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    14 views19 pages

    Lesson 8 Handouts

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    Khay Mae Donasco

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    © All Rights Reserved
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    CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON’T COPY PASTE FROM OTHERS Rikka Mae M. Donasco 07/07/2022 LESSON 8: HERPESVIRIDAE The word “_hurpe 2" is derived from the Greek word meaning “tp cree "and was historically used to describe the ) SID MOT Hode oF Tearswission Yyrek coda iin oainsn oF aloraaed skin Seve mor oy vuAical made] Cad Trquminal opnaiia ual gnasia AGE Ypang, uiilarun ‘pang, acuity | COMMON MANIFESTATION | Oral—Facial mucosal lesion [Guaita Usion Encephalitis cular lesions Sein Wiens todew walst wotonatal QURLL so Skin lesions below waist f ~ [Chicken embryo fibroblast | Does not grow well Replicates well | Neurovirulence co Ngee | Drug resistance = = “Antigenic homology foib avd 2 snus > 07 artiquic womaogy — | DNA homology WIA and 2 snows LOX Momadsoy WAL Ayunowic, KeeHeNe PATHOGENESIS & PATHOLOGY Characteristic histopathologic changes include _oalooniney__of infected cells, production of Gondry —_ type A _jnicanuUcor _ inclusion bodies, margination of chromatin, and formation Of mulkinactared giant cells. gf _ wane wewsooen CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON’T COPY PASTE FROM OTHERS HERPES SIMPLEX VIRUS ~ PRIMARY ACUTE INFECTION Both_gs~2 and HSV-2initially infect and replicate in the qauen-epithetiat “4 initiate lytic or productive infection at the site of contact. Transmission occurs through gods skin or mucosa from any site, but more commonly by: HSV-1: Qropnay 1 ©*\ith infected saliva or direct skin contact for HSV-1, and Sena crac or rarely’ _yurtica ‘mode (from mother to fetus) for HSV-2. HSV-1 is more often associated with disease " gowe am walst "or equal. herpes, whereas HSV.2 is most often associated with _queita infections or" bain ty wot” infections Virus then invades the local nerve ending and is transported by _aacogade oxana! flow to the dovsal_ root ganglia, where it replicates further, and then undergoes latency. Primary HSV infections are usually __yail in fact, most are However, in immunocompromised hosts, _ viewla occurs that leads to widespread organ involvement and systemic manifestations HERPES SIMPLEX VIRUS ~ LATENT INFECTION In humans, latent infection by __isv- 4 has been demonstrated in vigil nerve ganglia, and occasionally in the _$2- S>. superior cervical, and dorsal sensory nerve root ganglia Latent HSV-2 infection has been demonstrated in the __ sacral (52-53) region, CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON’ "T COPY PASTE FROM OTHERS HSV does not replicate in latent. ‘stage except for a small RNA, called _wi wo QUAL (encoded by 3 latency- associated viral gene) which maintains the _Jatust infection and prevents cell dean. HERPES SIMPLEX VIRUS ~ RECURRENT INFECTION (REACTIVATION) Reactivation of the latent virus can occur following various provocative stimuli, suchas peur uanal injury, physical or emotional stress, and exposure to uivaviows light. Via the axonal spread, virus goes back to the _puy\ mucosa producing \_site and further replicates in skin or lesions. Recurrent infections are less extensive and less. Severe because of presence of pre-existing host immunity that limits the local viral replication. CLINICAL FINDINGS ~ PRIMARY INFECTION Joo dl frost Hsv-1 HSV-2 weal | cineivostomatitis i a Aha. waist z PHARYNGOTONSILITIS 7 ~ | KERATOCONJUNCTIVITIS | 7 eS NEONATAL INFECITONS aE ¥ CLINICAL FINDINGS ~ RECURRENT INFECTION HSV-4 : v2 COLD SORES, FEVER & BLISTERS | 2 \; bears aha ois KERATITIS ape) a Inglamamation cornea : CLINICAL FINDINGS ~ PRIMARY OR RECURRENT INFECTION HSV-3 HsV-2 ‘CUTANEOUS HERPES SKIN ABOVE WAIST 4 al ‘SKIN BELOW WAIST th rt HAND OR ARMS is GENITAL HERPES 4[- + CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON’T COPY PASTE FROM OTHERS HERPES ENCEPHALITIS 4s 7 HERPES MENINGITIS 4 + LABORATORY DIAGNOSIS - HSV on, Pelumasor ais fPCR) assays can be used to detect virus in_yuidt. _ swabs, blood, _Cst and tissue and are sensitive and specific. wid : PCR amplification of viral DNA from cureisespinal is the most _suniiive. means of detection and is recommended for diagnosis of uusingitis /amaghalitic. Virus culture is commonly used, particularly for diagnosis of yuroudantaw disease, Inoculation of tissue cultures is used for viral isolation. HSV is relatively easy to cultivate, with cytopathic effects typically occurring in 3-2.daxu. The agent is then identified by nudvalsatina — test or immunofluorescence staining with specific antiserum. A rapid cytologic method isto stain scrapings obtained from the base of a_yuiick. _ (eg, with Giemsa’s stain); the presence of multinucleated giant cells indicates that iusganiras (HSV-1, HSV- 2, or varicella-zoster) is present. ‘Antibodies appear in_4-7.___days after infection and reach a peak in_2-4. weeks. ‘They persist with minor xuductiow. for the life of the host. Detection methods available include uAcalis cAion _, immunofluorescence, and enzyme-linked immunosorbent assay. EPIDEMIOLOGY & TREATMENT AND CONTROL- HSV HSV are worldwide in distribution. No animal reservoirs or vectors are involved with the human viruses. Transmission is by contact with infected secretions. The epidemiology of HSV-1 and HSV-2 differs. HSV-1 is more constantly present in humans than any other virus. HSV-2 is usually acquired as a_STO Several antiviral drugs have proved effective against HSV infections, including qujchovir_, dlaaysouc, and vidarabine. Newborns and persons with extsma should be protected from exposure to persons with active lesions, Patients with genital herpes should be counseled that asymptomatic shedding is frequent and that the risk of transmission can be reduced by antiviral therapy and con Aw usage. Experimental vaccines of various types are being developed. pata nin Se eee CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON’T COPY PASTE FROM OTHERS VARICELLA~ ZOSTER VIRUS (VZV) Varicella (chickenpox) is a mild, highly contagious disease, chiefly of children, characterized clinically ae eal edeaday._ eruption of the skin an mcous membranes. The disease may be seeeeinnadulte and in wanueacen™ viduals sterpes roster (uaequa__)'82 sporad, ncapactating dsease of elderly oF mmurmeampised Te Ce Gieed by gat and -dusada_‘esh limited distribution to theskin Innoited bya single sensor gana Te lesion afesmiartothore of wav Both diseases are caused by the same virus. Whereas varicella isthe acute disease that follows primary contact with the virus, _astae is the response of the partially ysunuuna__ host to reactivation of varicella virus present in latent form in neurons in sensory ganglia, Varicela-zoster virus is margasiaajccilyidentical to HSV. It has no animal reservoir. The virus propagates in cultures of snumonaepanac Sia produces typical jwivanuclt or inclusion bodies Varicella-zoster virus is inhaled; infects mucosal cells in nose and throat. @ The virus infects nearby lymph nodes, replicates, and enters the bloodstream (primary viremia). @ Infection of other body cells occurs, with replication in liver and spleen, resulting in secondary viremia. @ The virus causes successive crops of skin lesions, which evolve into blisters and crusts. © ‘nmune system eliminates the infection except for some virions that establish latent infections inside nerve cells. © immunity wanes with age or other reason, the virus persisting in the nerve ganglia can infect the skin, causing herpes zoster. @ Transmission to others occurs from respiratory secretions and skin. CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON’T COPY PASTE FROM OTHERS Noseuta CLINICAL FINDINGS - VZV ‘Giouivicat varicella is unusual, The incubation period of typical disease is _o=2 days. Malaise and aus are the earliest symptoms, soon followed by the rash, first on the Auante and then on the face, the limbs, and the _iauical__ and pharyngeal mucosa in the ‘mouth. ‘Successive fresh vesicles appear in crops, so that all stages of macules, papules, vesicles, and crusts may be seen at one time. The rash lasts about 5 days, and most children develop several hundred skin lesions. Immunocompromised patients are at increased risk of complications of varicella, including those with watiqnaa'Srgan transplants, or HIV infection and those receiving high doses of Lon cast oie Disseminated igtucassss\av coagulation may occur that is rapidly fatal. Children with \osseerio. are especially prone to developing severe, disseminated VZV disease, Herpes Zoster ju d, Herpes zoster usually occurs in persons iwununninst'S result of disease, therapy, or aging, butit occasionally develops in healthy young adults. it usually starts with severe pain in the area of skin or mucosa supplied by one or more groups of sensory nerves and ganglia and is often unilateral. Within a few days after onset, a_ceop _ of vesicles appears over the skin supplied by the affected nerves. The trunk, head, and neck are most commonly affected. The most common complication of zoster in elderly adults is gadwevettic euuvaigia —protracted pain that may continue for months. & + & (ae Oe vide soe oF VS ta Cousteny COE = BOL Herr CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON’T COPY PASTE FROM OTHERS LABORATORY DIAGNOSIS & EPIDEMIOLOGY- VZV Cytopathology: Causa staining ofthe scrapings from the ulcer base (Tuay\._—_ #mea’) reveals cytopathological changes similar to that of HSV infection, such as formation of muitisusisatcd giant cells. Virus isolation: Virus isolation in various cell lines can also produce HSV-like cytopathic effects such a5 _digguuw rounding and jnalsaring, of infected cells. \V2v-specific methods: Specific antigen detection by direct immunneiuactscunss. staining and PCR detecting __W1v -specific genes. EPIDEMIOLOGY Varicella and herpes zoster occur worldwide. Varicella (chickenpox) is highly communicable andisa common epidemic disease of d transfusion, though the riskis_lo» _with __lauk» _-reduced blood products. ‘Treatment, Prevention and Control Drug treatments of CMV infections have shown some encouraging results. Gaxciosu-_ has been shown to be successful in treating serious life-threatening CMV infections. Other drugs used to treat CMV infections are Foscarnet, anuxp\ovie and _volauhovie CUSTOMIZE YOUR HANDOUTS, ADD YOUR NAME AND PLEASE DON'T COPY PASTE FROM OTHERS HUMAN HERPES VIRUS 6 ~ HHV6 Ini a herpesvirus, now called human herpesvirus type 6 (HHV-6), was identified in cultures of peripheral blood \uyiausica from patients with lymphoproliferative diseases. HHV-6is_d-twegesinaus_ subfamily The virus morphologically similar to other herpesviruses with similar replication patterns of other herpesviruses. HHV-6 replicates in sid_tissue, especially Coes Tlymphocytes, and has two distinct variants, A and B, that are genetically disparate enough ‘that some consider them different species. Clinical Findings atu, HHV-6 type Bis the main etiologic agent of Siawi nO oseola), and both types Aand B can cause acute _tebiils illnesses with or without seizures or rashes. xanthem subitum generally occurs infants aged _t mo ~ ytav, Inthe first 6 months, infants are generally protected by the mother’s IgG. Exanthem subitum is characterized by fever {usually about ae for__2 days, followed by a faint Haun papulavrash spreading from the Fast the extremities, which begins during dueaacne. Exanthem subitum is one of the Six classic childhood Sayama — Epidemiology Of the herpesviruses, HHV-6is the most vagiai\y spread and is shed in the throats of tm %of babies by age 5 months, 70% by 12 months, and 30% of adults. Greater than 90% of ‘the population has antibody to this virus by the age of 5 years. Laboratory Diagnosis Primary virus infection can be documented by suiccenvuin. Active virus infection can be documented by culture, antigenemia, or DNA detection in the blood (by PCR). Because asymptomatic viremic reactivation is common, itis very difficult to use these tools to identify HHV-6 asthe cause of yumi _or other miscellaneous syndromes. ‘Treatment, Prevention and Control Definitive therapy has not been established, but lke the better characterized B-herpesvirus, CMV, HHV-6 appears to be susceptible in vitro to qov

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