Common Viral Pathogens Flashcards
Understand the basic ways to diagnose a viral infection using laboratory tests.
You can look for the actual virus:
• Tissue Culture
• Antigen via enzymatic reactions or IF to detect specific “parts” of the virus in, e.g. rapid flu test
• Polymerase Chain Reaction (PCR): amplify viral genome, can be qualitative or quantitative.
You can look for a host’s immune response to a viral infection by looking for antibodies that are specific for that virus.
• ELISA:
o Coat the plate with a viral antigen (can be the whole virus or part)
o Incubate the host’s serum on the plate to let the antibodies attach to the antigen on the bottom of the wells
o Then incubate the plate with an antibody that detects the host antibody (a secondary antibody)
o Then incubate the plate with a substrate that will allow visualization of the secondary antibody
• Example: Dx EBV by ordering a monospot test or a serologic panel. The monospot test detects the presence of a heterophile antibody (this is usually a rapid test). The EBV serologic panel usually consists of: VCA IgM, VCA IgG, and EBNA.
Know the hallmarks of herpes viruses and the 8 herpes viruses that infect humans
Hallmark: once a host is infected, the host is always infected. The virus establishes latency after infection that can become reactivated - may or may not cause disease. Treat w/ acyclovir
There are 8 herpes viruses which infect humans, all double-stranded DNA viruses: • HHV-1: HSV-1, oral • HHV-2: HSV-2, genital • HHV-3: VZV, chickenbox • HHV-4: EBV, mono, Burkitt's lymphoma • HHV-5: CMV, mono-like syndrome • HHV-6/7: Roseola (HHV-6a, HHV-6b), exanthem subitum • HHV-8: HHV-8 Kaposi's Sarcoma
HSV-1/HSV-2
Primary infection
• Usually asymptomatic, otherwise: lesions 1-3 days after inoculation, fever, contained rash @ inoc site (unless immunocompromised)
• Worse than recurrent infection
Reactivation infection
• Can be silent (STILL SHEDDING!) or symptomatic, but usually less so than primary infection
• Reactivation provoked by sunlight, stress, febrile illness, menstruation, immunosuppression
• Oral hangs out in trigem ganglia, genital in sacral ganglia
Pathogenesis
• ?
Diagnosis
• Clinical dx, but can do: Tzanck smear (sucks, non-specific), HSV culture, Direct Fluorescent Antigen, PCR
Treatment
• Severe infection: IV acyclovir
• Normal outbreaks: oral acyclovir (standing ‘scrip)
Prevention
• Barriers, hygiene, avoid contact. If bad enough, constant low dose acyclovir
VZV
Primary infection
• Chickenpox
• 10-21 days post-inoc: fever, malaise, ha, cough, RASH!
• Rash: “dew drops on rose petal,” trunk –> face + limbs, lasts 7 days
Reactivation infection
• VZV remains latent in the cranial, dorsal root and/or trigeminal ganglia
• Reactivation is ALWAYS symptomatic (unique)
• Virus reactivates in ganglion and tracks down the sensory nerve to the skin innervated by the nerve (hence dermatomal spread); lasts 2 weeks
Pathogenesis
• Virus gains entry via respiratory tract
• Spreads via lymphatics & replicates for 2-4d
• Primary viremia 4-6 days post-inoc
• Replication in liver, spleen and possibly other organs –> secondary viremia
• Secondary viremia spreads viral particles to the skin 14-16 days after initial exposure and causes the typical vesicular rash
Diagnosis
• Usually clinically, but can use Direct IFA, PCR, or culture
Treatment
• Self limited, but can administer acyclovir to help, nsaids for pain
Prevention
• Varicella vaccine: 12-15mos & 4-6y
• Varizig: IgG w/i 4 days of infection
• Zostavax @ 60y
EBV
Primary infection
• 95% of people get it. No prob when you’re a kid, but problem if you’re a little older
• Get it via saliva, incubates 4-6wks
• Symptoms: fever, sore throat, swollen lymph nodes fatigue
Pathogenesis
• EBV infects the nasopharyngeal epithelium, resulting in cell lysis and viral spread to adjacent structures such as the salivary glands and oropharyngeal lymphoid tissue
• Viremia –> liver, spleen, and infection of B lymphocytes
• Remains dormant or latent in the nasopharyngeal epithelium and B cells
• Periodically, the virus can reactivate and is commonly found intermittently in the saliva of infected persons, but pts are asymptomatic
Diagnosis
• Atypical lymphs seen on PBS
• Monospot test (Abs to EBV hemagglut sheep RBCs)
• Can do serology; IgM (at onset) to VCA = recent, IgG to VCA = prior, IgG to EBNA = old
Treatment
• Supportive care, boost immune system in immunocompromised
Prevention
• Avoid contact
CMV
Primary infection
• Incubation period: 2 weeks to 2 months
• Normal ppl & babies are asymptomatic (some get mild mono-like symptoms), no long-term health conseq.
• In immunocompromised pts: serious infection in most organs (CMV retinitis and colitis in HIV patients)
Reactivation infection
• Normal ppl: reactivation occurs, virus is shed (saliva & urine), but no symptoms
• Vertical Tx (mother to baby), but more common in pri.
• In immunocompromised: VERY serious disease. Non-focal viral syndrome or an organ-specific infection such as hepatitis or pneumonitis.
Pathogenesis
• CMV infects the epithelial cells of the salivary gland or the genital tract, resulting in a persistent infection and intermittent viral shedding.
• Viremia –> other organs and tissues
• Infection of the GU system –> CMV shed in urine
Diagnosis
• Serology (CMV IgM and IgG)
• Viral culture—easy to grow, but may take several days
• PCR
• Direct fluorescence test
• Tissue histology: Infected cells have “owl’s eye” appearance (densely staining body surrounded by a halo). Intracytoplasmic inclusions (multiple smaller inclusions) are also seen in CMV infection.
Treatment (for immunocompromised)
• gancyclovir or valganciclovir
• CMV-IG for preggos
• Babies, gan for now. Likely valgan later
Prevention
• CMV-IG monthly in immunocompromised
• Gan/Valgan post-transplant
For CMV, understand the significance of infection during pregnancy including features of congenital CMV.
- Very common
- When preg woman develops a primary CMV infection, there is a 3-5% chance that the child will be born with a congenital CMV infection.
- Most infected infants will be asymptomatic. Only 10-15% of the infected infants will have symptoms at birth (this is about 3-5% of the infants born to mothers with primary infections).
- Infection of the fetus can also occur if a pregnant women reactivates CMV, but the risk is much lower (<1% of babies will become infected and even fewer are symptomatic).
- Congenital CMV syndrome: low birth weight, Microcephaly, Hearing loss, Mental impairment, Hepatosplenomegaly, Skin rash (blueberry muffin spots), Jaundice, Chorioretinitis
EBV is implicated in several types of cancers:
Burkitt’s Lymphoma: endemic in Africa and occurs sporadically elsewhere in the world. A B cell tumor often affecting the jaw.
Hodgkin’s lymphoma
Nasopharyngeal carcinoma: highest incidence in Chinese
Lymphoproliferative disease: seen in immunocompromised patients, due to an uncontrolled proliferation of EBV-infected B cells
Describe the pathogenesis and the clinical manifestations of RSV infection in young children.
Pathogenesis
• Virus enters through mucosa of eye and nose
• Localized infection of respiratory tract, with cell-to-cell transfer of virus leading to spread from upper to lower respiratory tract
• Syncytia are formed
• Bronchiolitis results from:
- Mucosal edema
- Cell necrosis and sloughing
- Increased mucous secretion and plugging of bronchiolar lumina with epithelial debris and mucous
- Airway hyper-reactivity and bronchoconstriction also occur as a result of inflammation → wheezing
Clinical patterns
• In young children and premature infants, RSV is the most frequent cause of bronchiolitis and viral pneumonia.
• Symptoms: fever, runny nose, cough, wheezing with involvement of the lower respiratory tract
• Almost all children infected at least once by 2 y/o
• Seasonal illness which peaks in the winter (125k hospitalizations annually)
• Reinfection in adults and older children generally resembles a severe cold and confined to upper respiratory tract
• Bronchiolitis starts as an upper respiratory infection with congestion, sore throat, fever
• Cough deepens and becomes more prominent
• Lower respiratory tract involvement develops with increased respiratory rate, and intercostal muscle retraction, and wheezing
• Wheezing in child <2 yr of age is most likely bronchiolitis
Describe the pathogenesis of rotavirus and the clinical manifestations of the disease.
Pathogenesis
• Infects the mature absorptive epithelial cells or enterocytes (located at tips of villi) in the proximal 2/3 of the ileum
• Cell death leads to:
- Reduction of absorptive surface area of small intestine
- Loss of enzymes that break down complex sugars
- Increased fluid and osmotic load in gut → diarrhea
- Regeneration of villi takes 7-10 days (recovery period)
Manifests as severe diarrhea and/or gastroenteritis in infants and young children
