Herpes simplex

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Herpes Simplex Viruses

1. Notes
- subfamily: alpha, family: herpesviridae
- worldwide
- two distinct herpes simplex viruses: type 1 and type 2 (HSV-1, HSV-2) (Table 33–3). Their genomes are similar --> antigenic cross-reactivity between HSV-1 and HSV-2 --> preexisting immunity provides some protection against heterotypic infection.
(table 33.3)
- Growth: rapidly and highly cytolytic, 8–16 hours/cycle
- Antigens: (gD), Glycoprotein C, gE. Glycoprotein G is type-specific and allows for antigenic discrimination between HSV-1 (gG-1) and HSV-2 (gG-2).
2. Pathology
necrosis of infected cells together with the inflammatory response
Histopathologic: Cowdry type A and multinucleated giant cells.
Primary Infection
- HSV-1 spread by:
+ contact (infected individual's body prior to seroconversion), usually involving infected saliva or respiratory droplets
+ Hands, fingers: HSV must encounter mucosal surfaces or broken skin in order for an infection to be initiated (unbroken skin is resistant).
- HSV-2 (genital routes ) transmitted sexually / genital infection to a newborn
Viral replication occurs first at the site of infection. Virus then invades local nerve endings and is transported by retrograde axonal flow to dorsal root ganglia, where, after further replication, latency is established (viral ARN + host genes for the lifetime). (table 33.3)

- most are asymptomatic, rarely does systemic disease develop.
- reactivate virus: from the latent state
+ axonal injury
+ fever,
+ physical or emotional stress,
+ exposure to ultraviolet light.
The virus follows axons back to the peripheral site, and replication proceeds at the skin or mucous membranes. --> symptomatic, episodes of recurrent HSV-1 infection are usually manifested as cold sores (fever blisters) near the lip, …
3. Clinical Findings
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- Oropharyngeal Disease:
usually asymptomatic.
small children (1–5 years of age)
lasts 2–3 weeks.
Symptoms:
* include fever, sore throat, vesicular and ulcerative lesions, gingivostomatitis, and malaise.
* pharyngitis and tonsillitis. Localized lymphadenopathy may occur.
Recurrent disease is characterized by a cluster of vesicles most commonly localized at the border of the lip (Figure 33–5). Intense pain occurs at the outset but fades over 4–5 days.
- Keratoconjunctivitis = Inflammation of the conjunctiva and of the cornea
HSV-1, progressive --> permanent opacification and blindness. HSV-1 infections are second only to trauma as a cause of corneal blindness in the United States.
- Genital Herpes <-- transmit the infection to sexual partners
Lesions: vesiculoulcerative lesions of the penis of the male or of the cervix, vulva, vagina, and perineum of the female. Very painful
- Skin Infections
occur in abrasions
Eczema herpeticum chronic eczema. Rarely fatal
- Encephalitis
HSV-1 infections
high mortality rate
residual neurologic defects those who survive
- Neonatal Herpes
+ herpetic lesions in the birth canal (75% of neonatal herpes infections is HSV-2)
+ may be acquired in utero, during birth, or after birth
+ always symptomatic:
(1) lesions localized to the skin, eye, and mouth
(2) encephalitis with or without localized skin involvement
(3) disseminated disease involving multiple organs, including the central nervous system.
+ Death: viral pneumonitis, intravascular coagulopathy.
- Immunodeficiency
4. Immunity
During primary infections, IgM antibodies appear transiently and are followed by IgG and IgA antibodies that persist for long periods. The more severe the primary infection or the more frequent the recurrences, the greater the level of antibody response. However, the pattern of antibody response has not correlated with the frequency of disease recurrence. Cell-mediated immunity and nonspecific host factors (natural killer cells, interferon) are important in controlling both primary and recurrent HSV infections.
After recovery from a primary infection (inapparent, mild, or severe), the virus is carried in a latent state in the presence of antibodies. These antibodies do not prevent reinfection or reactivation of latent virus but may modify subsequent disease.
5. Laboratory Diagnosis
- Cytopathology
obtained from the base of a vesicle (eg, with Giemsa's stain) --> the presence of multinucleated giant cells indicates that herpesvirus (HSV-1, HSV-2, or varicella-zoster) is present, distinguishing lesions from those caused by coxsackieviruses and nonviral entities.
- Isolation and Identification of Virus
+ definitive diagnostic approach.
+ from herpetic lesions, throat washings, cerebrospinal fluid, and stool,
+ Nt test or immunofluorescence staining with specific antiserum
+ both during primary infection and during asymptomatic periods.
- Polymerase Chain Reaction (PCR)
sensitive and specific.
amplification of viral DNA from cerebrospinal fluid (biopsy brain tissue)
- Serology
Antibodies appear in 4–7 days after infection and reach a peak in 2–4 weeks. They persist with minor fluctuations for the life of the host.
limited by the multiple antigens (epidermiology meaning)
- Epidemiology
worldwide
HSV-1: children 6 months to 3 years of age (highest incidence)
HSV-2: 20% of adults in the United States possess HSV-2 antibodies
CM tinh duc 70s USA
6. Treatment, Prevention, & Control
- acyclovir, valacyclovir, and vidarabine. (details here)
- Vaccine:
+ The National Institutes of Health (NIH) in the United States is conducting phase III trials of Herpevac, a vaccine against HSV-2
+ Harvard Medical School: dl5-29, a replication-defective mutant virus
From : Medical Microbiology, 24th - Jawetz, Melnick, & Adelberg's
References: Wikipedia , ykhoa.net
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