosis:
- Ig from serum or CSF

Treatment : not available

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70
Q

III.20 Arenavirus - Lassavirus

A
  • Lassa: village in Nigeria
  • Lassavirus: Lassa fever
  • Reservoir: African rats

spread:
urine, contaminated food, human to human

Symp:

  • High fever, myalgia, haemorrhages
  • spleen and liver necrosis
  • oedema of face, lung
  • shock
  • Mortality 15-20%

Diagnosis:

  • PCR
  • serology

Th: supportive

Prevention:
rodent control, safe storage of food

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71
Q

III.21 Bunyaviruses (Hanta-.. Crimean-Congo hemorrhagic fever virus) characteristics

A
  • Name: Bunyamwera –> town in Uganda
  • BunyaVirales order (big family)
  • (-) ssRNA -circular-
  • Helical capsid
  • Enveloped with projections
  • Bunyavirales contain:
  • ->Hantaviridae: Hantaan virus
  • -> Arenaviridae
  • -> Nairoviridae: Crimean Congo hemorrhagic fever virus (CCHFV)

mostly causing viral haemorrhagic fevers

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72
Q

III.21 Bunyaviruses HANTAVIRUSES

transmission

A

Spread: zoonotic

- robovirus: rodent borne. from rodents with bite or bodily fluids

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73
Q

III.21 Bunyaviruses- HantaVirus

clinical

A

Diseases:

  1. Hantavirus pulmonary synd.:
    - American continent
    - by Sin Nombre virus (SNV)
    - reservoir: deer mice
    - flu-like symp –> sudden dyspnea, lung oedema, high mortality!
  2. Hemorrhagic fever with renal synd.:
    a) Nephropathia epidemica:
    - -> Scandinavia
    - -> by Puumala virus (PUUV)
    - -> reservoir: bank vole, by inhalation of dried fees
    b) Hemorrhagic fevers:
    - -> Korean haemorrhagic fever Hantaan virus
    - -> Seoul virus from rats
    - ->Fever, vomiting, rash, headache, high mortality

prevention:
- vaccine: Hantavax

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74
Q

III.21 Bunyaviruses Crimean-Congo hemorrhagic fever virus

transmission

A

Spread:

  • tick bite Hyalomma
  • animals
  • human to human
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75
Q

III.21 Bunyaviruses Crimean-Congo hemorrhagic fever virus

clinical

A

Symptoms:

  • Fever
  • vomiting
  • stiff neck
  • hepatomegaly
  • bleeding: into skin , mucosa , viscera
  • Shock
  • high mortality (30-40%)
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76
Q

III.21 Bunyaviruses Crimean-Congo hemorrhagic fever virus

diagnosis, treatment

A

Diagnosis:

  • PCR
  • serology

Th:
- supportive

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77
Q

III.21 Bunyaviruses Crimean-Congo hemorrhagic fever virus clinical

A

Crimean-Congo virus

Transmission via tick: Arbovirus/arthropod-borne - Crimean-Congo hemorrhagic fever (CCHF)

10 lesion involves leakage of RBCs and plasma through endothelium

Presents with fever, myalgia, headache, vomiting, diarrhea and bleeding into skin

Complications; liver failure, kidney damage, DIC, shock and death

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78
Q

III.22 Coronavirus characteristics

A
  • (+) ssRNA -positive sense-
  • Circular
  • Helical Nucleocapsid (crownlike)
  • Enveloped
  • Infects mammals and birds
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79
Q

III.22 Coronavirus SARS coronavirus (SARS CoV)

A
  • SARS: Severe Acute Respiratory Syndrome
  • Pandemic: started in 2002 in China (10% case fatality rate)
  • Symp: Fever, dry cough, headache, muscle pains, difficulty breathing
  • Origin: bats → civets → humans
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80
Q

III. 22 Coronavirus - (MERS CoV)

A
  • MERS coronavirus: Middle Eastern Respiratory Syndrome
  • Started in 2012, in Saudi Arabia 37% fatality
  • Origin: bats –> camels –> humans
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81
Q

III. Coronavirus - (SARS-Cov2)

A

• SARS CoV2: Severe acute respiratory syndrome coronavirus 2 –> official name of the virus
→ COVID-19: COronaVirus Disease 2019 –> name of the infection

  • First detected in Wuhan, China, in December 2019 –> Became a Public Health Emergency of International Concern in Jan 2020 –> pandemic in March 2020
  • Belongs to β coronaviruses SARS-CoV-2: 79.5 % genomic identity to SARS CoV
Origin: bats
--> 96.2% identity to a bat coronavirus
• Intermediate host: unknown
• Possible recombination of bat CoV with other CoV
• Under investigation
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82
Q

III. Coronavirus -CORONAVIRUSES SARS COV2-

structure, replication, transmission, effect

A

Structure:

- 4 structural proteins:
• Spike (S): allows entry by attaching to the ACE2 rec. of the host cell
• Envelope (E)
• Membrane (M)
• Nucleocapsid (N)
  • 16 nonstructural proteins (NSP): form the replicase-transcriptase complex (RTC)

Replication:

  • -> Receptor: ACE2-rec., expressed in the surface epith. of the lungs, heart and others
  • -> Increased concentrations of ACE2 in DM, cardiovascular disease, COPD, cigarette smoking
  • -> Transmembrane protease, serine 2 (TMPRSS2) –> cleaves S protein –> fusion

Transmission:
• Mainly with resp. droplets, hand to face contact from fomites
• Incubation period : usually 5 days

Effects
• Direct cytopathic effects: mainly to alveolar epith. (also liver & heart)
• Dysregulated immune response
–> Activation of the immune system –> cytokine release –> acute inflam. resp.
–> cytokine storm: overshooting imm. resp. –> very high Lvls of cytokines –> organ failure & death

83
Q

III.22 Coronavirus pathogenesis

A

Most coronaviruses infect and replicate the upper respiratory tract mucosa which leads to symptoms of a common cold

SARS strains replicate in respiratory tract –> viremia –> RES –> systemic infection

Extrapulmonary replication happens in GI, CNS and UT.

84
Q

III.22 Coronavirus clinical

A

Clinical course:
• Mild (80%)
- Uncomplicated course without dyspnea
- Lasts 1-2 w

• Severe 15%)

  • 5-7 d after symptom onset
  • dyspnea and hypoxia, pneumonia
  • Lasts 3-6 w

• Critical (5%)

  • Severe pneumonia (Resp. failure)
  • ARDS
  • coagulopathy
  • shock
  • multiple organ dysfunction syndrome (MODS)
  • Lasts 3-6 w

Mortality rate : 0.5 3%

85
Q

III.22 Coronavirus ddx

A

RT-qPCR (NAAT):

  • detetction of SARS-CoV2 specific genes sequences
  • Fast, most reliable method, specific and sensitive

• serology:

  1. Ag’s detection from resp. sample:
    - Possibly as an point of care (POC) test
    - less reliable, can be false negative
  2. Detection of antibodies from blood:
    - By rapid test or ELISA
    - Not as reliable as PCR in identifying fresh infection
    - Used for identify individuals who had a recent or past infection or immunisation
  3. Virus isolation & culture:
    - From sputum or other sample, on Vero cell line
    - For research use
    - CPE: is observed after 96h
    - Virus viability is determined by determining the plaque forming unit (PFU)
86
Q

III.22 Coronavirus treatment and prevention

A

TREATMENT:

Antiviral drugs: best effect in early phase

  1. Neutralizing mAbs prevents rec. binding:
    - -> Casiri.vimab , bamlani.vimab
  2. Inhibition of RNA dependent RNA polymerase
    - -> Remde.sivir
Immune resp. modulation: 
1. Tocilizu.mab: 
--> IL6 rec. inhibitor
--> mAb
2. Bari.citi.nib
inhibitor of janus kinase JAK 1 and 2
3. Corticosteroids:
--> Dexamethazon

VACCINATION:
• mRNA vaccines: Pfizer-BioNTech, Moderna
• Viral vector vaccines: Oxford AstraZeneca, Janssen, Sputnik
• Killed whole virus: Sinopharm, Sinovac, Co.vaxin, Covi.vac, CovIran
• Subunit : Epi.VAc.Corona

87
Q

III.22 Filovirsues characteristics

A
  • (-) ssRNA -negative sense-
  • Helical caspid (Filamentous shape)
  • Enveloped
  • Causes viral hemorrhagic fever in humans and other primates
  • BSL4 level, bioterrorist agents
  • Ebola virus genus (EBOV)
  • Marburg virus genus (MARV)
88
Q

III.22 Filovirsues EBOV

transmission and symps

A

Spread:
- Mainly in Sub Saharan Africa (Ebola: river in congo)
- Zoonosis: from bats and primates
- Human to human spread: all bodily fluids
(semen spreads the virus even after recovery)

Symptoms:

  • 1-2 weeks incubation
  • Fever, myalgia, headache
  • Internal and external bleeding –> shock
  • High mortality: 40 90%
89
Q

III.22 Filovirsues EBOV

Diagnosis, treatment, prevention

A

Diagnosis

  • In BSL4 lab only
  • Virus detection from bodily fluids
  • Serology for antibodies

Treatment:
- Not available (supportive only)

Prevention:
- Approved vaccine : Ervebo , since 2019
- Live attenuated recombinant vaccine
(Genetically modified vesicular stomatitis virus expresses surface glycoproteins of EBOV)

90
Q

III.22 Filovirsues MARV

transmission and symps

A

Spread:
- first recognised in 1967, Marburg, Germany
(researchers got the infection from African green monkeys)
- Zoonotic: from bats & monkeys
- Human to human: with bodily fluids

Symptoms:

  • Marburg virus disease (MVD) (viral hemorrhagic fever)
  • Fever, headache, vomiting, maculopapular rash, petechiae , hematomas
  • Encephalitis, confusion, visceral & mucosal bleeding, MOF, shock
  • High mortality
91
Q

III.22 Filovirsues MARV

diagnosis, treatment, prevention

A

Diagnosis:

  • PCR for viral RNA from serum
  • Serology for Ab’s

Treatment:
- Not available (supportive only)

Prevention:

  • No vaccine yet
  • Avoid contact
92
Q

III. 23 Flavivirus - Yellow Fever, Dengue Fever characteristics

A

(Flavus= yellow blonde in latin refers to jaundice caused by some of these viruses)

  • (+) ssRNA =mRNA
  • Icosahedral capsid
  • Enveloped

Common in Flavivirus genus:

  • Spread by vectors
  • Often asymp.n
  • Biphasic course of symp:
    1. Incubation period
    2. Aspecific symp, fever
    3. Asymptomatic phase
    4. CNS symp.

Arboviruses: Arthopod-borne
Many causes
viral haemorrhagic fever

93
Q

III. 23 Flavivirus - Yellow Fever vector

A

Aedes mosquitos, hosts are humans and monkeys

94
Q

III. 23 Flavivirus - Yellow Fever clinical

A 
Yellow fever:
Acute viral haemorhagic disease:
- 1 w incubation time
- Fever, headache
- In 15 20% more severe form develops: jaundice & liver, kidney damage, Haemorrhages, vomiting
(in this group mortality: 20 50%)
95
Q

III. 23 Flavivirus - Yellow Fever

diagnosis, treatment, prevention

A

Diagnosis:
difficult , as symptoms are similar to many other infections
DD: malaria , viral hepatitis, leptospirosis, dengue
-PCR: blood or urine
-Serology: Ab’s

Treatment:
- not available , only supportive care

Prevention:
- Vaccination: for babies living in affected areas at 9-12 m
and for travellers: 10 days prior travel
- Attenuated virus: single dose

-Vector control

96
Q

III. 23 Flavivirus - Dengue Fever vector

A

Spread: Aedes mosquito

97
Q

III. 23 Flavivirus - Dengue Fever clinical

A

Symptoms

  • 1-2 weeks incubation
  • Fever , rash , muscle pain
  • More severe form : dengue hemorrhagic fever
98
Q

III. 23 Flavivirus - Dengue Fever

diagnosis, treatment, prevention

A

Diagnosis:

  • PCR from serum
  • IgM, IgG (but cross reactivity with other flaviviruses)

Treatment:
- No specific treatment (Supportive care)

Prevention
- Insect repellents
- Vaccine: Deng.vaxia
–> only for those who live in affected areas and previously infected
(To prevent further, more severe infection)

99
Q

III. 24 Flavivirus - West Nile, Tick Born Encephalitis, Zika Virus characteristics

A

(Flavus= yellow blonde in latin refers to jaundice caused by some of these viruses)

  • (+) ssRNA =mRNA
  • Icosahedral capsid
  • Enveloped

Common in Flavivirus genus:

  • Spread by vectors
  • Often asymp.n
  • Biphasic course of symp:
    1. Incubation period
    2. Aspecific symp, fever
    3. Asymptomatic phase
    4. CNS symp.

Arboviruses: Arthopod-borne
Many causes
viral haemorrhagic fever

100
Q

III. 24 Flavivirus - Zika Virus vector

A

Spread:

  • Aedes mosquito
  • tropical/subtropical regions
  • transplacental spread
101
Q

III. 24 Flavivirus - Zika Virus

clinical

A

Symptoms:
In non-pregnant: -generally mild infection-
- fever, rash, myalgia,arthralgia, conjunctivitis
-Complication: CNS involvement, Guillan Barre

Transplacental:

  • infection of foetus
  • stillbirth, premature birth
  • Congenital Zika syndrome: Microcephaly, CNS damage, congenital glaucoma
102
Q

III. 24 Flavivirus - Zika Virus

diagnosis, treatment, prevention

A

Diagnosis:

  1. Adults:
    - PCR: blood , urine
    - Serology: cross reactivity with other Flaviviruses
  2. Pregnant:
    - Anamnesis travel or sex partner
    - Ultrasound sign of foetal damage
    - PCR: 3 times during pregnancy from mother’s serum
    - PCR: from amniotic fluid

Treatment: not available

Prevention:

  • Avoid travel while pregnant
  • Safe sex during pregnancy, if partner travelled
  • Mosquito control
103
Q

III. 24 Flavivirus - West Nile

treansmission

A

Spread: Culex mosquito

  • Traditionally tropical/subtropical regions
  • now spreads North
104
Q

III. 24 Flavivirus - West Nile

clinical

A

Symptoms:

  • Often asymptomatic (8/10)
  • 1-2 w incubation
  • West Nile fever: fever, diffuse maculo-papular rash, headache, myalgia
  • Rarely encephalitis, paralysis
105
Q

III. 24 Flavivirus - West Nile

diagnosis, treatment, prevention

A

Diagnosis:

  • PCR
  • Serology

Treatment: Not available

  • Supportive care
  • IVIG: intravenous polyclonal Ig’s

Prevention:

  • No specific prevention
  • Insect repellents, mosquito nets
  • Vaccine: under development
106
Q

III. 24 Flavivirus - Tick Born Encephalitis

transmission

A

Spread:

  • “Ixodes” tick bite
  • unpasteurised milk of infected animal
107
Q

III. 24 Flavivirus - Tick Born Encephalitis

clinical

A

Symptoms:

  • 1-2 weeks incubation
  • Fever, then 5-10 asymp. days
  • Encephalitis: headache, dizziness, photophobia, paralysis, vomiting
  • Usually full recovery
  • Mortality: 0.5-2% for EU subtype, 20% Far East subtype
108
Q

III. 24 Flavivirus - Tick borne Encephalitis

diagnosis, treatment, prevention

A

Diagnosis:

  • IgM and IgG from blood
  • IgM from CSF
  • PCR or virus isolation

Treatment:
- Not available

Prevention:

  • Vaccine: inactivated virus (Encepur)
  • 2-3 doses needed, and boosters every 5 y
  • not to be given during tick season
  • recommended for everybody
109
Q

III. 25 Calicivirus

characteristics

A
  • (+) ssRNA =mRNA
  • Icosahedral capsid
  • Naked
  • cannot be cultivated
  • Many strains have cup-shaped depression (calyx = cup)
  • Two genera of human pathogenic viruses;
  • -> Noro-virus & Sapo-virus
110
Q

III. 25 Calicivirus transmission

A

Fecal oral route
contaminated water (Resistant: may remain alive in water supply system)
contaminated food

111
Q

III. 25 Calicivirus clinical

A

Acute Gastroenteritis:

  • abd. cramps
  • vomiting
  • watery diarrhea – self-limiting gastroenteritis
  • resolves in 1-3 days
112
Q

III. 25 Calicivirus ddx

A
  • Clinical
  • ELISA
  • PCR
113
Q

III. 25 Calicivirus treatment

A
  • NOT available

- rehydration

114
Q

III. 25 Rotavirus characteristics

A
  • from REOviridae family
  • dsRNA, both positive & negative
  • Icosahedral capsid
  • Naked virus
115
Q

III. 25 Rotavirus Transmission

A

Fecal-oral

116
Q

III. 25 Rotavirus Clinical

A

GASTROENTERITIS:

  • mainly in children < 5y
  • fever, watery diarrhoea for 1 w (risk of dehydration)
  • Nosocomial epidemics occur
117
Q

III. 25 Rotavirus ddx

A
  • Immunochromatography rapid test: faeces

- PCR from faeces

118
Q

III. 25 Rotavirus treatment

A

supportive therapy

119
Q

III. 25 Rotavirus vaccine

A

Oral, live attenuated vaccine:

  • Rota.teq, Rota.rix
  • for infants 6-32 w old
  • not part of vaccination schedule
120
Q

III. 25 Astrovirus characteristics

A
  • (+) ssRNA
  • Icosahedral capsid
  • Naked virus
  • STAR shape
121
Q

III. 25 Astrovirus transmission

A

Fecal-oral route

122
Q

III. 25 Astrovirus clinical

A

Gastroenteritis:

  • in children and older people
  • Watery diarrhea, vomiting, abd pain
  • resolves 2-3 days
  • occur in winter
123
Q

III. 25 Astrovirus ddx

A
  • ELISA

- Hybridisation

124
Q

III. 25 Astrovirus treatment

A

Supportive

125
Q

III. 26 Orthomyxoviruses characteristics

A
  • (-)ssRNA -negative sense- segmented
  • Helical
  • Enveloped
  • RNA synthesis in nucleus (only RNA virus)
  • Possesses Hemagglutinin and Neuraminidase glycoproteins
126
Q

III. 26 Orthomyxoviruses transmission

A
  • Respiratory droplets & contaminated hand

- Seasonal spread: in fall and winter

127
Q

III. 26. Orthomyxoviruses Replication (of influenza)

A
  1. Attachment: HaemmAglutinin (HA) binds to sialic acid on cell surface
    - ->Target: resp. epith. cells
    - ->HA: important Ag’s , variable
  2. Uncoating
  3. Virus replication
  4. Assembly
  5. Release: mediated by NeurAminidase (NA) enzyme
    - ->cleaving the budding virus off from the cell
    - ->NA: important Ag’s , variable
128
Q

III. 26 Orthomyxoviruses - INFLUENZA “A” VIRUS

A

• Most virulent human influenza virus
• Subdivided into different serotypes based on surface Ag’s HA and NA
(eg . H1N1 and H3N2)
• Causes epidemics & pandemics
• Infects birds and mammals (different variants)

Avian influenza bird flu:

  • Aquatic birds are the natural reservoirs of influenza A virus (migration)
  • Infection of poultry: economic importance
  • Reassortment of bird and human strains: new variants –> potential for human pandemics
129
Q

III. Orthomyxoviruses - INFLUENZA “B” VIRUS

A
  • Exclusively infects humans
  • Less common than influenza A
  • Lower mutation rate, no Ag shift (lower diversity), lower risk for epidemics
  • Generally infects younger population
130
Q

III.26 Orthomyxovirus - INFLUENZA “C & D” VIRUSES

A
  • Mostly infect animals pigs , cattle

* C can cause human infections

131
Q

III. 26 Orthomyxoviruses variation

NEW VARIANTS OF INFLUENZA VIRUSES RISE AS A RESULT OF:

A
  • Antigenic shift:
  • Accumulation of point mutations
  • Gradual change
  • Occurs in influenza A and B
  • Antigenic drift:
  • Reassortment: mixing of genes between two organisms to make a new genetic sequence when 2 types infect same cell
  • Sudden change, explosive spread pandemics
  • Occurs only in influenza A virus
132
Q

III. 26 Orthomyxoviruses clinical

A
  • Influenza A, B and C (also known as flu)
- Symptoms:
• May be asymp.
• Sudden onset
• Fever : 38 to 39 C , chills
• Dry cough
• Muscle pain , fatigue , headache
133
Q

III.26. Orthomyxovirus - Influenza Complications?

A
  • Pneumonia: viral or bacterial superinfection
  • Sinus or ear infections
  • Myocarditis
  • Myositis
  • Encephalitis
  • Multiorgan failure , SIRS
  • Possibly lethal
134
Q

III. 26 Orthomyxoviruses ddx

A
  • Mostly based on clinical symptoms
  • RT PCR
  • Rapid antigen test
  • From respiratory sample usually nasopharynegal swab , in VTM

***More precise lab diagnosis for epidemiology (follow of epidemics):
• Virus isolation and cultivation on cell cultures or embryonated egg
• HA inhibition assay test for Ab’s

135
Q

III. 26 Orthomyxoviruses treatment

A

• Generally antivirals are not needed:
Bedrest , increased fluid intake , antipyretics

ANTIVIRALS:
1. Attachment is inhibited by Ab’s in immune people.
(monoclonal Ab’s in clinical trials for treatment)

  1. Uncoating Inhibited by adamantanes:
    - ->amanta.dine and rimanta.dine (resistance problem)
  2. Virus replication inhibition:
    - ->baloxa.vir
  3. Release:
    blocked by (NA) enzyme inhibitors
    –>zana.mivir, pera.mivir (Tamiflu)
136
Q

III. 26 Orthomyxoviruses vaccine

A

• Recommeded for everyone >6m , every season
• Especially important for risk groups & healthcare workers
•Tri/Tetravalent, inactivated or recombinant subunit:
–> Vaxi.grip , Fluarix , Influvac , Afluria
–> for 2 „A” types and 1-2 “B”s , intramuscular
• Nasal spray of live attenuated virus

137
Q

III. 27 - Paramyxoviruses - Mumps, Morbillivirus (measles) characteristics

A
  • Non-segmented (-) ssRNA genome
  • Helical
  • Enveloped
  • HN: HaemAgglutinin-NeurAminidase on surface
  • F-protein: glycoproteins for fusion
  • RNA synthesis in cytoplasm

PaRaMyxoviruses: Parainfluenza
RSV
Mumps , Measles , Metapneumo

138
Q

III. 27 - Paramyxoviruses - Morbilli (measles) clinical

A

Spread: resp. droplets

  • Most infectious virus
  • Occurs in regions with low vaccination rates (mostly in children)

Clinical features:
• Incubation period

• CATARRHAL STAGE: nonspecific symp:

  • Rhinitis (Coryza ), Cough, Conjunctivitis , fever
  • Koplik spot: Small white spots on oral mucosa

•EXANTHEM STAGE: MACULO-PAPULAR RASH

  • Confluent
  • starts behind ears , spreads towards feet
  • High fever, generalised lymphadenopathy
  • Heals with desquamation after 5-7 days
139
Q

III. 27 - Paramyxoviruses - Morbilli (measles) complications

A 
SHORT TERM:
• Bacterial superinfection:
- Measles --> temporary immunosuppression --> Lymphocyte count ↓↓ --> immune amnesia
- Otitis media
- Pneumonia (most common cause of death)
• Gastroenteritis , viral pneumonia
• Acute encephalitis Frequency: 1:1000

LONG TERM:
• Subacute sclerotizing pan-encephalitis - SSPE
- 10 yrs after measles infection
- Generalised demyelinating inflammation of the brain
- 100% lethal in a few years , no cure
- Sy: dementia , personality change , epilepsy, vegetative state
- Cause: persistence of measles in brain as slow virus
- Frequency: 1-2:10,000 measles cases

140
Q

III. 27 - Paramyxoviruses - Morbilli ddx

A
  • Based on clinical symptoms
  • Serology : Measles specific IgM
  • RT PCR
141
Q

III. 27 - Paramyxoviruses - Morbilli treatment and prevention

A

TREATMENT:
• Not available
- vitamin A reduces morbidity and mortality

PREVENTION ! :
• MMR (mumps-morbilli-rubella) vaccine for every child at 15 m & 6,11 yrs of age
• Post-exposure prophylaxis (PEP ): active immunisation of healthy , passive for immunosupressed

142
Q

III. 27 - Paramyxoviruses - Mumps clinical

A
  • Spread:
    resp. droplets (unvaccinated) , in children mainly
  • -> Highly infectious

*Pathomechanism:
Initial replication in Nasopharyngeal mucosa → viraemia → parotid gland → dissemination possible to testes, ovaries , pancreas , CNS

Clinical course:
- Prodrome: fever
- Inflamm. of the salivary glands PAROTITIS (Swelling of parotid, salivary, lymph nodes, pain
Earache -earlobe turned upwards-)

143
Q

III.27 Paramyxoviruses - Mumps complications

A
  • Orchitis: inflam of the testicles (Mostly post-pubertal age)
  • Meningitis
  • Encephalitis
  • Pancreatitis: link to later diabetes mellitus 1
144
Q

III. 27 - Paramyxoviruses - Mumps ddx

A
  • RT-PCR

- serology: mumps virus specific IgM

145
Q

III. 27 - Paramyxoviruses - Mumps treatment and prevention

A 
- Treatment: 
only supportive (antipyretics, bedrest)
  • PREVENTION:
    MMR (mumps-morbilli-rubella) for every child at 15m and 6, 11 yrs
146
Q

III. 28 - Paramyxoviruses - RSV, Parainfluenzavirus characteristics

A
  • RSV: Resp. Syncytial Virus
  • (-) ssRNA -negative sense-
  • non-segmented
  • Helical
  • Enveloped: HA, NA, F glycoproteins RNA synthesis in cytoplasm
147
Q

III. 28 - Paramyxoviruses - RSV clinical

A

Spread:

  • resp. droplets
  • Common infection
  • nosocomial spread also possible

Clinical forms:
• Common cold , rhinitis
• Acute exacerbation of COPD and old people
• Bronchiolitis:
- in infants
- URTI followed by tacwypnoe , cyanosis , wheezing

148
Q

III. 28 - Paramyxoviruses - RSV Diagnosis, Treatment, Prevention

A

Diagnosis:

  • clinical
  • RSV PCR from nasal sample if necessary

Treatment:
- Bronchodilators, epinephrine, corticosteroids

Prevention:
Palivizumab for premature babies
(mRNA vaccine in trial)

149
Q

III. 28 - Paramyxoviruses - Parainfluenzavirus 1-4 clinical

A

Spread:

  • resp. droplets
  • common infections Infects epith. cells of resp. tract
  • Common cold URTI: not severe
  • Bronchiolitis, pneumonia: more severe

• Croup: Acute Laryngo-Tracheo-Bronchitis: children age 0,5-6y
–> Acute obstructive laryngitis –> tracheal swelling Hoarseness, barky cough, tachypnoea, Dyspnoea (Usually at night, in autumn, winter)

150
Q

III. 28 Paramyxoviruses - Parainfluenza virus 1-4 DDX and treatment

A

D:

  • Clinical sign
  • X ray: steeple signs

Tx:

  • cold humid air
  • steroid inhalation or suppository Rectodelt
  • salbutamol inhalation for bronchodilatation
  • intubation
151
Q

III. 29 Picornavirus - Poliovirus characteristics

A
  • (+) ssRNA -positive sense- =mRNA
  • icosahedral
  • Naked
  • Member of Enterovirus genus (of the Picornaviridae family)
  • Polio has 3 serotypes – 1, 2, and 3
152
Q

III. 29 Picornavirus - Poliovirus transmission

A
  • because member of Enteroviruses:
  • -> very resistant (pH, heat, detergents) –> enhances spread
  • -> fecoral spread (but rarely causes enteric disease)
153
Q

III. 29 Picornavirus - Poliovirus pathogenesis and clinical

A

–> Replicates in lymphoid.T. & tonsils (Peyer’s patches)
–> viremia to Ant. Horn of spinal cord & brain stem.
–> Replicates in motor neurons
–> causing cell lysis (leading to asymmetrical flaccid paralysis)
(severity and location depends on the infected neurons)
====> can affect: Limbs, Cranial n., Resp. muscles

  • Asymptomatic infection is possible
  • Symptomatic: Febrile illness, Aseptic meningitis
  • Severe: 1%

===> possible outcome:

  • Recovery
  • residual paralysis
  • death
154
Q

III. 29 Picornavirus - Poliovirus

Ddx, Th, Prevention

A

DDx:

  • cultivation
  • Serology

Th:
- not available (supportive only)

Prevention:

  • vaccine: since 1995
    1. IPV: inactivated PV. (Salk v.)
  • -> 2,3,4, 15m then 3,6 yrs
    2. OPV: oral live PV (Sabine v.)
  • ->risk for vaccine related poliomyelitis
  • -> not used in Hungary
155
Q

III. 30 Picornavirus - Coxasckie A Virus

transmission, Clinical

A

Transmission:
- Fecal-oral route

Clinical:
1. Herpangina:
- Fever
- Sore throat
- Vomiting
- soft palate vesicular ulcerations
(self limited, only supportive th)
  1. Hand-Foot-Mouth disease:
    - vesicular exanthem
    - fever
  2. Hemorrhagic conjunctivitis
156
Q

III. 30 Picornavirus - Coxasckie B Virus

clinical

A
  1. Pleurodynia
    - Fever
    - Unilateral severe plueritic hest pain
    - abd pain
    - vomiting
  2. Myocarditis, pericarditis
    - fever
    - heart failure
    - high mortality
  3. infection of langrhans cells
    - maybe associated with insulin dependant DM
157
Q

III. 30 Picornavirus - Echovirus transmission

A

Fecal-oral route –> can infect any tissue (broad tropism)

158
Q

III. 30 Picornavirus - Coxasckie Virus characteristics

A
  • (+)ssRNA -positive sense- =mRNA
  • Icosahedral capsid
  • Naked
  • 30 serotypes
  • we focus on A and B
159
Q

III. 30 Picornavirus - Echovirus characteristics

A

ssRNA, positive sense
Icosahedral capsid
Naked

160
Q

III. 30 Picornavirus -Rhinovirus characteristics

A
  • ssRNA, positive sense
  • Icosahedral capsid
  • Naked
  • 100 serotypes
  • sensitive to pH, Temp
  • Can survive on objects
161
Q

III. 30 Picornavirus - Echovirus clinical

A
  1. aseptic meningitis (~ nr.1 cause)
    - headache and meningeal irritation
  2. Acute febrile URTI with RASH
    - viral exanthem, non-specific rash
  3. Necrotizing hepatitis
    - in newborns

(no treatment or prevention available)

162
Q

III. 30 Picornavirus -Rhinovirus transmission

A
  • Respiratory droplets and by hands –> URTI (multiply in Nose)
  • Unable to replicate in GI tract as enteroviruses
  • Rhinoviruses have Ag drift, as seen in influenza
163
Q

III. 30 Picornavirus -Rhinovirus clinical

A
  • URTI
  • common cold
    –> sneezing, Rhinorrhea, Sore throat, Headache
    RARELY fever !!!
164
Q

III. 30 Picornavirus - Enterovirus

clinical

A
  • very resistant to environmental factors (pH, heat, detergents)
  • Fecoral spread (rarely causes enteric disease)
  • initial multiplication: mucosa of pharynx and tonsils –> viraemia
  • 70 serotypes
  • most infectious: Asymp
  • Humoral immunity is important here
  • Exclusively human pathogen
165
Q

III. 30 Picornavirus - Enterovirus characteristics

A
  • (+) ssRNA =mRNA
  • Icosahedral capsid
  • Naked
  • 5 genera:
  • -> Entero (coxsackie, polio, Echo)
  • -> Rhino
  • -> Hepato (hepatitis A)
  • -> cardio
166
Q

III. 31 Rhabdoviruses characteristics

A
  • (-) ssRNA -negative sense-
  • Bullet shaped (rhabdo=ROD)
  • Enveloped

Includes:

  • Lyssa virus genus (Rabies)
  • Vesiculovirus genus (vesicular stomatitis virus (VSV))
167
Q

III. 31 Rhabdoviruses

transmission

A

Spread: zoonosis

  • worldwide
  • by Bite or bodily fluids of animals or human: dog, cat, fox, wolf, bat
  • Aerosol: from bat dropings
168
Q

III. 31 Rhabdoviruses

pathogenesis

A
  1. At entry: virus infects muscle, nerves –> replicates (long incubation)
  2. Ascending spread: DRG & brain
    (speed depends on the proximity of entry to brain)
  3. Demyelinisation & Negri bodies formation in CNS
  4. Descending infection: to salivary gland & other organs
169
Q

III. 31 Rhabdoviruses clinical

A

Symptoms:

  • incubation: 20-90 days
  • Prodromal stage: fever, headache
  1. Encephalitic rabies:
    - -> fever
    - -> Hydrophobia
    - -> pharyngeal spasms
    - -> hyperactivity subsiding to paralysis
    - -> coma and death
  2. Paralytic rabies : descending flaccid paralyis
170
Q

III. 31 Rhabdoviruses diagnosis

A

Diagnosis:

  • anamnesis
  • PCR: from saliva or CSF
  • Ab’s: from serum or CSF
  • Post mortem: Negri bodies
171
Q

III. 31 Rhabdoviruses treatment

A

Treatment:

  • No treatment after onset of symp! (100% mortality)
  • POSTEXPOSURE ACTIVE IMMUNISATION: if risk of rabies suspected (before symp)
  • Inactivated virus vaccine: series of injections (Pasteur)
172
Q

III. 31 Rhabdoviruses Prevention

A

Prevention:

  • Vaccination of dogs yearly! (live attenuated)
  • Immunisation of wild reservoir animals with vaccine containing food (ORV oral rabies vaccine)
  • Pre-exposure prophylaxis for people at high risk eg. hunters
  • Avoid animal contact especially at risk countries
173
Q

III. 33 Togavirus characteristics

A

ssRNA, positive sense
Icosahedral capsid
Enveloped

Includes Alpha- and Rubiviruses

174
Q

III. 33 Togavirus Alphavirus transmission

A

Via mosquitos (vectors – where replication occurs) – Humans are dead-end hosts

175
Q

III. 33 Togavirus Alphavirus ddx

A

Serology

RT-PRC

176
Q

III. 33 Togavirus Alphavirus prevention

A

Killed vaccine for EEE and WEE

vaccination of horses

177
Q

III. 33 Togavirus Rubiviruses characteristics

A
  • Rubi-virus genus (Rubella name: little red)
  • Used to belong to Togavirus family (toga : coat in Latin)
  • (+) ssRNA
  • icosahedral
  • enveloped
178
Q

III. 33 Togavirus Rubiviruses transmission

A

Spread:

  • Aerosol
  • Respiratory droplets (unvaccinated), mostly in children
179
Q

III. 33 Togavirus Rubiviruses Clinical

A

Symptoms:
• 2 w incubation (most contagious)
• Low grade fever, lymphadenomegaly, headache, pink eye
• Maculopapular rash: starts on face, spreads down
–> In children it is milder (maybe asymp)
–> In adults more systemic signs: arthritis, arthralgia
(Self-limiting illness in non pregnant)

CONGENITAL RUBELLA SYNDROME CRS
- reason for vaccination
- Transplacental spread of virus to foetus:
–> Risk of congenital malformation in first 20 w of pregnancy → In utero death, premature birth or congenital defects:
•Ear: Hearing impairment
•Heart: congenital heart defects
•Eye: cataracts/congenital glaucoma, pigmentary retinopathy
•Late onset manifestations:
–> CNS: intellectual disability, Diabetes mellitus, Thyroid dysfunction

180
Q

III. 33 Togavirus Rubiviruses treatment and diagnosis and prevention

A 
Th: 
Not available (just supportive)

DDx:
-Lab diagnosis: if pregnant, or to DD from other conditions-

• Serology: IgM from mother (may be false positive in pregancy) or newborn
–> Confirmation: Low avidity IgG / 4 fold increase in IgG titere
–> Vaccinated: has Ab’s
• Screening of pregnant
• PCR: from pharynx or urine of newborn or placenta

Prevention:
-MMR: live attenuated rubella virus, at age 15 m, booster at 11 yrs (in hungary)

181
Q

III. 34 Hepatitis A characteristics

A
  • (+) ssRNA =mRNA
  • Icosahedral capsid
  • Naked
  • Hepatovirus genus (from Enterovirus from Picornaviruses)
  • Only 1 serotype
  • Resistant to environmental factors
182
Q

III. 34 Hepatitis A

transmission and clinical

A

Spread: fecooral food, water, bad hygiene, undercooked shellfish

  • ->intestine –> liver (via circulation) –> Infects hepatocytes –> Kupffer cells
  • -> immune response against infected hepatocytes –> Liver damage

Clinical:

  • Long incubation
  • Acute hepatitis (never chronic)
  • -> Fatigue, faver, nausea, jaundice
  • Sometimes subclinical (rarely fulminant)
  • lifelong immunity develops
183
Q

III. 34 Hepatitis A

diagnosis, treatment, prevention

A

Diagnosis:
- serology : Anti-HAV (IgM +)

Therapy: not available

Prevention:

  • active immunisation for travellers to endemic areas
  • passive : anti-HAV human Ig’s
184
Q

III. 34 Hepatitis E characteristics

A

ssRNA positive sense

resistance to heat and acid

185
Q

III. 34 Hepatitis E clinical

A

severe in pregnancy

186
Q

III. 34 Hepatitis E treatment

A

none

187
Q

III. 34 Hepatitis E prevention

A

vaccination in China

188
Q

III. 34 Hepatitis E ddx

A

Anti-HEV IgM

189
Q

III. 35 Hepatitis B characteristics

A

dsDNA, circular
Icosahedral capsid
Enveloped
Replicates in and outside the nucleus

Uses reverse transcriptase (but does not integrate into the host chromosome)

190
Q

III. 35 Hepatitis B pathogenesis

A

Infects the liver, but can also infect kidney and pancreas

Symptoms and disease due to type 3 HSR (immune complexes of HBsAg+Anti-HBs Ag)

191
Q

III. 35 Hepatitis B treatment

A
  • Lamivudine – cytidine analogue (inhibit viral DNA synthesis)
  • Nucleoside Reverse Transcriptase Inhibitor (NRTI)
  • Interferon a
  • For kids at risk – Anti-HepB Immunoglobulins
192
Q

III. 35 Hepatitis B transmission

A

Blood contamination (e.g. parenteral, needles etc.)

Sexual contact

Vertical infection (perinatal) – TORCHES

193
Q

III. 35 Hepatitis D characteristics

A

envelope

ssRNA negative - circular

194
Q

III. 35 Hepatitis C ddx

A
  • Acute infection ~ ALT will rise and eventually fall after 6 months – Viral RNA persist in serum after 6 months
  • ELISA of anti-HCV antibodies or PCR of RNA genome for diagnosis – Western-blot for confirmation (like HIV)
  • Associated with cryoglobulins – precipitating Ig (mostly IgM) in cooler temperatures
  • Liver biopsy – shows lymphocytes in the portal triad
195
Q

III. 35 Hepatitis B prevention

A

Recombinant vaccine made of HBsAg given by 3 injections (at birth, 1 month and 6 months)

196
Q

III. 35 Hepatitis C pathogenesis

A

HCB binds to CD81 (tetraspanin) surface receptors (of hepatocytes and B-cells). It can also coat itself in LDL and use the LDL receptor to enter the hepatocytes. Cell-mediated immune response (CD8+) will cause resolution of infection and tissue damage. Chronic infection leads to exhaustion of CD8+ T-cells.

197
Q

III. 35 Hepatitis C characteristics

A

ssRNA, positive sense

Icosahedral capsid

Enveloped

Member of the Flaciciridae family

Virus-encoded RNA polymerase lacks proofreading exonuclease activity in the 3’-5’ direction. This makes the virus prone to mutation, causing antigenic variability (of envelope proteins). The virus mutates so quickly there is no protection from it ~ no vaccination

198
Q

III. 35 Hepatitis C transmission

A

Blood transfusions
Needle sharing (I.V drug users, accidental pricks from carrier, tattooing etc.)
sexual contact

199
Q

III. 35 Hepatitis C clinical

A

Acute hepatitis

  • fever, malaise, headache, anorexia, vomiting, dark urine and jaundice

Chronic hepatitis ~ 60-80% of hepatitis C infections will become chronic

  • Same symptoms, but also chronic fatigue
  • Extrahepatic manifestations include
    Membranous nephropathy and membranoproliferative glomerulonephritis
  • Can progress to cirrhosis (used also to grade the disease severity)
  • Can progress to hepatocellular carcinoma – primary cause
200
Q

III. 35 Hepatitis C treatment

A
  • Ribavirin (nucleoside inhibitor, guanosine analogue)
  • Interferon a
  • Protease inhibitors (Broceprevir or Telaprevir)
201
Q

III. 35 Hepatitis D transmission

A

parental

202
Q

III. 35 Hepatitis D clinical

A

acute hepatitis

203
Q

III. 35 Hepatitis D ddx

A

anti-HDV ELISA

mrts (19 decks)

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