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Micro Flashcards

1
Q

III.11 Adenovirus characteristics

A
  • dsDNA
  • Icosahedral capsid
  • Naked
  • Fiber antigens for attachment to receptor and agglutination of RBCs
  • Human adenovirus has 57 serotypes (number 14 most severe), differentiated by hemagglutinin inhibition
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2
Q

III.11 Adenovirus Transmission

A

Contact, respiratory droplets, feces and aerosol

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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: virus is lytic – production occurs/replication
  • In non-permissive cells: can be chronic of oncogenic (transformation occurs)
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4
Q

III.11 Adenovirus Clinical

A

a) Respiratory diseases: Tonsillitis (#1 cause), pharyngitis, pharyngoconjunctival fever, pneumonia, pertussis-like symptoms
b) Enteric infection: Watery diarrhea
c) Eye infection: Epidemic keratoconjunctivitis, follicular conjunctivitis
d) UTI: Acute hemorrhagic cystitis
e) Immune suppressed patients: Pneumonia, hepatitis, encephalitis
* Reactivation can occur in case of immunosuppressed patients

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5
Q

III.11 Adenovirus Ddx

A

Serology, cultivation on HeLA, epithelial cell culture –> strong CPE (cytopathic effect), rapid test for diarrhea

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6
Q

III.11 Adenovirus treatment

A

none - supportive

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7
Q

III.11 Adenovirus vaccine

A

Live attenuated (serotype 4 and 7) –> only for military recruits

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8
Q

III.12 Herepesvirus : HSV1 and HSV2 characteristics

A
  • dsDNA – linear
  • Icosahedral capsid – Encode glycoproteins for attachment, fusion, immune escape
  • Enveloped – Sensitive to acid, detergents etc.
  • α-herpesvirus
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9
Q

III.12 Herepesvirus : HSV1 and HSV2 Transmission

A

Saliva, vaginal secretions, transcervical (perinatal), TORCH

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10
Q

III.12 Herepesvirus : HSV1 and HSV2 Pathogenesis

A

The virus targets Mucoepithelial cells:
Viral replication in site of infection –> local nerve ending invasion –> retrograde axonal transport to dorsal root ganglia –> latency

*Generally: acute infection (early proteins) –> latency (viral genome present, but no viral proteins produced – periodic reactivation i.e. due to UV, stress etc.

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11
Q

III.12 Herepesvirus : HSV1 clinical

A
  • Herpes labialis (cold sores) and gingivostomatitis Keratoconjuntivitis
  • Herpetic Whitlow – rash on fingers
  • Erythema multiforme – back of hands/feet
  • Encephalitis – due to necrosis and hemorrhage of neurons
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12
Q

III.12 Herepesvirus : HSV2 clinical

A
  • Genital herpes – inguinal lymphadenopathy and painful genital lesion
  • Neonatal herpes – transcervical or transplacental (liver involvement/encephalitis)
  • Aseptic meningitis
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13
Q

III.12 Herepesvirus : HSV1 and HSV2 ddx

A

Scrapings of the base of lesions – cultivation on HeLA

PCR of CSF – for encephalitis

Serology to distinguish HSV-1 and HSV-2

Genital infections – virus isolation from vesicles –> Tzanck smear
*Tzanck smear - Cytology that will show multinucleated giant cells, intranuclear eosinophilic Cowdry type A inclusion bodies are also seen

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14
Q

III.12 Herepesvirus : HSV1 and HSV2 treatment

A

Acyclovir (inhibition of DNA synthesis) – does not prevent latent infection

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15
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus characteristics

A
  • dsDNA
  • Icosahedral capsid ~ 150nm
  • Enveloped
  • α-herpesvirus
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16
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus transmission

A

Respiratory droplets, contact(rare), TORCH

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17
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus Pathogenesis

A

Primary infection in mucosa of respiratory tract –>blood and lymphatics –> dissemination to skin –> dermal vesiculopapular rash –> chicken pox –> latency in sensory ganglia –> reactivation –> migrates along neural pathways to skin –> Shingles

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18
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus Clinical

A

Primary infection: Varicella (chicken pox)

  • Asynchronous rash forms small, itchy blisters all over the body (different stages; Macula, vesicles, scabs).
  • Presents with fever, headache, pharyngitis, malaise (general discomfort), rhinitis.
  • Adults present with pneumonia, encephalitis. Highly contagious!

Secondary infection (recurrence): Zoster (Shingles)

  • Pain in a given dermatome with rash limited to said dermatome.
  • Develops in immunocompromised patients
  • Can cause post-herpetic neuralgia (chronic pain that lasts for years due to damage of nerves addected by virus) *

Herpes Zoster ophthalmicus – Vision loss when CNV/I is affected

Congenital varicella syndrome –> Limb hypoplasia, cutaneous dermal scarring, blindness

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19
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus ddx

A

Serology –> Examine skin lesion scraping

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

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20
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus treatment

A

Acyclovir

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21
Q

III.13 Herpesvirus - VZV - Varicella Zoster Virus Vaccine

A

Passive (VZ-Ig) – immunosuppressed patient, ineffective in active cases

Active; live, attenuated – cell mediated immunity

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22
Q

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

A
  • large linear dsDNA
  • Icosahedral capsid
  • Enveloped
  • gamma-herpesvirus
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23
Q

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

A

Saliva and respiratory secretions (90% of population is seropositive)

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24
Q

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

A

Infects permissive nasopharyngeal epithelial cells, salivary and lymphoid tissues.

Latent infection in B-cells;
Binds CDRI and produce LMP1 (latent membrane protein 1) –>
a) NFKB activation and B-cell proliferation
b) Bcl2 ⊣ apoptosis

This causes production of atypical CD8+ T-cells – Downey cells against it

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25
Q

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

A

a) Infectious mononucleosis – “Kissing disease” (transmitted by saliva)
Exudative tonsillitis, lymphadenopathy, splenomegaly.
Presence of atypical lymphocytes used to distinguish from CLL.
Paul-Bunnel reaction positive – it has heterophile antibody

b) Hairy oral leukoplakia – non-precancerous hyperproliferation of lingual epithelial cells
oral thrush

c) Burkitt lymphoma – Tumor growth in lymph nodes; maxilla and mandible (joint).
Due to translocation of c-myc oncogene which becomes active promotor (t(8;14)).

Endemic type – Associated with endemic areas of malaria
Sporadic/non-African type – commonly affects the ileocecal region
Immunodeficient type – associated with AIDS

d) Nasopharyngeal carcinoma – commonly in Asians. Tumor cell of epithelial origin
e) Hodgkin’s (B-cell) lymphoma – Dx by presence of Reed-Sternberg cells

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26
Q

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

A

Blood smear –> Downey cells

Monospot test – a form of heterophile Ab-test –> heterophile Abs positive – IgM agglutination to Paul-Bunnel antigens on sheep RBCs.

Heterophile Abs are produced due to B-cell induction by EBV

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27
Q

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

A

symptomatic treatment for mono

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28
Q

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

A
  • dsDNA
  • Icosahedral capsid ~ 150nm
  • Enveloped
  • beta-herpesvirus
  • Latency in monocytes, macrophages, T-cells
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29
Q

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

A

Direct and sexual contact by bodily fluids
transplantation
TORCH

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30
Q

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

A

Infects salivary glands epithelial cells by binding to the integrin receptors.
Established persistent in fibroblasts, epithelial cells, macrophages, etc.

Latency is established in mononuclear leukocytes (B-cells, T-cells, macrophages).
Reactivation occurs by immunosuppression.

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31
Q

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

A

a) Congenital CMV infection – CNS damage causes sensorineural deafness.
Periventricular calcifications lead to seizures. Thrombocytic purpura w/ “blueberry Muffin” rash, jaundice, hepatosplenomegaly, pneumonitis, fetal hydrops

b) Mononucleosis – negative heterophile
c) Esophagitis – with linear ulcerations

d) CMV colitis – with ulcerated walls
e) Interstitial pneumonitis – leads to severe systemic infection due to reactivation in transplant patients or AIDS

f) CMV Retinitis – common in AIDS patients with a CD4+ count under 50 cells/&L. Blind spots, vision loss, retinal
necrosis and pizza pie retinopathy on fundoscopic exam

g) Hepatitis – in pregnancy

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32
Q

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

A

Histology –> intranuclear basophilic Owl’s eyes inclusions. Take sample from buffy coat (the layer of WBC from a centrifuged blood) and stain with Pap or H&E

PCR –> DNA detection and amplification

Cell culture –> fibroblast culture

Serology –> ELISA, Paul-Bunnel antigen detection

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33
Q

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

A

Immunocompetent people which are asymptomatic do not require treatment

Severe infection in immunocopromised people, Gancyclovir, Cidofovir and Foscarnet (for resistance, UL97 mut) can be given.

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34
Q

III.16 Herpesvirus - HHV6 characteristics

A

dsDNA
Icosahedral capsid ~ 150 nm
Enveloped
beta-herpesvirus

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35
Q

III.16 Herpesvirus - HHV6 Transmission

A

salvia

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36
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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37
Q

III.16 Herpesvirus - HHV6 clinical

A

in immunocompromised (HHV6a)

  • Encephalitis
  • Pneumonitis
  • Chorioretinitis

Neonatal HHV-6B ~ Roseda infantum (exanthema subitum)

  • Primarily in children 3-6 months old
  • Fever that could lead to febrile seizures
  • Maculopapular rash that spares the face
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38
Q

III.16 Herpesvirus - HHV6 ddx

A

Clinical picture

PRC, serology – Virus isolation from lymphocytes

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39
Q

III.16 Herpesvirus - HHV6 treatment

A

Self-limited

Gancyclovir, symptomatic, no vaccine

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40
Q

III.16 Herpesvirus - HHV 7 clinical

A

Also causes Exanthema subitum, but less frequently than HHV-6. Same symptoms

Others: 
- Pytiriasis rosea (Herald patches), “gloves and socks syndrome”
Severe cases: 
- encephalitis
- flaccid paralysis
- hepatitis, gastritis
- lowered lymphocyte count
- LAD
- diarrhea
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41
Q

III.16 Herpesvirus - HHV8 characteristics

A

dsDNA
Icosahedral capsid
Enveloped
gamma-herpesvirus

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42
Q

III.16 Herpesvirus - HHV8 transmission

A

Saliva, sexual contact – higher prevalence in Russian men, Sub-Saharan Africa and Mediterranean

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43
Q

III.16 Herpesvirus - HHV8 pathogenesis

A

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

HHV-8 activates VEGF

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44
Q

III.16 Herpesvirus - HHV8 clinical

A

a) Kaposi sarcoma
Opportunistic infection associated with AIDS
Lesions on nose, extremities, mucus membrane
Lesions may be plaque, patches, macule or nodule – arise from mesenchymal cells Angiogenesis within lesion causes violet color
Commonly affects hard palate, and also seen in GI

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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45
Q

III.16 Herpesvirus - HHV8 ddx

A

Clinical, antibody detection, viral DNA by PCR

Differential diagnosis from bacillary angiomatosis (B. henslae) by microscopic exam (will show neutrophil infiltrate, instead of lymphocytes as with HHV-8)

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46
Q

III.16 Herpesvirus - HHV8 treatment

A

Liquid nitrogen

interferon-alpha

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47
Q

III. 17 Parvovirus characteristics

A

ssDNA
Icosahedral capsid ~20-25 nm (smallest virus)
No envelope

Erythrovirus –> Parvovirus B19 ~ only one to cause human disease

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48
Q

III. 17 Parvovirus transmission

A

Respiratory droplets, fomites, TORCH

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49
Q

III. 17 Parvovirus clinical

A

a) Erythema Infectiosum ~ “fifth disease”
Slapped cheek syndrome – starts as fever, then rash
Teenagers may develop papular purpuric gloves and socks syndrome Adults may develop arthralgia, arthritis and edema

b) Fetal hydrops
Can cross-placenta; occurs in the first 2 trimesters of pregnancy
This is due to CHF (congestive heart failure) leading to severe anemia and edema

c) Aplastic anemia
Infection can lead to lower erythropoiesis
This may cause anemia which is only significant in patients with blood disorders (i.e. sickle cell, Thalassemia, Hereditary spherocytosis)
Bone marrow depletion – severe situation if chronic anemia is present

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50
Q

III. 17 Parvovirus ddx

A

Clinical, serology

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51
Q

III. 17 Parvovirus treatment

A

self-limiting

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52
Q

III. 17 Parvovirus pathogenesis

A

Parvovirus B19

Target cells: Normoblasts –> failure of RBC production

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53
Q

III. 18 Papilloma Virus characteristics

A

cdsDNA
Icosahedral capsid
naked

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54
Q

III. 18 Papilloma Virus Transmission

A

Direct and sexual contact (can also infect children during delivery)

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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55
Q

III. 18 Papilloma Virus ddx

A

Clinical – for cutaneous warts

PCR – to distinguish serotype

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56
Q

III. 18 Papilloma Virus treatment

A

Cryotherapy

Cidofovir

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57
Q

III. 18 Papilloma Virus prevention

A

Guardisol – using capsid proteins (recombinant)

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58
Q

III. 18 Polymoavirus characteristics

A

cdsDNA
Icosahedral capsid
naked

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59
Q

III. 18 Polymoavirus Transmission

A

Respiratory droplets, saliva

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60
Q

III. 18 Polymoavirus Pathogenesis

A

Infects tonsils and lymphocytes, then spreads by viremia to kidney.
secondary viremia occurs and become latent in immunocompetent or reactive in immunosuppressed.

1) BK virus (from first patient) ~ latency in kidney
Nephropathy (nephritis and urethral 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 leukoencephalopathy (PML) ~ infection of oligodendrocytes causing demyelination of CNS.
Multifocal brain lesions in white matter (DDX; Toxoplasma)
Symptoms are deranged speech, vision and coordination loss, paralysis of limbs, death
Usually occurs in AIDS patients

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61
Q

III. 18 Polymoavirus ddx

A

MRI/CT
ELISA
PCR of CSF

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62
Q

III. 18 Polymoavirus treatment

A

none

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63
Q

III. 18 Papilloma Virus clinical

A

1) Mucosotropic genotypes

a) Low risk serotypes; 6-11
Condyloma Accuminata (anogenital warts)
Laryngeal papilloma

b) High risk serotypes; 16-18, 31, 33
Pre-neoplastic condition (associated with dysplasia) CIN/VIN/VAIN, penis, anus, mouth, throat
E6 ⊣ p53
E7 ⊣ Retinoblastoma

2) Cutaneous genotypes; 1-4
Low risk serotypes
Hyperkeratosis (growth of basal and spinosum) leads to formation of warts

Common warts (2-4): Found on hands/fingers

Plantar warts (1): Found on soles – deeper and more painful

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64
Q

III.19 Poxvirus characteristics

A

dsDNA ~ replicates in cytoplasm
Complex structure ~ 300 nm (Biggest virus!)
Enveloped
2 lateral bodies

Variola virus ~ Smallpox

Vaccinia virus ~ Vaccination of smallpox

Cow pox virus ~ Share antigenic determinant with variola virus (Jenner)

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65
Q

III.19 Poxvirus transmission

A

Respiratory droplets, contact

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66
Q

III.19 Poxvirus clinical

A

1) Smallpox (Variola – minor or major depending on immune status)

Virus enters the upper respiratory tract and disseminates via lymphatics causing viremia After second viremia, it infects all dermal tissues and internal organs – “pocks”
5-7 day of incubation;
Flu-like symptoms for 2-4 days followed by a rash (macule – papule – vesicle – pustule –>
synchronous). The vesicles are deep and hemorrhagic.

2) Molluscum contagiosum virus
Benign epithelial tumor (wart-like). 
Acquired by direct contact 
Common on trunk and genitalia. 
Treated by liquid nitrogen
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67
Q

III.19 Poxvirus ddx

A

Isolation from vesicles – intra-cytoplasmic eosinophilic

Guarnieri inclusion bodies (site of viral replication)

Embryonated egg – chorioallantoic membrane inoculation

Serology

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68
Q

III.19 Poxvirus vaccine

A

Live attenuated- Cowpox vaccine is efficient against cowpox and smallpox

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69
Q

III.20 Arenavirus characteristics

A

ssRNA ~ Ambisense, has both positive and negative sense sections

Helical ~ 50-300 nm

Enveloped with projections

Natural host; rodents

“Sandy” – ribosome granules of host cell origin

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70
Q

III.20 Arenavirus transmission

A

Zoonotic, rodents shedding virus via saliva, urine and feces

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71
Q

III.20 Arenavirus pathogenesis

A

Arenaviruses usually cause persistent infections. They infiltrate macrophages leading to release of IFN and cytokines that causes cell and vascular damage. T-cell induced effects will cause further tissue destruction. Incubation time is 10-14 days.

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72
Q

III.20 Arenavirus ddx

A

Grainy appearance on EM, serology, RT-PCR

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73
Q

III.20 Arenavirus treatment

A

Ribavirin for Lassa fever, supportive therapy for LCM

  • Virus could be inactivated by heating, low pH, irradiation and detergents
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74
Q

III.20 Arenavirus -Lymphocytic choriomeningitis virus (LCM)

A

Ranges from asymptomatic (in immune competent) to aseptic meningitis

Biphasic disease; 10 phase with fever, flu-like symptoms and myalgia to the 20 phase with meningitis, encephalitis, lymphocytic infiltration of choroid plexus

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75
Q

III.20 Arenavirus - Lassavirus

A

Hemorrhagic fever with 50% mortality due to hypovolemic shock. May present with coagulopathy, petechia, no vasculitis

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76
Q

III.20 Arenavirus - Machupovirus

A

Similar symptoms to Lassavirus, but less severe * Different endemic areas

Lassa- Hemorrhagic fever with 50% mortality due to hypovolemic shock. May present with coagulopathy, petechia, no vasculitis

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77
Q

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

A

ssRNA ~ 3 segments. Circular, negative
Helical capsid

Enveloped with projections

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78
Q

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

A

Arboviruses (arthropod-borne), except Hantavirus (rodent-borne)

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79
Q

III.21 Bunyaviruses- HantaVirus clinical

A

Hantavirus (aka Sin Nombre)

Transmission via rodent feces or urine
- Hemorrhagic fever with Renal syndrome (HFRS)

Hemorrhagic fever (leakage of RBC and plasma through endothelium)

Pre-renal azotemia - Pulmonary syndrome
Pulmonary edema due to capillary leak

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80
Q

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

A

PCR – Hantavirus
RVFP + CEO – ELISA
Crimean-Congo – ELISA

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81
Q

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

A

none

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82
Q

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

A

Inactivated Henta in Asia

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83
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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84
Q

III.22 Coronavirus characteristics

A

ssRNA, positive sense

Helical capsid

Enveloped ~ glycoproteins give a halo.

Three proteins (open reading frame, nucleocapsid protein, enveloped protein) Cell receptors – SARS-CoV, SARS-CoV-2: ACE2

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85
Q

III.22 Coronavirus transmission

A

Respiratory droplets

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86
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.

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87
Q

III.22 Coronavirus clinical

A
  • Common cold: URT infection Mild symptoms, no fever
  • SARS-CoV: LRT infection
    Acute bronchitis that leads to ARDS
    Flu-like illness with fever, dry cough, dyspnea, progressive hypoxia
    CT shows ground glass opacities, multifocal consolidation lesions
    (Pneumonia, ARDS, cytokine storm, MOF)
  • MERS: endemic version of SARS
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88
Q

III.22 Coronavirus ddx

A

PCR

serology

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89
Q

III.22 Coronavirus treatment

A

Supportive therapy

Antiviral treatment (i.e. HIV protease inhibitor – ritonavir) can reduce incidence of severe/critical cases

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90
Q

III.22 Filovirsues characteristics

A

ssRNA
negative sense
Helical capsid
Enveloped

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91
Q

III.22 Filovirsues transmission

A

From monkeys to human, and then human-to-human (bodily fluids)

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92
Q

III.22 Filovirsues clinical

A
  • Marburg virus
  • Ebola virus

Severe form of hemorrhagic fever, could lead to hypovolemic shock and multiple organ failure

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93
Q

III.22 Filovirsues ddx

A

Careful to avoid accidental infection
– level 4 isolation required

Marburg virus in tissue culture, Ebola virus in animal inoculation

Serology

RT-PCR

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94
Q

III.22 Filovirsues treatment

A

No treatment - Remdesivir

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95
Q

III. 23 Flavivirus - Yellow Fever, Dengue Fever characteristics

A

ssRNA, positive sense

Icosahedral capsid

Enveloped

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96
Q

III. 23 Flavivirus - Yellow Fever vector

A

Aedes mosquitos, hosts are humans and monkeys

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97
Q

III. 23 Flavivirus - Yellow Fever clinical

A

Yellow fever

Jaundice, backache, bloody diarrhea, nausea, vomiting, headache

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98
Q

III. 23 Flavivirus - Dengue Fever vector

A

Aedes mosquitos, hosts are humans and monkeys

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99
Q

III. 23 Flavivirus - Dengue Fever clinical

A

Dengue fever/breakbone fever:

Infects bone marrow; presents with fever, headache, vomiting, muscle/joint pain and measles-like rash that blanches when compressed

In severe dengue we can see thrombocytopenia, hemorrhagic fever, renal failure

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100
Q

III. 23 Flavivirus - Yellow Fever, Dengue Fever ddx

A

ELISA
HAI (hemagglutinin inhibition)
Latex particle agglutination

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101
Q

III. 23 Flavivirus - Yellow Fever, Dengue Fever treatment

A

supportive

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102
Q

III. 23 Flavivirus - Yellow Fever, Dengue Fever vaccine

A

yellow fever - live attenuated

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103
Q

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

A

ssRNA, positive sense

Icosahedral capsid

Enveloped

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104
Q

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

A

ELISA
HAI (hemagglutinin inhibition)
Latex particle agglutination

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105
Q

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

A

supportive

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106
Q

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

A

inactivated vaccine - tick-borne encephalitis

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107
Q

III. 24 Flavivirus - Zika Virus vector

A

Aedes mosquitos

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108
Q

III. 24 Flavivirus - Zika Virus clinical

A

Fever, rash, myalgia, arthralgia

Congenital Zika syndrome – microcephaly, CNS damage

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109
Q

III. 24 Flavivirus - West Nile vector

A

Culex mosquitos, hosts are birds (killed by virus)

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110
Q

III. 24 Flavivirus - West Nile clinical

A

Complications; encephalitis, meningitis, flaccid paralysis, seizures, coma

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111
Q

III. 24 Flavivirus - tick borne encephalitis (Fruehsommer-meningo-encephalitis virus) vector

A

Ixodes tick, hosts are animals, tick-transovarian infection, can spread by goat milk

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112
Q

III. 24 Flavivirus - tick borne encephalitis (Fruehsommer-meningo-encephalitis virus) clinical

A

Biphasic; influenza-like symptoms, febrile illness

Aseptic meningitis/meningoencephalitis

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113
Q

III. 25 Calicivirus characteristics

A

ssRNA, positive sense

Icosahedral capsid

Naked virus

Many strains have cup-shaped depression (calyx = cup)

Divided into two genera of human pathogenic viruses; Norovirus (aka. Norwalk virus) and Sapovirus

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114
Q

III. 25 Calicivirus transmission

A

Fecal oral route
contaminated water
aerosol

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115
Q

III. 25 Calicivirus clinical

A

Nausea
vomiting
watery diarrhea – self-limiting gastroenteritis

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116
Q

III. 25 Calicivirus ddx

A

Serology
RT-PCR
radioimmunoassay

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117
Q

III. 25 Calicivirus treatment

A

rehydration

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118
Q

III. 25 Rotavirus characteristics

A

dsRNA, both positive and negative
Icosahedral capsid
Naked virus

All viruses have between 10-12 segments

All viruses have unique, double protein shell (coat) made of inner/outer capsid (resembles couch wheel)

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119
Q

III. 25 Rotavirus Transmission

A

Fecal-oral

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120
Q

III. 25 Rotavirus Clinical

A 
NSP4 viral enterotoxin 
increases Cl- permeability which prevents absorption of water leading to 
- watery diarrhea
- vomiting 
- dehydration
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121
Q

III. 25 Rotavirus ddx

A

ELISA – from stool (virion)

Blood – Ab titer

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122
Q

III. 25 Rotavirus treatment

A

supportive therpay

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123
Q

III. 25 Rotavirus vaccine

A

Live attenuated – needs to be given before 3 months or else there’s an increased risk for intussusception

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124
Q

III. 25 Astrovirus characteristics

A

ssRNA
positive sense
Icosahedral capsid
Naked virus

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125
Q

III. 25 Astrovirus transmission

A

Fecal-oral route

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126
Q

III. 25 Astrovirus clinical

A

Watery diarrhea for 2-3 days

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127
Q

III. 25 Astrovirus ddx

A

Serology

RT-PCR

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128
Q

III. 25 Astrovirus treatment

A

Supportive

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129
Q

III. 26 Orthomyxoviruses characteristics

A

ssRNA, negative sense

Helical

Enveloped

RNA synthesis in nucleus (only RNA virus)

Possesses Hemagglutinin and Neuraminidase glycoproteins

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130
Q

III. 26 Orthomyxoviruses transmission

A

Respiratory droplets, bodily fluids

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131
Q

III. 26 Orthomyxoviruses variation

A
  • Antigenic drift: small, slow change of Antigen – change by point mutation.

Neutral Antibody against HA block binding to cells. Mutations in HA epitopes prevents neutral Aantibody from binding.
Influenza A, B – causes epidemic/seasonal flu

  • Antigenic shift: great, fast change of Ag – co-infection of 2 different strains causes gene reassortment
    Gives new subtypes due to genetic recombination of H and N segments of human and non-human species.
No cross-protective immunity against virus with new HA
i.e. H1N1 - Spanish flu
H2N2 - Asian flu
H3N1 - Hong Kong Flu
H5N1 Hong Kong avian flu
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132
Q

III. 26 Orthomyxoviruses pathogenesis

A

HA binds sialic acid on cell membrane of epithelial cells in lung/throat. Many different HA antigens (H1, H2, H3) are seen in influenza. These antigens detect cell tropism (which cell the virus can infect). Anti-HA antibodies protects the person from infection with the same stain in the future. M2 protein (a H+ channel which adjusts the pH for the virus need) gets the virus ready for viral encoding. After replication in nucleus, the virus binds host cell via the same residues as HA. NA cleaves Sialic acid from membrane to rely new virion from cell.

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133
Q

III. 26 Orthomyxoviruses clinical

A

Influenza A, B and C (also known as flu)

Upper respiratory tract infection with headache, high fever, malaise, chills, myalgia and coughing (GI symptoms in kids)

Complications include pneumonia and bronchitis

Associated with Guillan Barré syndrome: ascending paralysis, albuminocytological dissociation, elevation in CSF proteins with normal WBC count.

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134
Q

III. 26 Orthomyxoviruses ddx

A

Clinical or HA serotyping to detect virus type

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135
Q

III. 26 Orthomyxoviruses treatment

A

Amantadine (only for influenza A) and Rimantadine ~ M2 ion channel modifier

Osettamavir ~ Neuraminidase inhibition (Tamiflu)

  • Aspirin is contraindicated in children after infection (Reye’s syndrome) – Fatty liver, LF, encephalitis, rash etc
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136
Q

III. 26 Orthomyxoviruses vaccine

A

Trivalent type consists of 2 A strains and 1 B strain/or tetravalent with 2A2B

  • Inactivated (killed): given intramuscular
  • Live attenuated: given intranasally (as spray)
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137
Q

III. 27 - Paramyxoviruses - Mumps, Morbillivirus characteristics

A

ssRNA, negative sense, non-segmented
Helical

Enveloped – HA, NA, F glycoproteins RNA synthesis in cytoplasm

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138
Q

III. 27 - Paramyxoviruses - Mumps clinical

A 
Mumps virus (Rubulavirus). 
Enters upper respiratory tract --> spread to lymph node --> viremia.

Painful edematous enlargement of parotid and other glands ~ inflammation salivary glands, parotitis, pancreatitis, orchitis, adrenal gland etc.

Symptoms includes fever, headache and malaise. If CNS is also affected it could lead to meningoencephalitis which can eventually leads to deafness.

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139
Q

III. 27 - Paramyxoviruses - Mumps ddx

A

ELISA

HAI

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140
Q

III. 27 - Paramyxoviruses - Mumps prevention

A

live attenuated vaccine, MMR vaccine

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141
Q

III. 27 - Paramyxoviruses - Morbilli clinical

A

4 C’s; cough, coryza (runny, stuffy nose), conjunctivitis, koplik.

Symptoms include

  • Koplik spots (vesicles on buccal mucosa)
  • maculopapular rash (confluent, DDX from Rubella)
  • acute rhinitis and conjunctivitis.

Complications are otitis media, bronchitis, giant cell pneumonia (with Warthrin-Finkeldy cells), subacute sclerosing panencephalitis (SSPE) which leads to CNS degeneration.

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142
Q

III. 27 - Paramyxoviruses - Morbilli ddx

A

ELISA

HAI

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143
Q

III. 27 - Paramyxoviruses - Morbilli prevention

A

live attenuated vaccine, MMR vaccine

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144
Q

III. 28 - Paramyxoviruses - RSV, Parainfluenzavirus characteristics

A

ssRNA, negative sense, non-segmented
Helical

Enveloped – HA, NA, F glycoproteins RNA synthesis in cytoplasm

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145
Q

III. 28 - Paramyxoviruses - RSV clinical

A

Atypical pneumonia in first year, bronchitis, bronchiole necrosis can occur

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146
Q

III. 28 - Paramyxoviruses - RSV characteristics

A

Respiratory syncitial virus (RSV)

F glycoprotein

i.e. pneumovirus

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147
Q

III. 28 - Paramyxoviruses - Parainfluenzavirus 1,2 clinical

A

Croup (laryngotracheobronchitis) in first 5 years

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148
Q

III. 28 - Paramyxoviruses - Parainfluenzavirus 3 clinical

A

Pneumonia in first year

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149
Q

III. 28 - Paramyxoviruses - Parainfluenzavirus 4 clinical

A

Upper RTI, mild catarrhal symptoms

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150
Q

III. 29 Picornavirus - Poliovirus characteristics

A

ssRNA, positive sense

Naked

Member of Enterovirus genus of the Picornaviridae family

Polio has 3 serotypes – 1, 2, and 3

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151
Q

III. 29 Picornavirus - Poliovirus transmission

A

Fecal-oral route

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152
Q

III. 29 Picornavirus - Poliovirus pathogenesis

A

Replicates in lymphoid tissue and tonsils (Peyer’s patches). Spreads (viremia) from lymphoid tissue to anterior horn of spinal cord and brain stem. Replicates in motor neurons, causing cell lysis (leading to paralysis)

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153
Q

III. 29 Picornavirus - Poliovirus clinical

A
  • Asymptomatic illness – 75% of cases
  • Absortive Poliomyelitis – 20% of cases (presents with URT infection and GI disturbances)
  • Non-paralytic poliomyelitis – 0,1-0,5% of cases
    Causes acute flaccid paralysis in which muscles become weak, floppy and paralyzed. Most commonly in lower limb (vary from 1 to 4 limbs – tetraplegia).
    Depending on the site paralysis, can be classified as spinal, bulbospinal, bulbar. Bulbar polio is the most severe since it paralyzes respiratory muscles.
  • Post-polio syndrome – occurs 15-30 years after
    Loss of muscle function (due to late harm of neurons)
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154
Q

III. 29 Picornavirus - Poliovirus ddx

A

Specimen from throat (few days) or from feces (for 30 days)
Serology
RT-PCR, virus is absent from CSF despite meningitis

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155
Q

III. 29 Picornavirus - Poliovirus treatment

A

Supportive. Iron-lung earlier (negative pressure respirator)

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156
Q

III. 29 Picornavirus - Poliovirus prevention

A
  • Inactivated (killed) trivalent poliovirus vaccine (IPV) – Salk vaccine (given IM) ~ Does not form IgA
  • Live attenuated bivalent poliovirus vaccine (OPV) – Sabin vaccine (given orally) ~ Forms IgA and IgG

Can infect immunocompromised, no longer used in USA/Hungary because of its potential to shed in feces.

Polio is found in three different countries today; Afghanistan, Pakistan, Nigeria

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157
Q

III. 30 Picornavirus - Coxasckie Virus characteristics

A

ssRNA, positive sense
Icosahedral capsid
Naked

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158
Q

III. 30 Picornavirus - Coxasckie Virus transmission

A

Fecal-oral route

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159
Q

III. 30 Picornavirus - Coxasckie Virus pathogenesis

A

Replicates in enterocytes and lymphocytes of intestines.

Primary viremia –> target tissue (i.e. cardiac myocyte) –> 2nd viral replication –> secondary viremia

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160
Q

III. 30 Picornavirus - Coxasckie Virus A clinical

A
  • Hand, foot, mouth disease ~ usually A16 serotype
    Red vesicular rash and mild fever. Appear on hands, feet and in the mouth
  • Herpengina
    Sore throat, fever and vomiting
    Vesicular ulcerated lesions around posterior part of soft palate and uvula
  • Acute hemorrhagic cystitis ~ usually A24 serotype
    Extremely contagious, subconjunctival hemorrhages and conjunctivitis

Aseptic meningitis

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161
Q

III. 30 Picornavirus - Coxasckie Virus B clinical

A
  • Pleurodynia (Bornholm disease) aka Devil’s grip
    Sudden onset of fever with lower chest and pleuritic pain – unilateral
  • Myocarditis and pericarditis
    Sudden fever, cyanosis, cardiomegaly® heart failure

Dilative cardiomyopathy

Aseptic meningitis ~ both Cox A and B

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162
Q

III. 30 Picornavirus - Coxasckie Virus ddx

A

Virus isolation – throat, stool, CSF

Inoculation in mice –> Cox A (fast, flaccid paralysis)
–> Cox B (slow, spastic paralysis)

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163
Q

III. 30 Picornavirus - Coxasckie Virus treatment

A

supportive

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164
Q

III. 30 Picornavirus -Rhinovirus characteristics

A

ssRNA, positive sense
Icosahedral capsid
Naked

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165
Q

III. 30 Picornavirus -Rhinovirus transmission

A

Respiratory droplets –> Upper respiratory tract infection

Unable to replicate in GI tract as enteroviruses

Rhinoviruses have Ag drift, as seen in influenza

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166
Q

III. 30 Picornavirus -Rhinovirus clinical

A

Upper respiratory tract infection ~ common cold

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167
Q

III. 30 Picornavirus - Echovirus characteristics

A

ssRNA, positive sense
Icosahedral capsid
Naked

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168
Q

III. 30 Picornavirus - Echovirus transmission

A

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

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169
Q

III. 30 Picornavirus - Echovirus clinical

A 
Gastroenteritis
Boston-exanthema (fever, sore throat, exanthemas)
maculopapular rash
aseptic meningitis (~ nr.1 cause)
necrotizing hepatitis in neonates
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170
Q

III. 30 Picornavirus - Enterovirus characteristics

A

ssRNA, positive sense
Icosahedral capsid
Naked

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171
Q

III. 30 Picornavirus - Enterovirus D68 clinical

A

EV-D68, infants, children and teens. Mild to severe respiratory illness, however, the full spectrum of EV-D68 is not well defined. Most start with common cold symptoms of runny nose and cough. Some, but not all, may also have fever. For more severe cases, difficulty breathing, wheezing or problems catching your breath may occur.

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172
Q

III. 30 Picornavirus - Enterovirus A71 clinical

A

One of the major causative agents for hand, foot and mouth disease, and is sometimes associated with severe central nervous system diseases. Increases in the level of mRNAs encoding chemokines, proteins involved in protein degradation, complement proteins, and pro-apoptosis proteins have been implicated.

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173
Q

III. 31 Rhabdoviruses characteristics

A

ssRNA, negative sense
Helical
Enveloped

Includes:
- Vesiculovirus genus (vesicular stomatitis virus (VSV))

  • Lyssa virus genus (Rabies virus, Rabies-like virus)

Described as bullet-shaped on EM

174
Q

III. 31 Rhabdoviruses clinical

A

Caused by Rabies virus, typical zoonotic infection from animals to humans

  • Urban rabies: domestic animals i.e. dogs
  • Sylvan rabies: wild animals i.e. bats, foxes
175
Q

III. 31 Rhabdoviruses pathogenesis

A

The virus envelope is covered with glycoproteins for attachment and neutralizing Abs.
GPs bind to nAch receptors at the neuromuscular junction, then replicate inside the muscle (at wound). After replication period of days/weeks, the virus travels retrograde from peripheral nerve to dorsal root ganglion and spinal cord until it rapidly infects the brain.

Disseminate via afferent neurons to innervation sites in head (salivary gland, retina etc.)

Length of incubation depends on the proximality of the wound to CNS – the closer, the shorter

176
Q

III. 31 Rhabdoviruses phases

A
  • Prodromal phase
    Fever, nausea, pain at site of bite
  • Neurological phase
    Muscle: spasm of throat causing dysphagia and foaming of mouth

CNS: Increased saliva production, encephalitis and sweating, hydrophobia, seizures, disorientation, hallucinations, coma.
* Ab detectable in serum and in CNS

  • Death
177
Q

III. 31 Rhabdoviruses ddx

A

Clinical symptoms, RT-PCR from saliva, serum, CSF

Negri inclusion bodies (intracytoplasmic eosinophilic bodies) in pyramidal cells and purkinje cells of hippocampus

178
Q

III. 31 Rhabdoviruses treatment

A

Fatal if not treated

Post-exposure vaccination – passive immunization via Abs

Pre-exposure vaccination – inactivated (killed), given to people exposed to animals

179
Q

III. 32 Retrovirus and AIDS characteristics

A

ssRNA, positive sense, diploid

Conical capsid

Enveloped

180
Q

III. 32 Retrovirus types

A

Oncornaviruses: HTLV 1, 2, 5 (Human T-cell lymphotrophic viruses)

Lentivirinae: HIV1 (AIDS), HIV2 (AIDS related syndrome)

Simple retroviruses have 3 major groups
- Gag (p24 = capsid protein, p17 = matrix protein, p7 = core nucleocapsid proteins)

  • Pol (reverse transcriptase, integrase, protease)
  • Env (gp120, gp41)

Complex retroviruses (i.e. HTLV, HIV) which have several regulatory proteins (regulate splicing). Reverse transcriptase converts RNA to DNA which can be installed into host cell genome

Oncornaviruses (HTLV) –> Leukemias, sarcomas, carcinomas.

Lentiviruses attack T-cells –> diminishing the hosts cell immune response (AIDS)

181
Q

III. 32 Retrovirus and AIDS - HIV transmission

A

Bodily fluids

TORCH

182
Q

III. 32 Retrovirus and AIDS - HIV Pathogenesis

A

Gp41 promotes cell-cell fusion, gp120 binds to CD4 receptors (and CCR5 and CXCR4) on T-cells. Following infection, HIV can remain latent for many years. Eventually infected T-cells lose their ability to function ® loss of humoral (CD4+ count <200) and cell mediated immunity.

183
Q

III. 32 AIDS - clinical

A

Severe diseases related to AIDS

  • Lymphadenopathy and fever
  • Opportunistic infection i.e. M. tuberculosis, oral candidiasis
  • Malignancies i.e. Kaposi sarcoma (HHV8), Burkitt’s lymphoma, and DLBL (Diffuse large B-cell lymphoma)
  • AIDS related dementia
184
Q

III. 32 Retrovirus and AIDS ddx

A

Clinical symptoms, patient history
HIV Ab measurement ~ using
ELISA Positive result confirmed using WB

185
Q

III. 32 Retrovirus and AIDS treatment

A

Nucleoside RT inhibitor (Retrovir), non-nucleoside RT inhibitor (Rescriptovir), protease inhibitor (Crixivan), integrase inhibitor Given in combination to tackle virus in different ways.

186
Q

III. 32 Retrovirus and AIDS - HTLV transmission

A

Bodily fluids and TORCH, sex, blood, breast-feeding

187
Q

III. 32 Retrovirus and AIDS - HTLV pathogenesis

A

Spreads in CD4+ T-cells after transmission.
Neurons also express HTLV-1 receptor.

There is a long latency period before leukemia onset:

  • Tropical spastic paraparesis – progressive weakness in lower extremities
  • Adult T-cell leukemia – develops after a long latency period (~30-50 years)

Initial form = leukocytosis, abnormal lymphocytes

Mature form = Pleomorphic neoplastic cells with T-cell markers

Chronic form = Skin lesions (like Sezary syndrome), leukopenia, and no visceral involvement

188
Q

III. 32 Retrovirus and AIDS - HTLV ddx

A

ELISA – presence of HTLV-specific Ab
PCR – Viral genome
Labs, bone marrow

189
Q

III. 32 Retrovirus and AIDS - HTLV treatment

A

Glucocorticoids – tropical spastic paralysis

Chemotherapy – Leukemia

Zidovudine and INF-alpha - Virus

190
Q

III. 33 Togavirus characteristics

A

ssRNA, positive sense
Icosahedral capsid
Enveloped

Includes Alpha- and Rubiviruses

191
Q

III. 33 Togavirus Alphavirus transmission

A

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

192
Q

III. 33 Togavirus Alphavirus ddx

A

Serology

RT-PRC

193
Q

III. 33 Togavirus Alphavirus prevention

A

Killed vaccine for EEE and WEE

vaccination of horses

194
Q

III. 33 Togavirus Rubiviruses characteristics

A

One species; Rubella virus – humans are only host for Rubella

Rubella ~ German measles
One of the five classic childhood exanthema
1. Measles (Morbilli/Robeola)
2. Scarlet fever (S. pyogenes)
3. Rubella (German measles)
4. Erythema infectiosum (Parvovirus B19)
5. Roseola infantum (HHV6)

Child rubella – lymphadenopathy, maculopapular rash (pink, pinpoints, moves faster –> DDX from measles)

Adult rubella – lymphadenopathy, bone and joint pain, thrombocytopenia

Congenital rubella – developmental abnormalities (cataracts, deafness, patent ductus arteriosus, pulmonic stenosis, microcephaly, jaundice, purpuric rash), abortion

195
Q

III. 33 Togavirus Rubiviruses transmission

A

Respiratory droplets

196
Q

III. 33 Togavirus Rubiviruses ddx

A

Serology

RT-PCR

197
Q

III. 33 Togavirus Rubiviruses treatment

A

Supportive, prevention with live attenuated vaccine

198
Q

III. 34 Hepatitis A characteristics

A

Resistance to heat and acid
ssRNA positive sense
naked

199
Q

III. 34 Hepatitis A epidemiology

A

Infectious hepatitis (HAV) is endemic throughout the world – low mortality ~ no carrier state

200
Q

III. 34 Hepatitis A transmission

A

fecal-oral

201
Q

III. 34 Hepatitis A ddx

A

Anti-HAV IgM

202
Q

III. 34 Hepatitis A treatment

A

none

203
Q

III. 34 Hepatitis A treatment

A

vaccine

204
Q

III. 34 Hepatitis A pathogenesis

A

Ingestion of virus –> spread to bloodstream by penetrating epithelium of the oropharynx or intestine –> reaches the parenchyma of the liver –> replicates in hepatocytes and Kupffer cells (without lysis) –> release of new virions into bile –> shed in large quantities in the stool

205
Q

III. 34 Hepatitis A clinical

A

Acute hepatitis

  • Children: mild disease, often asymptomatic (10% jaundice)
  • Adults: fever, fatigue, nausea, dark urine, pale stool, itchy skin and jaundice
  • Smokers that develop hepatitis A tend to develop aversion to smoking (tobacco)
206
Q

III. 34 Hepatitis E characteristics

A

ssRNA positive sense

resistance to heat and acid

207
Q

III. 34 Hepatitis E treatment

A

none

208
Q

III. 34 Hepatitis E prevention

A

vaccination in China

209
Q

III. 34 Hepatitis E clinical

A

severe in pregnancy

210
Q

III. 34 Hepatitis E ddx

A

Anti-HEV IgM

211
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)

212
Q

III. 35 Hepatitis B transmission

A

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

Sexual contact

Vertical infection (perinatal) – TORCHES

213
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)

214
Q

III. 35 Hepatitis B clinical

A

Acute hepatitis

  • Prodromal serum sickness (fever, malaise) with rash and arthralgia
  • Polyarthritis nodosa – systemic vasculitis affecting medium to small arteries
  • Glomerular nephritis ~ 2 forms
    Membranous nephropathy – more common Membranoproliferative glomerulonephritis

Chronic hepatitis ~ 5-10% chance to develop chronic hepatitis; newborns have ~90% chance

  • Can progress to cirrhosis and to hepatocellular carcinoma
215
Q

III. 35 Hepatitis B ddx

A

ALT (Alanine aminotransferase) rises during acute infection and then falls close to normal after symptomatic phase.

Neonates often have a normal ALT level.

216
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
217
Q

III. 35 Hepatitis B prevention

A

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

218
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

219
Q

III. 35 Hepatitis C transmission

A

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

220
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
221
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
222
Q

III. 35 Hepatitis C treatment

A
  • Ribavirin (nucleoside inhibitor, guanosine analogue)
  • Interferon a
  • Protease inhibitors (Broceprevir or Telaprevir)
223
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.

224
Q

III. 35 Hepatitis D characteristics

A

envelope

ssRNA negative - circular

225
Q

III. 35 Hepatitis D transmission

A

parental

226
Q

III. 35 Hepatitis D clinical

A

acute hepatitis

227
Q

III. 35 Hepatitis D ddx

A

anti-HDV ELISA

228
Q

IV. 7 Coccidioides immitis characteristics

A

Dimorphic – molds in the cold, yeast in the heat

Coccidioides yeast cells > RBC

229
Q

IV. 7 Coccidioides immitis clinical

A

Disease is caused by inhalation of infectious arthroconidia Endemic regions: Southwestern USA, Mexico

Immunocompetent:
~ asymptomatic, pneumonia, fever, arthralgia, erythema nodosum

Immunocompromised:
~ Progressive pulmonary infection, “the great imitator”, wide variety of lesions; skin, bone, lung, meninges (coccoidal granuloma)

Tissue form:
~ Spherule – thick walled structure with endospores.
Disruption of wall leads to spore release which can form new spherules in neighboring tissues

230
Q

IV. 7 Coccidioides immitis ddx

A

~ Microscopic exam of sample from i.e. sputum

~ Serology – Ab titers

~ Skin test – coccidioidin or spherulin

231
Q

IV. 7 Coccidioides immitis treatment

A

Surgery + Amphotericin B/Azoles

232
Q

IV. 7 Histoplasma capsulatum characteristics clinical

A

Grows in soil, especially in soil contaminated with excretions of bat/birds
Endemic regions: Caves; USA, Latin-America

Histoplasma yeast cells < RBC Systemic fungi

233
Q

IV. 7 Histoplasma capsulatum ddx

A

~ Direct exam of specimen – Blastosphores inside macrophages
~ Latex agglutination
~ Rapid serum and urine antigen test
~ Skin test: Histoplasmin

234
Q

IV. 7 Histoplasma capsulatum treatment

A

~ Surgery + Amphotericin B/Azoles

235
Q

IV. 7 Histoplasma capsulatum clinical

A

Acute histoplasmosis:
~ After inhalation, the microconidia are phagocytosed by pulmonary macrophages. Conversion to parasitic yeast form, occurs intracellular

Disseminated histoplasmosis:
~ Occurs in immunocompromised patients, AIDS: Calcified, destructive lesions on lung, hepatosplenomegaly with calcifications, erythema nodosum

236
Q

IV. 8 Blastomyces dermatitidis characteristics

A

systemic infection

Endemic regions: North America Dimorphic fungi found in decaying organic material (i.e. woods)

In tissue: broad-based budding yeast Mold form: Mycella with/typical piriform mycroconidia

237
Q

IV. 8 Blastomyces dermatitidis clinical

A

Blastomycosis – by inhalation of conidia spores (RBC size)

  • Pulmonary disease
  • Extrapulmonary: skin, bone, GU, CNS - Disseminated disease in immunocomp
238
Q

IV. 8 Blastomyces dermatitidis ddx

A

Direct exam of specimen (spherules)

239
Q

IV. 8 Blastomyces dermatitidis treatment

A

Amphotericin B or Azoles

240
Q

IV. 8 Paracoccidiodes brasiliensis characteristics

A

Endemic regions:
Similar to Blastomycosis, but located in south and central America

Dimorphic fungi, likely soil associated
In tissue:

Thin to thick walled, multiplying, captain’s wheel

241
Q

Paracoccidiodes brasiliensis clinical

A

Brazilian Blastomycosis - Respiratory droplet

~ Self-limiting pulmonary disease

~ Extrapulmonary: skin, mucosa, bones, LN, viscera, meninges

~ Disseminated disease in immunocompromised patients and children

242
Q

Paracoccidiodes brasiliensis ddx

A

When yeast buds look like “captain’s wheel”

243
Q

Paracoccidiodes brasiliensis treatment

A

Amphotericin B

244
Q

IV. 9 Cryptococcus neoformans characteristics

A

Ubiquitous saphrophyte, found worldwide especially in pigeon excretions.
Only yeast form

245
Q

IV. 9 Cryptococcus neoformans virulence factors

A

Think capsule, melanin

Opportunistic fungal infection causing pneumonia and meningitis with soap bubble lesions and cysts in grey matter. Typical in immunodeficient patient.

246
Q

IV. 9 Cryptococcus neoformans ddx

A

~ CSF specimen – India ink for capsule detection (black background, transparent fungi), latex agglutination for
polysaccharide capsule

~ Lung tissue – stain capsule with Mucicarmine (red), culture with Saboraud with cycloheximide (sample from BPL), urease positive

247
Q

IV. 9 Cryptococcus neoformans treatment

A

Amphotericin B, Flucytosine

248
Q

IV. 9 Pneumocystis jirovecii characteristics

A

Thought to be a protozoa until recently. Now, based on its RNA it is a fungus related to ascomycetes (obligate extracellular)

Pneumocystis is present in lung of many animals, i.e. rats and rabbits

Causes diffuse interstitial pneumonia in immunodeficient patients (ground-glass appearance on X-ray)

Frequency of infection is rising due to i.e. HIV, transplantations, AIDS

249
Q

IV. 9 Pneumocystis jirovecii ddx

A

~ Microscopical exam with Giemsa stain

~ Methamine-silver (BAL) – disc shaped yeast

~ Lung biopsy

250
Q

IV. 9 Pneumocystis jirovecii treatment

A

Sulphonamide, Trimetroprim (=Bactrim)

251
Q

IV. 10 Aspergillus species characteristics

A

opportunistic fungi

Allergic bronchopulmonary Aspergillosis
- Asthmatic attacks, hypersensitivity pneumonitis, Aspergilloma which may progress to fibrotic lung disease

Invasive Aspergillosis
- Most frequently involves lungs and paranasal sinuses. Fungus may disseminate from lungs, via blood to i.e. brain, liver, kidney, heart. Main portal of entry is the respiratory tract. Predisposing factors are; neutropenia due to i.e. chemotherapy

252
Q

IV. 10 Aspergillus species transmission

A

Inhaled conidiospores from peanuts, rice, grains etc.

253
Q

IV. 10 Aspergillus species ddx

A

~ Histopathology – Grocott stain

~ Isolation from specimen, culture and ID – septate hyphae branch at acute angle (~45°)

~ Ag (galactomannan test) from serum

~ Imaging – ring enhancing lesions in brain (DDX: lymphoma, toxoplasmosis)

254
Q

IV. 10 Aspergillus species treatment

A

Amphotericin B

surgery for Aspergilloma

255
Q

IV. 10 Penicillium genus characteristics

A

P. marneffei is a pathogenic dimorphic fungus

Present in soil, prominent infection in immunodeficient patients

Infection reminds of cryptococcus and histoplasmosis and other diseases – prominent in immunodeficient patients

256
Q

IV. 10 Penicillium genus ddx

A

Microscopic detection of eliprical fission yeast inside macrophages

257
Q

IV. 10 Penicillium genus treatment

A

Amphotericin B

258
Q

IV. 10 Zygomycoses characteristics

A

Caused by Rhizopus, Rhizomucor, Absidia, Mucor ssp and other members of zygomycetes – Invasive sinopulm infection (Mucormycosis)

Especially severe form of zygomycosis is known as Rhinocerebral syndrome (black eschar, necrosis in nasal cavity) which occurs in DM with ketoacidosis.

Causative molds are:
~ Conidiobolus – facial area of adults

~ Basidiobolus – limbs of children
Risk factors are DMKA, neutropenia, corticosteroids

Both Aspergillus ssp, and zygomyceses tend to invade blood vessels

259
Q

IV. 10 Zygomycoses ddx

A

Non-separate hyphae branching at 90°

260
Q

IV. 10 Zygomycoses treatment

A

Itraconazole, oral KI, facial surgery

261
Q

IV. 11 Candida genus characteristics

A

Opportunistic fungi

Candida species includes; C. krusei, C. glabrata, C. tropicalis, C. parapsilosis C. albicans is the most important

WHEN CULTIVATED: MOLD IN HEAT, YEAST IN COLD!

Candidiasis may be superficial or deep

~ Superficial candidiasis may involve epidermal and mucosal surfaces (endogenous transmission, normal flora). i.e. oral
soar, diaper rash, candida vulvovaginitis

~ Deep candidiasis involves the liver, kidney and spleen mainly. GI tract and IV catheters are major portals of entry.

262
Q

IV. 11 Candida genus clinical

A

Immunocompetent:
~ Soor, vaginal flour, intertrigo (skin)

Immunocompromised:
~ General oral candidiasis, candida esophagitis (CD4 count under 100), candidemia (sepsis, infective endocarditis)

263
Q

IV. 11 Candida genus risk factors

A

~ Broad spectrum antibiotics
~ Chemotherapy
~ Corticosteroids
~ IV catheters

264
Q

IV. 11 Candida genus ddx

A

~ Microscopic exam

~ Cultivation: Saburaud, chrom agar

~ Identification: old methods – rice meal agar (chlamydospores), new methods – biochemical test (on glucose containing
serum is forms pseduhyphae), molecular methods, MALDI-TOF

~ Catalase positive

265
Q

IV. 11 Candida genus treatment

A

~ Mild/local: Azoles
~ Oral: Nystatin
~ Disseminated: Amphotericin B

Prophylaxis for transplant patients: oral fluconazole

266
Q

IV. 13 Entamoeba histolytica characteristics

A

Amoebic dysentery: Abdominal pain, blood and pus in stool (small volume, blood and mucus)

Source of infection: carriers, cyst-shedding humans

Fecal-oral transmission: contaminated water, anal transmission is rare

267
Q

IV. 13 Entamoeba histolytica virulence factors

A
  • Adhesion molecule (Gal/GalNac Lectin)
  • Amoeboporin
  • Pseudopodia (locomotion)
  • Histolytic enzymes: protease, cysteine kinase, phospholipase A, hyaluronidase, collagenase, elastase, RNAase
268
Q

IV. 13 Entamoeba histolytica pathogenesis

A

Ingestion of cysts → Reach stomach → Formation of trophozoite → Replication → Attachment to host cells by GalNAC → Local necrosis via cytokines → Invasion of intestinal wall and RBC (to feed) → Dissemination to other organs → Secondary organ involvement (lymphatic spread)

Extra-intestinal Amebiasis, when amoeba invades intestinal wall

~ Flask shaped ulcers in colon with extension to peritoneum and other organs

~ Abscess formation (i.e. brain, lung, liver)

269
Q

IV. 13 Entamoeba histolytica ddx

A

Fecal antigen test: trophozoite and cyst seen

Serology: ELISA for confirmation/differentiation from commensal

Histology: Flask-shaped ulcers

270
Q

IV. 13 Entamoeba histolytica treatment

A

Active disease – Metronidazole (10 days), Tinidazole (5 days)

Cyst carriers – Paromomycin

271
Q

IV. 13 Entamoeba histolytica prophylaxis

A

Boil water, chlorination does not work

272
Q

IV. 13 Entamoeba coli characteristics

A

Part of normal flora

When found in stool it’s often confused with E. histolytica

273
Q

IV. 13 Entamoeba coli ddx

A

~ Cyst contains 1-8 nuclei (E. histolytica: 1-4)

~ Does not ingest RBC

~ Differentiated by antigen detection

274
Q

IV. 14 Acanthamoeba characteristics

A

Acanthamoeba spp → A. castellani, A. keratitis = Trophozoite (infective term) and cyst → Found in soil and lakes (free living)

275
Q

IV. 14 Acanthamoeba pathogenesis

A

Trophozoits travel via cribriform plate → into CNS Trophozoits/cysts may also be inhaled into respiratory tract

276
Q

IV. 14 Acanthamoeba clinical

A

Granulomatous amebic encephalitis (GAE)

  • Infects immunocompromised patients causing brain abscesses, edema of brain tissue, dissemination causing
    granulomatous disease
  • Slower course of disease (DDX Naegleria)

Amoebic keratitis

  • Source: eye trauma, contact lens contamination
  • Results in corneal ulceration and pain
277
Q

IV. 14 Acanthamoeba ddx

A 
NICE
N – Nasal discharge
I – Iodine stained smear
C – Corneal scraping
E – Examination of CSF
  • Both trophozoites and cysts are seen in tissues (ddx from naegleria)
278
Q

IV. 14 Acanthamoeba treatment

A

Pentamidine

279
Q

IV. 14 Naegleria genus characteristics

A

same as acanthamoeba

280
Q

IV. 14 Naegleria genus clincial

A

Primary Amebic Meningoencephalitis (PAM)

~ Destruction of brain tissue, leads to death (rapid: 4-5 days)

~ Symptoms: prefrontal headache, nausea, high fever, stiff neck, altered olfaction

~ CSF is purulent: contain motile amoeba and blood

~ Diagnosis: NICE, but only trophozoites seen in tissues

~ Treatment. Amphotericin B, Rifampin

281
Q

IV.15 Giardia lamblia characteristics

A

Flagellate

Trophozoite is kite-shaped, bi-nucleated with 4 flagella
Cyst is drug, chlorine and filtration resistant, with 4 nuclei

Both cyst and trophozoite from are detected in fecal samples.
Found mainly in non-hygienic water sources

282
Q

IV.15 Giardia lamblia clinical

A

Giardiasis – Beaver fever, backpackers’ diarrhea

Can be asymptomatic and symptomatic.

Symptoms are ranging from mild diarrhea to severe malabsorption syndrome (steatorrhea).
Rarely blood/pus in stool since no tissue destruction (ddx: entamoeba)

283
Q

IV.15 Giardia lamblia ddx

A

~ Fecal antigen test – Trophozoites and cysts seen

~ Duodenal aspiration – since it resides in duodenum

~ Enterotest – gelatin on a string (capsule)

284
Q

IV.15 Giardia lamblia treatment

A

Metronidazole

285
Q

IV. 15 Balantidium coli characteristics

A

Ciliate

Trophozoite is ciliated (motile), 2 nuclei (one micro and one macronucleus)

Cysts are smaller, surrounded by wall, 1 macronucleus

286
Q

IV. 15 Balantidium coli clinical

A

Balantidiasis

Bloody diarrhea, abdominal cramps (tenesmus) → Fatal, but rare

287
Q

IV. 15 Balantidium coli ddx

A

Stool examination

288
Q

IV. 15 Balantidium coli treatment

A

Tetracycline (first choice)

Metronidazole

289
Q

IV.15 Giardia lamblia pathogenesis

A

Fecal-oral transmission

Infection is initiated by ingestion of cysts, which reach duodenum and form trophozoites.

The trophozoites multiply by binary fission and attach to intestinal wall via ventral sucking disc (does not invade intestinal wall, ddx from Entamoeba)

290
Q

IV. 15 Balantidium coli pathogenesis

A

Found in pigs and monkeys

Fecal-oral transmission

Ingestion of cysts, trophozoite invasion into mucosa of large intestine, cecum, terminal ileum

291
Q

IV. 16 Cryptosporodium spp characteristics

A

Sporozoa
Sexual cycle: sporogony
Asexual cycle: schizogony

292
Q

IV. 16 Cryptosporodium spp pathogenesis

A

affects SI mucosa via fecal-oral contamination of water

I) Ingestion of cyst with 4 motile sporozites (infective stage)

II) Sporozites attach to the intestinal epithelium and mature (schizogony)

III) Sexual form develops (gametogony) and produces fertilized oocysts with zygote inside

IV) Oocyst matures in intestine or is excreted to the environment via stool

293
Q

IV. 16 Cryptosporodium spp clinical

A

Cryptosporidiosis - Severe watery diarrhea and dehydration (around 2 weeks)

294
Q

IV. 16 Cryptosporodium spp ddx

A

Fecal antigen test

Acid-fast stain of stool – contains oocyst

295
Q

IV. 16 Cryptosporodium spp treatment

A

Rehydration, probiotics

Spiramycin in immunocompromised

296
Q

IV. 16 Blastocystis hominis characteristics

A

Amoeba

One of the most common parasitic infections in the world – number 1 in the US Reservoir:
Animal intestine

Transmission: Animal feces in cyst form

297
Q

IV. 16 Blastocystis hominis pathogenesis

A

I) Ingested feces from environment

II) Cyst change to vacular form in GI and replicate, or change further to other forms i.e. amoeba or granular form

III) Release of new cysts via stool

298
Q

IV. 16 Blastocystis hominis clinical

A

Symptoms range from asymptomatic to diarrhea, nausea, abdominal cramps

299
Q

IV. 16 Blastocystis hominis ddx

A

Wet mount

Trichrome from stool

300
Q

IV. 16 Blastocystis hominis treatment

A

Metronidazole

301
Q

IV. 17 Trichomonas vaginalis characteristics

A

Flagellates, only trophozoite from (4 flagella, 1 nucleus)

Genital pathogen (in urethra, vagina/prostate), transmission by sexual contact, thermal baths, WC, birth canal

302
Q

IV. 17 Trichomonas vaginalis pathogenesis

A

During intercourse, trophozoites in vaginal/prostatic secretions are passed and placed in vagina or urethra. Here the trophozoites multiply by longitudinal binary fission. Trophozoites are both the infective and diagnostic form

303
Q

IV. 17 Trichomonas vaginalis clinical

A

Trichomoniasis
Yellow/green discharge with fish-like odor

Burning, itching, preterm delivery
Vaginitis, prostatitis, cervicitis (strawberry)

304
Q

IV. 17 Trichomonas vaginalis ddx

A

Wet mount with blue-methylene stain: trophozoites with corkscrew motility
Grows on elevated pH
Giemsa stain

305
Q

IV. 17 Trichomonas vaginalis treatment

A

Metronidazole (also for sex partners)

306
Q

IV. 18 Plasmodia characteristics

A

Sporozoa
4 species that infect humans:
P. ovale and P. vivax (tertian paroxysm, 48h asexual reproduction), P. malariae (quatrain paroxysm, 72h asexual reproduction), P. falciparum (most malignant)

Plasmodium ssp are sporozoan parasites of blood
2 hosts are needed:
- (Anopheles) Mosquitos for sexual reproduction (sporogony)
- Human/animals for asexual reproduction (schizogony)

307
Q

IV. 18 Plasmodia life cycle

A

~ Infection initiated by mosquito bite, releases sporozoites into blood

~ Sporozoites are carried to the liver for asexual reproduction (schizogony). Hepatocytes (liver stage schizonts) containing
2-40’000 merozoites (5-21 days)

~ Merozoite attach to RBC (1/RBC), developing into immature ring-shaped trophozoites, and later to blood stage schizonts
containing 8-36 merozoites.

~ Rupture of RBC – symptomatic

~ Gametocytes will then be sucked back up of the same mosquito and the life cycle is complete
* Sexual reproduction in mosquitos is known as sporogonic cycle

308
Q

IV. 18 Plasmodia clinical

A

Malaria
Headache, fever, fatigue, coughing, sweating, nausea. Cerebral malaria, pulmonary edema, shock, coma, renal failure, hepatosplenomegaly, anemia. (Black urine)

309
Q

IV. 18 Plasmodia ddx

A

Smear, PCR
Blood films
- Thick film: hemolyzed by distilled H2O – used for detection of Plasmodium

  • Thin film: methanol fixed, non-hemolyzed – for detection of species
310
Q

IV. 18 Plasmodia prophylaxis

A

P. falciparum vaccine (2018), made from fusion protein Doxycycline, chloroquine, mefloquine

311
Q

IV. 19 Trypansoma brucei characteristics

A

Flagellates

T. brucei gambiense – human reservoir, tse-tse fly vector, sleeping sickness, West Africa

T. brucei rhodesiense – antelope, tse-tse fly vector, sleeping sickness, East Africa

312
Q

IV. 19 Trypansoma brucei pathogenesis

A

Blood: Trypomastigote

Tissue: Amastigote (IC)

Undergo antigenic variation, evade immunity,
chronic infection

Trypomastigote enter by the wound of the tsetse fly bite. Travel in blood/lymph/CNS and reproduce at target site by binary fission. Ingested back from blood by fly, then multiply in fly1s midgut. Migrate and mature to epimastigote in salivary glands. Develop to trypomastigote in salivary glands (ready to infect)

313
Q

IV. 19 Trypansoma brucei clinical

A

Sleeping sickness/African trypanosomiasis

~ Ulcer at the site of bite

~ Fever, chills, anorexia

~ Lymphadenopathy – cervical (Winterbottom’s sign) and axillary

~ CNS – lethargy (lack of energy), somnolence (sleepiness), dementia, meningoencephalitis

~ Coma, eventually death

  • Differentiation between species → T. b. rhodesiense has shorter incubation time, rapidly progressing, more virulent. It is easier to detect in blood
314
Q

IV. 19 Trypansoma brucei ddx

A

Blood films (thick and thin) → Showing trypomastigotes (ALWAYS extracellular)

Serology from CSF → High Ig levels

315
Q

IV. 19 Trypansoma brucei treatment

A

Suramin – for acute infections

Melarsoprol – chronic/CNS infections

316
Q

IV. 20 Trypanosoma cruzi characteristics

A

Flagellates

Armadillo/cat/dog reservoir, kissing bug (Recluviid bug) vector, Latin-America, Chagas disease

317
Q

IV. 20 Trypanosoma cruzi pathogenesis

A

Trypomastigotes are passed in the feces of bug and enters the wound (aided by scratching). Migrate to different tissues forming small, oval amastigote, then multiply by binary fission. Rupture and destroy the host cells. Trypomastigotes can be ingested back by the kissing bug where they form epimastigotes in bugs midgut, then develop into trypomastigotes

318
Q

IV. 20 Trypanosoma cruzi clinical

A

Chagas disease/American trypanosomiasis

Acute form 
~ most severe in children under 5 years
~ Chagoma at bug bite site
~ Romana sign: periorbital edema
~ Fever, malaise, myalgia, fatigue

Chronic form
~ Dilated cardiomyopathy, megacolon, mega esophagus
~ Granulomas in brain

319
Q

IV. 20 Trypanosoma cruzi ddx

A

Blood films in acute phase ~ showing trypomastigotes (difficult to find)

Biopsy of infected tissues, then serology

Xenodiagnosis

320
Q

IV. 20 Trypanosoma cruzi treatment

A

Nifurtimox

Benznidazole

321
Q

IV. 21 Leishmaniae characteristics

A

Hemoflagellates – infects blood and tissues

Obligate intracellular parasites of reticuloendothelial system, bone marrow, spleen, lymph nodes

Organism is not seen in peripheral blood

322
Q

IV. 21 Leishmaniae pathogenesis

A

Fly bites and injects promastigotes into skin → invade macrophages and form amastigotes which replicate → cell rupture and release of the amastigotes → invades other cells and replicate again → Ingestion from blood back to fly → promastigote development → move to proboscis (nose of fly) and is ready to infect again.

323
Q

IV. 21 Leishmaniae - L. tropica

A

Reservoir: rodents, dogs

Vector: phlebotomus fly

Disease: Cutaneous leishmaniosis ~ tropical sore/ulcer (secondary bacterial infections)

Location: Asia, Africa

324
Q

IV. 21 Leishmaniae - L. braziliensis

A

Reservoir: rodents, dogs

Vector: phlebotomus fly

Disease: Mucocutaneous Leishmaniosis
~ Espundia (disfiguring of the face) → secondary bacterial infections with mucous membrane involvement

Location: South America

325
Q

IV. 21 Leishmaniae - L. donoconi

A

Reservoir: dogs, cats, foxes

Vector: Phlebotomus fly

Disease: Visceral Leishmaniosis (~ Kala azar, black fever, dumdum fever) with
~ Fever, chills, sweating – like malaria

~ Deep tissue involvement – Hepatosplenomegaly, anemia, pancytopenia

~ Granulomatous lesions of the skin

Location: Southeast Asia i.e. Bangladesh, Nepal

326
Q

IV. 21 Leishmaniae ddx

A

Aspirate from lymph node – Giemsa staining of biopsied tissues

Montenegro skin test – T4 HSR

327
Q

IV. 21 Leishmaniae treatment

A

Sodium stibogluconate (and IFN gamma)

328
Q

IV. 21 Leishmaniae prophylaxis

A

Protection from phlebotomus fly bite

329
Q

IV. 22 Toxoplasma gondii characteristics

A

Obligate intracellular sporozoan

Definite host: cats where gametocysts and oocyst develop

Secondary host: i.e. humans where tachyzoites and bradyzoites develop

330
Q

IV. 22 Toxoplasma gondii transmission

A

Route of human transmission

1) Cat stool
2) Undercooked meat
3) Contaminated vegetables
4) Transplacental (TORCH)

T. gondii develops and has it’s sexual cycle in cat intestine → Oocyst released in feces → 3-4 days of incubation in environment → ingested by human → sporozoites infect cells → develop into tachyzoites which replicate fast in macrophages (blood) and delivery into tissues where cyst develop → Bradyzoite reproduction in cyst (responsible for chronic infection)

331
Q

IV. 22 Toxoplasma gondii clinical

A

Toxoplasmosis

In immunocompetent:
Asymptomatic, lymphadenopathy with fever. DDX; mono, but heterophile is negative

In pregnant women: Flu-like symptoms and heterophile negative
I) Early placental crossing
- Intracranial calcifications
- Hydro-/microcephaly, convulsions - Chorioretinitis and deafness

II) Late placental crossing
- Unapparent, but may lead to blindness in adolescence

In immunocompromised patients: Meningoencephalitis
Number 1 leading cause of focal DNA disease in AIDS patients.
If CD4+ count is <100, and seropositive for IgG, prophylactic TMP-SMX should be given

332
Q

IV. 22 Toxoplasma gondii ddx

A

Serology: specific markers is IgM (after two weeks no IgG, then IgM is false positive)

Avidity test: To distinguish if recent or past infection (look for IgG)

PCR: from CSF, in HIV patients

333
Q

IV. 22 Toxoplasma gondii treatment

A

Self-limiting in immunocompetent patients

Sulfadiazine and pyrimethamine

Spiramycin for pregnant women

334
Q

IV. 24 Taenia saginata characteristics

A

Aka. Beef tapeworm
Cestode (tapeworm)

Intermediate host: cattle

Definite host: human

Transmitted via undercooked beef – cysterici are ingested 12m, 1-2mm in diameter with 4 suckers

335
Q

IV. 24 Taenia saginata life cycle

A

Mature proglottidis give off eggs → cyst formation (cysticercosis) in intermediate host (i.e. cows) → Humans infected by eating meat → SI maturation → enteral taeniasis

336
Q

IV. 24 Taenia saginata ddx

A

Proglottis or eggs in stool – eggs (thick double wall) only detect taenia genus, proglottis can differentiate spp

337
Q

IV. 24 Taenia saginata treatment

A

Niclosamide and mebendazole

338
Q

IV. 25 Taenia solium characteristics

A

Aka. Pork tapeworm

Intermediate host: Pigs

Definite host: Humans

Accidental intermediate host: Human (cysticercosis) ONLY SOLIUM

Transmitted via undercooked pork – cysticerci are ingested (eggs are transmitted via contaminated water) 6m, has rostellum with hooklets

339
Q

IV. 25 Taenia solium life cycle

A

Mature proglottids give off eggs → cyst formation (cysticercosis) in intermediate host (i.e. cows) → Humans infected by eating meat → SI maturation → enteral taeniasis

340
Q

IV. 25 Taenia solium clinical

A

~ Subcutaneous cysticerosis
~ Cerebral cysticerosis
~ Enteral taeniasis

341
Q

IV. 25 Taenia solium ddx

A

Proglottids in stool
Cysts in tissue on CT scan
Serology – Ag detection of CSF by ELISA

342
Q

IV. 25 Taenia solium treatment

A

Praziquantel
Niclosamide
+ corticosteroids and surgery

343
Q

IV. 26 Diphyllobothrium latum characteristics

A

Aka. Fish tapeworm → largest tapeworm Definite host: humans

Reservoir: bears, other mammals Intermediate host: Fish

344
Q

IV. 26 Diphyllobothrium latum pathogenesis

A

Humans infected by eating fish containing larvae, small intestinal maturation

345
Q

IV. 26 Diphyllobothrium latum clinical

A

Abdominal pain with nausea and diarrhea, pernicious anemia due to B12 requirement of the parasite

346
Q

IV. 26 Diphyllobothrium latum ddx

A

Finding eggs in stool

347
Q

IV. 26 Diphyllobothrium latum treatment

A

Praziquantel

Niclosamide

348
Q

IV. 26 Hymenolepis nana charcteristics

A

Dwarf tapeworm, 1-3 cm

Most prevalent in conditions of poor sanitation, and is endemic in tropical regions = hymenolepiasis

349
Q

IV. 26 Hymenolepis nana pathogenesis

A

Swallowed eggs → SI maturation → developing helminths * some eggs pass out with feces

Asymptomatic infection – diagnosis based on finding eggs in stool

350
Q

IV. 26 Hymenolepis nana treatment

A

Praziquantel

Niclosamide

351
Q

IV. 27 Echinococcus species characteristics

A

E. granulosus: Carnivores, domestic animals ~ dog tapeworm

E. multilocularis: Wolf, fox ~ small fox tapeworm I

ntermediate host: Herbivores (sheep, cattle)

Definite host: Dogs

Accidental, dead-end host: humans

352
Q

IV. 27 Echinococcus granulosus life cycle

A

After ingestion of eggs, the onchospheres penetrate the intestinal wall and reach host organs ~ liver/lung

They form cyst within a week, consisting of an external acellular part, and an internal/germinal.

The larvae develop from the germinal layer

353
Q

IV. 27 Echinococcus granulosus hydatidosis

A

Hydatid cysts in lung, liver, brain

Fluid inside cyst is toxic → anaphylactic shock, death

354
Q

IV. 27 Echinococcus granulosus ddx

A

Presence of isolated hooklets

CT or echography

ELISA, western blot

355
Q

IV. 27 Echinococcus granulosus treatment

A

Sugery

Albendazole

356
Q

IV. 27 Echinococcus multilocularis life cycle

A

Adult worm in small intestine of animal (reservoir), embryonated eggs in feces of that animal → orally into human OR from cyts in intermediate host until it reaches human → The activated onchosphere penetrates the small intestine, enters blood vessels and reaches liver via portal vein.

357
Q

IV. 27 Echinococcus multilocularis pathogenesis

A 
Alveolar echinococcosis (AE)
The liver is the organ primarily affected, but could metastasize to any organ (brain, lungs etc). 
Causes infiltatrive growth – hepatomegaly, jaundice, abdominal pain
358
Q

IV. 27 Echinococcus multilocularis ddx

A

CT/MRI

ELISA

359
Q

IV. 27 Echinococcus multilocularis treatment

A

Surgery, chemotherapy

Benzimidazole

360
Q

IV. 28 Fasciola Hepatica characteristics

A

Sheep liver fluke, high prevalence in Europe and south America

Definitive host: sheep, cattle, humans

Intermediate host: snails

361
Q

IV. 28 Fasciola Hepatica organs affected

A

Biliary ducts

liver

362
Q

IV. 28 Fasciola Hepatica pathogenesis

A

Consumption of larvae → Encystation in duodenum → Liver (maturation, necrosis of liver) → egg in bile duct → pass out with feces

363
Q

IV. 28 Fasciola Hepatica clinical

A

Fever, severe eosinophilia, hepatosplenomegaly, bile duct obstruction

364
Q

IV. 28 Fasciola Hepatica ddx

A

Eggs in feces

365
Q

IV. 28 Fasciola Hepatica treatment

A

Triclabendazole

Bithionol

366
Q

IV. 29 Paragonimus westermani characteristics

A

Lung fluke, high prevalence in Asia

Source of infection: eating undercooked freshwater crabs or crayfish (larvae)

367
Q

IV. 29 Paragonimus westermani pathogenesis

A

Fluke develops in stomach → migration via intestinal wall → through diaphragm → pleural cavity where the adults lay eggs in lungs

368
Q

IV. 29 Paragonimus westermani clincal

A

Pneumonia – can be fatal due to penetration of brain, heart, spinal cord

Fever, eosinophilia, chest pain, bloody sputum, lung tissue fibrosis (night sweats, pleuritis, bronchopneumonia)

369
Q

IV. 29 Paragonimus westermani ddx

A

Eggs in feces/sputum

370
Q

IV. 29 Paragonimus westermani treatment

A

Praziquantel + bithionol

371
Q

IV. 30 Schistosomes characteristics

A

Only fluke with separate sexes

S. hematobium → IM hosts are snails (Bulinus) – urinary tract

S. mansoni → IM hosts are snails (biomphalaria) – GI

S. japonicum → IM hosts are snails (onchomelania) – GI

372
Q

IV. 30 Schistosomes life cycle

A

1) Eggs hatch in water, releasing miracidia
2) Miracidia penetrate snail tissue and form sporocysts

3) Cercariae (infective form larvae) released
by snails, these are free-swimming

4) Cercariae penetrate human skin, loose tails and becomes schistosomulae
5) Blood stream → Liver: maturation
6) Migration to large intestine or venous plexus of urinary bladder

373
Q

IV. 30 Schistosomes clinical

A

Hepatosplenic schistosomiasis

~ Results from eggs embolization in hepatic venules

~ Formation of granulomas and portal fibrosis

~ Hepatosplenomegaly and hepatic insufficiency

374
Q

IV. 30 Schistosomes ddx

A

serology

375
Q

IV. 30 Schistosomes treatment

A

Praziquantel

376
Q

IV. 30 Schistosomes manosoni

A

S. mansoni → female lays eggs ~ 300 eggs/day → Africa

Adult Schistosomes live in pairs in the portal system and in the mesenteric venules

377
Q

IV. 30 Schistosomes japonicum

A

S. japonicum → Female lays eggs ~ 2000 eggs/day → Southeast Asia

S. mansoni → female lays eggs ~ 300 eggs/day → Africa

378
Q

IV. 30 Schistosomes hematobium characteristics

A

Female lays ~ 150 eggs/day

Adult schistosomes lives in pairs in pelvic veins (especially in venous plexus around urinary bladder)

379
Q

IV. 30 Schistosomes hematobium clinical

A

Urinary schistosomiasis

~ Eggs induce granuloma formation, bladder wall enlargement, hematuria

~ Hyperplasia of mucosa, fibrosis and calcification with polyp formation in urinary bladder and urethral stenosis

~ Hydronephrosis and cancer are late complications

~ Damage to seminal vesicles

380
Q

IV. 30 Schistosomes hematobium ddx

A

Eggs in urinary sediment ~ motility
Eggs in feces
ELISA, IF, RIA

381
Q

IV. 30 Schistosomes hematobium treatment

A

Praziquantel

382
Q

IV. 31 Ancylostoma dudenale and Necator americanus charcteristics

A

Intestinal nematodes
Hookworm

A. duodenale ~ old world hookworm
A. braziliense
N. americanus ~ new world hookworm

383
Q

IV. 31 Ancylostoma dudenale and Necator americanus pathogenesis

A

Bare foot in environment → larvae infect through skin → enter blood stream → infection of lung, pharynx, SI (cough/swallow) → sucking blood (0,3-0,9 ml/day) (A. duodenale → 0,15 ml, N. americanus → 0,03 ml)

384
Q

IV. 31 Ancylostoma dudenale and Necator americanus clinical

A

Hookworm infection
~ Live attached to mucosa of small intestine, where they feed on villous tissue

~ Hypochromic microcytic anemia (IDA)

~ Epigastric pain, hypoproteinemia, eosinophilia

Cutaneous larva migrans
~ A. braziliense

~ Intense skin scratching from dog/cat hookworm

385
Q

IV. 31 Ancylostoma dudenale and Necator americanus ddx

A

Larvae in feces

386
Q

IV. 31 Ancylostoma dudenale and Necator americanus treatment

A

Mebendazole/albendazole

Iron supplement

387
Q

IV. 32 Toxocara canis Toxocara cait characteristics

A

Geohelminths = Toxocara (cati, canis) ~ nematode

388
Q

IV. 32 Toxocara canis Toxocara cait pathogenesis

A
  1. Entry through mouth (eggs excreted by dog or cat)
  2. Larvae hatch in small intestine and penetrate mucosa
  3. Larvae enter portal system (some are trapped in liver)
  4. Larvae enter systemic circulation → dissemination (dead-end infection)
  5. Diseases depends on number of larvae ingested and the degree of the allergic response
389
Q

IV. 32 Toxocara canis Toxocara cait ddx

A

Larvae in tissue (~10cm)
ELISA – serology
No adult worms in human

390
Q

IV. 32 Toxocara canis Toxocara cait treatment

A

Albendazole

391
Q

IV. 32 Toxocara canis Toxocara cait clinical

A

Visceral larva migrans:
fever, cough, malaise, leukocytosis with hypereosinophilia, hepatomegaly, high titers of isohemagglutinins * myocarditis, encephalitis, pneumonia

Ocular larva migrans:
retinal granulomas and uveitis → blindness

392
Q

IV. 33 Trichinella spiralis characteristics

A

Nematode

Adult form lives in SI of flesh-eating mammals, i.e. pigs

Viable, encysted larvae is found in the meat (muscles of animals)

393
Q

IV. 33 Trichinella spiralis pathogenesis

A

Cycle
1) Entry by ingestion of cyst: contaminated meat

2) Excystation and maturation in SI
3) Larvae enter systemic circulation → dissemination ~ dead-end infection

394
Q

IV. 33 Trichinella spiralis clinical

A

Trichinellosis

Larvae encyst in striated muscle, causing inflammation, pain, myalgia, acute enteritis, fever, periorbital edema

395
Q

IV. 33 Trichinella spiralis ddx

A

Larvae in muscle biopsy

Serology – ELISA

396
Q

IV. 33 Trichinella spiralis treatment

A

Mebendazole

albendazole

397
Q

IV. 34 Enterobius vermicularis characteristics

A

Nematode

Pinworm – male: 2-5mm, female: 10-13mm

398
Q

IV. 34 Enterobius vermicularis pathogenesis

A

1) Entry through mouth – eggs (form environment) contain larvae
2) Eggs hatch in small intestine – migrate to large intestine and mature
3) Migrate to perianal area → lay eggs (1000/day) → perianal itch → scratch → autoinfection

399
Q

IV. 34 Enterobius vermicularis clinical

A

Perianal prurutis

400
Q

IV. 34 Enterobius vermicularis ddx

A

Eggs in perianal region – scotch tape smear used to see larva in eggs. *made in the morning before defecation/bathing

401
Q

IV. 34 Enterobius vermicularis treatment

A

Mebendazole

402
Q

IV. 35 Acaris lumbricoides characteristics

A

nematodes
Geohelminth
Most common and largest roundworm: males: 15-20 cm, female: 20-35cm

403
Q

IV. 35 Acaris lumbricoides pathogenesis

A

1) Entry through mouth, eggs containing infective larvae from soil
2) Hatch in small intestine, enter blood stream
3) Infection of lung, trachea, esophagus, small intestine

404
Q

IV. 35 Acaris lumbricoides clinical

A

Ascariasis
Larvae migrates through lung → pneumonitis
Migration into bile duct, gall bladder and liver → tissue damage

Peritonitis, abdominal pain, intestinal obstruction
* Protein deficiency (Kwashiorkor syndrome)

405
Q

IV. 35 Acaris lumbricoides ddx

A

Eggs in feces

406
Q

IV. 35 Acaris lumbricoides treatment

A

Mebendazole

407
Q

IV. 35 Trichuris trichuria characteristics

A

Geohelminth

Whipworm: males: 30-45mm, female: 35-50mm

408
Q

IV. 35 Trichuris trichuria pathogenesis

A

1) Entry through mouth: eggs contain larvae

2) Hatch in small intestine, migrate and mature in cecum, appendix, colon

409
Q

IV. 35 Trichuris trichuria clinical

A

Mucosal damage, abdominal pain, bloody stool (anemia), appendicitis, rectal prolapse

410
Q

IV. 35 Trichuris trichuria ddx

A

Eggs in feces (lemon-shaped)

411
Q

IV. 35 Trichuris trichuria treatment

A

Mebendazole

412
Q

IV 36. Strongyloides stercoralis characteristics

A

Geohelminth
Rhabditiform larvae = non-infective
Filariform larvae = infective

413
Q

IV 36. Strongyloides stercoralis clinical

A

Abdominal pain, nausea, vomiting, diarrhea, paralytic ileus, hepatitis

414
Q

IV 36. Strongyloides stercoralis ddx

A

Rhabditiform larvae in stool Hypereosinophilia
Antibody detection
Immunologic diagnosis by IF

415
Q

IV 36. Strongyloides stercoralis treatment

A

Thiabendazole and ivermectine

416
Q

IV. 36 Dirofilaria repens characteristics

A

Intermediate host: mosquito
Final host: Dogs, humans (rarely)

Larvae migrate to
~ Subcutaneous tissue → painless nodule

~ Very rarely to lungs lungs (coin-like lesion on X-ray)

~ Sometimes tissue under conjunctiva

  • Adults die before fully matured – cannot spread further
417
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis characteristics

A

Wucheria bancrofti: mosquitos of genus culex, anopheles, aedes

Brugia malayi: mosquitos of genus mansonia, anopheles, aedes

418
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis pathogenesis

A

1) Larvae enter via mosquito bite
2) Larvae mature to filaria (adult) in lymphatics and produce microfilariae which enter blood and spread
3) Disease → Adenolymphangitis, eosinophilia, Elephantiasis (LL, scrotum) *Brufia never genitals
4) Microfilariae ingested back into mosquitos

419
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis ddx

A

Detection of microfilaria in blood smear (at night) ~ mosquito activity

420
Q

IV. 37 Worms causing filariasis - Lymphatic filariasis treatment

A

Diethylcarbamazine (DEC) and Ivermectin

Spraying for mosquitos, nets etc.

421
Q

IV. 37 Worms causing filariasis - Loaisis - Loa Loa characteristics

A

Transmitted by chrysops fly/Mango fly

After bite, the larvae travel subcutaneously where it produces microfilaria which travels through blood (most frequently to conjunctiva)

422
Q

IV. 37 Worms causing filariasis - Loaisis - Loa Loa ddx

A

Detection of microfilaria in blood smear ~ 3-7cm

423
Q

IV. 37 Worms causing filariasis - Loaisis - Loa Loa treatment

A

Diethylcarbamazine ~ for 10 years

Corticosteroids for allergic reaction
Surgery of the eye

424
Q

IV. 37 Worms causing filariasis - Onchocera volvulus pathogenesis

A

Transmitted by black fly/simulium

  1. Larvae enter via bite
  2. Larvae mature to filaria in subcutaneous nodules and produce microfilaria
  3. Microfliaria cause
  4. Microfilaria ingested back by black fly
425
Q

IV. 37 Worms causing filariasis - Onchocera volvulus ddx

A

Examination of blood free skin nips

426
Q

IV. 37 Worms causing filariasis - Onchocera volvulus treatment

A

Ivermectin, surgical removal of skin nodule

427
Q

IV. 37 Worms causing filariasis - Onchocera volvulus clinical

A

River blindness: due to hyperpigmentation and scarring of cornea

Skin lesions: pruritic dermatitis (elephant skin), depigmentation, loss of elasticity, subcutaneous nodules

428
Q

IV. 37 Worms causing filariasis - Dracunculus medinensis pathogenesis

A

Transmitted through water (copepods with larvae; intermediate host)

Copepods ingested and die in stomach

They release the larvae which penetrates the abdominal wall and mature.

Once the female matured in the abdominal cavity, it migrates to the surface of the skin (usually in lower limb) and making painful ulcers

429
Q

IV. 37 Worms causing filariasis - Dracunculus medinensis ddx

A

Female emerges from ulcer

430
Q

IV. 37 Worms causing filariasis - Dracunculus medinensis treatment

A

Slowly wrapping the worm on a stick

431
Q

V. 35 Protozoa and Helminths causing Ophthalmic Infections and their ddx

A

protozoa

  • Acanthamobea - keratitis
    ddx: specimen CSF, culture with Gram negative bacilli on agar
  • Taxoplasma gondii - chorioretinitis
    ddx: serology, retinal exam, ELISA

helminth

  • loa loa - chorioretinitis
    ddx: serology - contains microfilana
  • onchocera volvulis - chorioretinitis
    ddx: biopsy, serology
  • Toxocara ssp - ocular larva migrans
    ddx: serology
  • Dirofilaria - occular infection
    ddx: serology

MRTs cmplt (4 decks)

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