*(XVI) Viruses (2)*Herpes Flashcards
A person has Cytomegalovirus. it can be found in his/her […]
A person has Cytomegalovirus. it can be found in his/her circulating leukocytes and kidney
Clinical manifestation of cytomegalovirus (CMV) infection
BABIES (most women have anti-CMV IgGs so its okay. but if it’s a NEW infection during pregnancy, that’s a problem):
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ADULTS:
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Clinical manifestation of cytomegalovirus (CMV) infection
BABIES (most women have anti-CMV IgGs so its okay. but if it’s a NEW infection during pregnancy, that’s a problem):
1. Congenital CMV infection
- Foetal infection following maternal viraemia in any trimester of pregnancy
- Varied sequelae: usually mild but severe in 20% (CID occurs)
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**Cytomegalic inclusion disease
- 20% of infants that get it from their mother present with severe disease
- jaundice, hepatosplenomegaly, insterstitial pneumonitis, thrombocytopenia, hemolytic anemia
- neurologic sequealae: microencephaly, periventricular calcification, chorioretinitis, optic atrophy, mental retardation, spasticity, epilepsy
- affected organs show enlarged cells with large intranuclear “owl’s eyes” (hence CMV’s name) -
perinatal hepatitis
- Hepatomegaly. Abnormal LFT.
- Jaundice +.
ADULTS:
4. Infectious mononucleosis syndrome (named syndrome because classic disease is by EBV)
- may be spontaneous in otherwise healthy young adults
- very similar to Infectious mononucleosis in EBV (but no heterophile antibodies, less pharyngitis, less lymphoadenopathy)
- often post-perfusion or open heart surgery
Complications:
- Guillain-Barre syndrome
- disemminated CMV in AIDS (fever, leukopaenia, pnemonitis, hepatitis, retinitis, colitis)
Clinical manifestation of Epstein-Barr Virus
Most people are asymptomatic.
Some will present with the classic
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Complications:
- Hepatitis. May have jaundice, abnormal LFT.
- Pneumonitis.
- Neurological –aseptic meningitis, encephalitis, myelitis, optic neuritis, acute cerebellar ataxia, Guillain-Barre Syndrome, peripheral neuropathy, Bell’s palsy.
- Haematological –haemolytic anaemia, thrombocytopaenia, splenic rupture.
- Myocarditis, pericarditis.
- Burkitt’s lymphoma, Classical Hodgekin lymphomas
- nasopharyngeal carcinoma
- Immunoblastic lymphoma
- Chronic fatigue syndrome
- Seriously so many complications what the heck
Clinical manifestation of Epstein-Barr Virus
Most people are asymptomatic.
Some will present with the classic
Infectious mononucleosis (aka glandular fever//mono)
- High fever (up to 2 weeks)
- More mononuclear cells and atypical lymphocytes
- Lethargy, anorexia, PHARYNGITIS, exudative tonsillitis, hepatosplenomegaly, LYMPHADENOPATHY, rash
- heterophile antibodies found
Complications:
- Hepatitis. May have jaundice, abnormal LFT.
- Pneumonitis.
- Neurological –aseptic meningitis, encephalitis, myelitis, optic neuritis, acute cerebellar ataxia, Guillain-Barre Syndrome, peripheral neuropathy, Bell’s palsy.
- Haematological –haemolytic anaemia, thrombocytopaenia, splenic rupture.
- Myocarditis, pericarditis.
- Burkitt’s lymphoma, Classical Hodgekin lymphomas
- nasopharyngeal carcinoma
- Immunoblastic lymphoma
- Chronic fatigue syndrome
- Seriously so many complications what the heck
Differentials:
HIV
CMV (no heterophile antibodies, less pharyngitis and lymphadenopathy)
acute toxoplasmosis
strep pharyngitis (no mononuclear cells)
Clinical manifestation of Herpes Simplex Virus Type 1: Mn: WEAK GAL
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Clinical complications of Herpes Simplex Virus Type 1:
- Disseminated herpes in immunocompromised subjects. Herpes hepatitis, etc
Clinical manifestation of Herpes Simplex Virus Type 1: Mn: WEAK GAL
- Acute herpetic gingivostomatitis (ok it just means sudden herpes gums lips mouth inflammation lol #breakitdown)
- vesicular eruption in buccal mucosa
- ulceration of gums with grey slough
- fever
- Commonest primary disease (especially in young children) - Herpes labialis
- Cold sore. Herpes febrilis.
- recurrent activation of HSV1 in trigeminal ganglion
- Vesicles at mucocutaneous junction of lips or near nose, later with painful ulers - Herpetic whitlow
- implantation of HSV into fingers (esp healthcare workers who don’t wear gloves)
- serous exudate (as opposed to purulent exudate in Staph whitlow) - Eczema herpticum (Kaposi’s varicelliform eruption)
- superinfection of chronic eczematous skin
- extensive vesiculation and fever (significant mortality) - Keratoconjunctivitis
- Edema and vesicles of eyelids
- Cornea - dendritic keratitis, opacification ,blindness (Care with steroids!) - Asceptic meningitis
- Acute necrotizing encephalitis (rare, but severe)
- retrograde transmission of HSV from trigeminal nerve axon to brain.
- sudden fever, confusion, headache, temporal lobe necrosis (high morbidity and mortality)
- CSF -lymphocytosis, PCR for HSV
- Brain biopsy –viral isolation, IF
Clinical complications of Herpes Simplex Virus Type 1:
- Disseminated herpes in immunocompromised subjects. Herpes hepatitis, etc
Clinical manifestation of Herpes Simplex Virus Type 2:
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Clinical complications of Herpes Simplex Virus Type 2:
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Clinical manifestation of Herpes Simplex Virus Type 2:
Herpes Progenitalis
- Sexually transmitted vesiculoulcerative lesions of genitalia –penis, perineum, vulva, vagina, cervix
- fever, malaise, lymphadenopathy
- recurrent activation of HSV2 in lumbar/sacral ganglia causing painful perianal lesions
Neonatal Herpes
-Severe generalized infection acquired from infected birth canal of mother (especially without protective maternal antibodies).
- jaundice, hepatosplenomegaly, thrombocytopenia, large cutaneous vesicle
- prevention: caesarian delivery prior to membrane rupture
Clinical complications of Herpes Simplex Virus Type 2:
Cervical and Vulvar Carcinoma
- High frequency of HSV2 antibodies in patients compared with matched controls.
- Occasional detection of HSV2 DNA, RNA and antigens in biopsies.
- Stronger association with human papillomaviruses, especially types 16 and 18 (vaccines available against HPV 16 and 18)
Clinical manifestations of VZV (vvv IMPT!!!)
Symptoms of Varicella
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Complications
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2. Aseptic meningitis
3. Neurological Syndrome
4. Post-infectious encephalomyelitis (1 week after rash)
5. pneumonia
6. haemorrhagic (fulminating varicella) due to thrombocytopenia or DIVC
7. arthritis
8. Congenital varicella –rare transplacental infection in neonates born to mothers with varicella in early pregnancy.
9. Neonatal varicella –Child contracted disease from mother near time of delivery when little or no protection from maternal antibodies. High mortality in severe disease.
10. Overwhelming varicella in immunocompromised (can be lethal)
Symptoms of Zoster
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- Skin distribution corresponds to […]
- Thoracic (50%) - “belt of roses”
- Cervical (20%)
- Lumbar (20%)
- Trigeminal nerve (15%), Involvement of ophthalmic division may cause iridocyclitis, keratitis, corneal ulceration - […]
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Complications
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Clinical manifestations of VZV (vvv IMPT!!!)
Symptoms of Varicella
1. Fever, headache, malaise, abdominal pain
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Crops of vesicles (later pustules) in waves
- centrepetal distribution (more in trunks than extremities)
- usually more severe in adults
Complications
1. Skin superinfection if not kept clean (Staphylococcus, Streptococcus)
2. Aseptic meningitis
3. Neurological Syndrome
4. Post-infectious encephalomyelitis (1 week after rash)
5. pneumonia
6. haemorrhagic (fulminating varicella) due to thrombocytopenia or DIVC
7. arthritis
8. Congenital varicella –rare transplacental infection in neonates born to mothers with varicella in early pregnancy.
9. Neonatal varicella –Child contracted disease from mother near time of delivery when little or no protection from maternal antibodies. High mortality in severe disease.
10. Overwhelming varicella in immunocompromised (can be lethal)
Symptoms of Zoster
1. Painful vesicular eruption, morphologically similar to Varicella
- Virus present in skin lesions and corresponding sensory ganglia
- Skin distribution corresponds to one or more sensory root ganglia
- Thoracic (50%) - “belt of roses”
- Cervical (20%)
- Lumbar (20%)
- Trigeminal nerve (15%), Involvement of ophthalmic division may cause iridocyclitis, keratitis, corneal ulceration -
Geniculate ganglion (ramsay-hunt syndrome, vesicles in external auditory canal, tympanic membrane anterior tongue, facial nerve palsy)
- More severe if cranial dermatomic distribution e.g. ophthalmic zoster
Complications
1. Post-herpatic neuralgia (pain after vesicles go away. very painful phantom pain. Virus still moves around nerves)
2. Diseminated zoster (Vesicles outside involved dermatome(s) in immunosuppressed)
3. Encephalomyelitis, Lymphocyctic pleocytosis in CSF
4. Bacterial superinfection
Epstein Barr Virus (HHV4) is mainly found in […]% of world population. (some children and young adults present with symptoms)
Cytomegalovirus (HHV5) is mainly found in […]
Epstein Barr Virus (HHV4) is mainly found in 90% of world population. (some children and young adults present with symptoms)
Cytomegalovirus (HHV5) is mainly found in 50% of the adults (usually asymptomatic in health host)
Herpes Simplex Virus (type 1 and 2) Clinical Features
Primary Infection:
- Replicates in mucous membrane or skin at initial site of infection
- Disseminated, leading to […] (depending on immunocompetence)
Latent Period:
After primary infection, people develop antibodies for it (all adults eventually get this).
- But in non-immune subjects, HSV travels along sensory nerves to sensory ganglia where it persists lifelong in a […] state
- […] ganglia in type 1
- […] ganglia in type 2
Reactivation:
- virus reactivates when person becomes […]
Herpes Simplex Virus (type 1 and 2) Clinical Features
Primary Infection:
- Replicates in mucous membrane or skin at initial site of infection
- Disseminated, leading to viremia (depending on immunocompetence)
Latent Period:
After primary infection, people develop antibodies for it (all adults eventually get this).
- But in non-immune subjects, HSV travels along sensory nerves to sensory ganglia where it persists lifelong in a latent state
- Trigeminal ganglia in type 1
- Sacral/Lumbar ganglia in type 2
Reactivation:
- virus reactivates when person becomes immunocompromised/fever/stress/menstruation
Herpes Simplex Virus (type 1 and 2) Pathology
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- proliferation, ballooning degeneration, acidophilic intranuclear inclusions. - […]
- meningitis, perivascular infiltration, neuronal degeneration. - […]
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Herpes Simplex Virus (type 1 and 2) Pathology
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Vesicular eruption
- proliferation, ballooning degeneration, acidophilic intranuclear inclusions. -
Encephalitis
- meningitis, perivascular infiltration, neuronal degeneration. -
Early inclusion
- Cowdry type A inclusion body
Vesicular eruption = virus proliferates in infected cells until they balloon & lyse to fill vesicle with serous fluid of cytoplasmic & viral content
Herpes Simplex Virus Type 1 mainly infects the […] –> hence transmitted by […]
Herpes Simplex Virus Type 2 mainly infects the […] –> hence transmitted by […]
Herpes Simplex Virus Type 1 mainly infects the lips –> hence transmitted by kissing/contact with oral secretions/serous exudates
Herpes Simplex Virus Type 2 mainly infects the genitals –> hence transmitted by STD, perinatally
Mainly as in 80% of the time!
“1 kiss 2 bang”
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not I say one…
HHV6 is a Human B-lymphotropic virus that is associated with […]
Mild disease of children between 6 months & 3 years of age
- Occasionally confused with rubella
- Incubation period of 1-2 weeks
- Abrupt onset with high pyrexia, lymphadenopathy & convulsions
- Rubelliform rash appears after fever disappears except on face
- Leukopaenia with relative lymphocytosis
- Spontaneous recovery
Symptomatic treatment with anti-pyrexias
HHV6 is a Human B-lymphotropic virus that is associated with exanthema subitum (roseola infantum)
Mild disease of children between 6 months & 3 years of age
- Occasionally confused with rubella
- Incubation period of 1-2 weeks
- Abrupt onset with high pyrexia, lymphadenopathy & convulsions
- Rubelliform rash appears after fever disappears except on face
- Leukopaenia with relative lymphocytosis
- Spontaneous recovery
Symptomatic treatment with anti-pyrexias
HHV7 also associated with […] but is a less frequent cause.
HHV7 also associated with exanthem subitum (roseola infantum) but is a less frequent cause.
Tbh just throw this card away man HAHHAHA jk im wont cuz im OCD.
HHV8 is classically known as […]
- It causes Kaposi’s Sarcoma in AIDS
- Malignancy of vascular endothelial cells which manifests as purple lesions in skin, oral cavity, GIT & lungs
- Transmitted sexually or va transplantation
No antivirals or vaccines available
HHV8 is classically known as Kaposi’s sarcoma-associated herpesvirus (KSHV)
- It causes Kaposi’s Sarcoma in AIDS
- Malignancy of vascular endothelial cells which manifests as purple lesions in skin, oral cavity, GIT & lungs
- Transmitted sexually or va transplantation
No antivirals or vaccines available
HSV Immunology Principals
- Newborns have passive maternal antibodies lasting 6 months
- HSV 1 infection acquired […]. Almost 100% have antibodies by adulthood.
- HSV 2 acquired usually […]. About 20% of sexually–active adults have antibodies.
- Neutralizing antibodies formed after primary infection DO NOT prevent reactivation because of location of latent virus in […] sites.
- Reactivation DOES NOT stimulate rise in […].
HSV Immunology Principals
- Newborns have passive maternal antibodies lasting 6 months
- HSV 1 infection acquired early in life. Almost 100% have antibodies by adulthood.
- HSV 2 acquired usually after puberty. About 20% of sexually–active adults have antibodies.
- Neutralizing antibodies formed after primary infection DO NOT prevent reactivation because of location of latent virus in “immunoprivileged” sites.
- Reactivation DOES NOT stimulate rise in antibody titre.
HSV Lab Diagnosis
- Specimens: vesicle fluid, skin swab, saliva, tears, corneal scrapings, brain biopsy
- Tissue Culture: CPE of rounded cells in 48-72 hr.
- Antigen Detection NT or IF with specific antisera
- PCR: Detect HSV1 DNA in CSF (for acute necrotizing encephalitis)
- Serology: […]: for primary HSV infection, significant rise in titre 2-4 weeks after primary infection (however, not useful in recurrent infection due to pre-existing high levels of antibodies with no rise in titre detectable)
HSV Lab Diagnosis
- Specimens: vesicle fluid, skin swab, saliva, tears, corneal scrapings, brain biopsy
- Tissue Culture: CPE of rounded cells in 48-72 hr.
- Antigen Detection NT or IF with specific antisera
- PCR: Detect HSV1 DNA in CSF (for acute necrotizing encephalitis)
- Serology: Anti-HSV IgM: for primary HSV infection, significant rise in titre 2-4 weeks after primary infection (however, not useful in recurrent infection due to pre-existing high levels of antibodies with no rise in titre detectable)
CPE = Cytopathic effect = structural changes in a host cell resulting from viral infection. CPE occurs when the infecting virus causes lysis (dissolution) of the host cell or when the cell dies without lysis because of its inability to reproduce.
NT = Neutralization Test = serum and virus are reacted together in equal volumes and inoculated into a susceptible animal host or cell culture. If antibodies to the virus are present then clinical disease or CPE will not be observed; that is, the virus replication will be inhibited and virus is neutralized.
IF = Immunofluorescence assay = a standard virologic technique to identify the presence of antibodies by their specific ability to react with viral antigens expressed in infected cells; bound antibodies are visualized by incubation with fluorescently labeled antihuman antibody.
