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  1. Parvoviruses group includes several species-specific viruses of animals B - 19   * Is a human pathogen - Named so after code number of human serum in which it was discovered
  1. Icosahedral       
  2. Non enveloped
  3. Single stranded DNA virus with outer capsid made of two structural proteins
  4. Individual virus particles contain DNA strands of +ve & -ve polarity
  5. Thermostable, retains infectivity after incubation at 60° C for 16 hrs
  6. Fails to grow in conventional cell culture lines and animal model
  7. Only replicates in vitro in erythroid progenitor cells derived from human bone marrow,  umblical cord,    peripheral blood or fetal liver
b. Causes variety of disorders
  1. Erythema infectiosum
  2. Acute arthropathy
  3. Transient aplastic crisis & pure red cell aplasia in immunocompromised
  4. Fetal infections - manifested by death or non-immune hydrops fetalis
B 19 binds specifically to cellular receptors, erythrocyte P antigen, hence the tropism of B19 for erythroid precsursor cells particularly pronormoblast and normoblasts
c. Clinical manifestation :
  1. Erythema Infectiosum/Fifth disease
  2. Most common manifestation of parvovirus B19 infection
  3. A mild illness, facial rash (typical presentation) with a "Slapped cheek" appearance preceded by fever. Rash spreads on arms, legs and has lacy, reticular, erythematous appearance. Trunk, palm and soles less commonly involved.  Rash can be maculopapular, morbilliform, vesicular, purpuric or pruritic
  4. Rash resolves in about a week but recur intermittently for several weeks, after stress,  exercise, exposure to sunlight, bathing and change in environment temperature
ii. Arthropathy : -
  • Most common manifestation in adults. Uncommon in children Symmetrical, peripheral involving wrists, hands , knees most frequently
  • Usually resolves in 3 weeks, non destructive, may last for many months, even years
iii. Transient Aplastic Crisis :
  • parvovirus B19 causes transient aplastic crisis in patients with chronic hemolytic disease, eg : sickle cell disease, hereditary spherocytosis, thalassemias etc.
  • Patients have intense reticulocytopenia
  • Patients with transient aplastic crisis unlike others like arthritis & arthropathy can transmit B19 infection to other people
iv. Chronic anemia in Immunodeficient patients : Unable to eliminate B19 infection due to inadequate production of IgG antibodies thus persistence of infection
v. Fetal and congenital infections :
  • Maternal B19 infections generally do not adversely affect the fetus
  • < 10% of maternal B19 infection usually lead to fetal death
  • If infected usually death due to development of non immune fetal hydrops. Where in fetus has severe anemia & CHF
  • For prevention - pregnant women with known exposure to B19 should have IgM monitored and check for elevated level of α AFP, USG for Hydrops fetalis
d. Diagnosis
  • Acute infection shows raised IgM
  • Bone marrow biopsy
  • Fetal infection: Presence of B19 DNA in amniotic fluid or Fetal blood
e. Treatment :
  • Erythema infectiosum - Self immunity
  • Arthritis and Arthropathy - NSAIDS
  • Aplastic crisis - Erythrocyte transfusion
  • Immunodeficient patient - I/V anti Parvovirus IgG
  • No vaccine for Parvovirus B19 is currently available - A baculo virus infected insect cell line that expresses non infectious immunogenic B19 capsid proteins is being evaluated as a vaccine candidate
3. Adeno virus
  1. DNA virus: Double stranded DNA, non-enveloped, icosahedral symmetry. Space vehicle shaped.
    50 distinct antigenic types have been isolated from humans.
  2. Have been used as gene vectors
  3. Human adenoviruses are divided into six groups (A-F) based on their physical, chemical and biological properties
a. Clinical features:
Group Principal types Disease
B 3,7,14 Pharyngoconjunctival fever (swimming pool conjunctivitis)
3,7,14,21 Acute respiratory disease
3,7 Pneumonia, acute febrile pharyngitis in small children
11, 21 Acute haemorrhagic cystitis
34,35 Pneumonia with dissemination (AIDS patients)
C 1,2,5,6 Acute febrile pharyngitis in small children
1,2,5 Hepatitis in children with liver transplant
D 8,19,37 Epidemic keratoconjunctivitis (ship yard eye)
E 4 Acute respiratory disease with fever
F 40,41 Infantile gastroenteritis ( difficult to cultivate)
b. Laboratory Diagnosis:
Culture: primary human embryonic kidney cells, Hep-2, HeLa; CPE- Rounding and clustering of cells

Antigen detection: Immunofluorescence, ELISA, latex agglutination, electron microscopy
Treatment: symptomatic

Vaccine - Live attenuated / killed, for prevention of acute respiratory disease, useful for military recruits
4. Herpesviruses
  • Spherical ds DNA virus, 120-200nm in diameter
  • Comprise of four structural elements: envelope, tegument, capsid and core
  • Envelope is outer most; tegument is present between envelope and capsid. Inner to tegument is icosahedral capsid, which contains double stranded DNA
  • These groups of viruses establish latent infections which get reactivated in immunosuppressed hosts
Classification of human herpesviruses
Subfamily Growth cycle Cytopathology Site of latent infection Official name Common name
Alphaherpesvirinae Short Cytolytic Neurons HHV1
Varicella-zoster virus
Betaherpesvirinae Long Cytomegalic Glands, kidneys HHV5 CMV
Lymphoproliferative Lymphoid tissue HHV6
Gammaherpesvirinae Variable Lymphoproliferative Lymphoid tissue HHV4
Kaposi’s sarcoma associated
a. Herpes simplex virus
i. Two types HS1 & HSV2
  • HSV1: infects mouth, eye, CNS (regions above the waste), but is also responsible for few cases of genital herpes.
  • HSV2: infects genital and anal regions
  • Infections caused by herpes simplex can be divided into primary infection, latent infection & reactivation
ii. Primary infections-usually more severe
iii. Transmitted by contact through damaged skin or mucosa, classic lesion is a vesicle
iv. HSV1 cause following primary infections
  • Acute gingivostomatitis
  • Herpetic whitlow
  • Keratoconjunctivitis
  • Eczema herpeticum
  • Encephalitis (involves temporal lobes)
  • Generalized infections
v. HSV2 causes following primary infections
  • Genital herpes (painful vesicles, fever, malaise, swollen lymph nodes)
  • Aseptic meningitis
  • Neonatal infection
  • Acquired during passage of the baby through infected birth canal, abortion, congenital defects
  • Disseminated disease: mortality rate: 80%
  • Encephalitis
  • Localized infection (skin, eye, mouth)
vi. Latent infection
  • HSV1: cranial (trigeminal) ganglia and HSV2: sacral ganglia
  • Within the sensory ganglia, viral DNA exists as a free circular episome
vii. Reactivation-Provoked by various stimuli like common cold, fever, stress etc.
viii. Virions migrate back to the nerve endings, where infection of the epithelial cells results in cluster of vesicles commonly found at the mucocutaneous junctions of the lips, nose, eyes
ix. Laboratory diagnosis
  • Direct examination: electron microscopy (virions), fluorescence microscopy (viral antigens), light microscopy (Tzank smear: multinucleated giant cells with faceted nuclei, homogeneously stained ground glass chromatin with eosinophilic intranuclear inclusions)
  • Culture: human fibroblast/ vero cell line, swollen rounded cells (CPE), immunofluorescent staining of the infected cells
  • Serological tests: CFT, Nt, Immunofluorescence, ELISA
    Treatment: Acyclovir
b. Varicella zoster
  • 2 distinct clinical entities :- Varicella / Chicken pox- Herpes Zoster / Shingles
  • Mode of infection : Respiratory route
  • Vesicles:  Corium + dermis - ballooning, multinucleated giant cells, Eosinophilic intranuclear IB
  • Pulmonary Involvement : Interstitial pneumonitis
  • Multinucleated giant cells
i. Chicken Pox :
  • Humans are only reservoir for VZV
  • Secondary attack rate : 90% ( 70 - 90%)
  • Late winter + Early spring
  • Age : 5 - 9yrs,   I.P. 10 - 21 days
  • Infectious : 48 hrs prior to onset of vesicular rash, during the period of vesicular formation (4- 5days) & until all vesicles are erupted and scab is formed
  • Skin lesions: maculopapules / vesicles/ scabs-multiple crops appear daily.
  • Immunocompromised patients: Have more lesions & greater risk of visceral complications (30 - 50%) & fatal (15%)
  • Most common , infectious complication = S. pyogenes / S. aureus
  • Most common extracutaneous site involved: CNS (acute cerebellar ataxia + meningeal irritation)
  • Others CNS manifestations: aseptic meningitis, Reye's syndrome, GBS & transverse Myositis
  • Varicella pneumonia : is serious complication , more common in adults
  • Perinatal varicella: ↑ mortality, if maternal disease 5days before delivery or 48hrs thereafter (Mortality = 30%)      
  • Congenital Varicella: Limb hypoplasia, cicatricial skin lesions, microcephaly, chorioretinitis
c. Herpes Zoster :
  • 6th - 8th decade
  • T3 - L3, if ophthalmic division of trigeminal nerve:  Zoster opthalamicus
  • Zoster associated pain: Continuation of pain from onset to resolution
  • 1st dermatomal pain (48 - 72 hrs), then rash ( 3 - 5days)
i. Ramsay Hunt syndrome :
  • Pain & vesicles in external auditory canal
  • Loss taste in anterior 2/3rd of tongue & develop ipsilateral facial palsy ( Geniculate ganglion of sensory branch of VII nerve involved)
  • Most debilitating complication: pain associated with neuritis & post herpetic neuralgia
  • Patient with HIV, Hodgkin’s, non Hodgkin’s lymphoma & bone marrow transplant are at increased risk
ii. Lab. Investigation :
  • TZANCK smear
  • Isolation of VZV in susceptible tissue culture cell
  • 3. Demonstration of seroconversion. Demonstration of a 4 fold / greater rise in antibody titre between convalescent and acute phase sera by ELISA, CFT, Nt, IFA
  • PCR
iii. Prophylaxis :
  • VZIG & ZIG: within 96hrs (pref. 72 hrs)
  • Vaccine: OKA strain (life attenuated vaccine)
iv. Treatment :
  • Acyclovir , vidarabine, valacyclovir
  • Acute Neuritis / Neuralgia : Analgesics / Glucocorticoids

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