lecture 13/14 – Flashcards
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| ETIOLOGY -fastidious -GN -non motile -oxidase positive -diplococcus -kidney bean shape gram stain VIRULENCE FACTORS capsular types no crossreactivity type B capsule is same as e.coli k1 |
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| EPIDEMIOLOGY carriers: -colonization site is nasopharynx -carrier state persists days to months -non immune and short term; group specific immune carriers are responsible for spread of disease, via aerosols -carriers quite common in epidemic situation but few develop disease |
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| infections require close contact, susceptibility (lack of antibodies for capsules) and predisposing condition - tobacco smoke exposure, crowding, binge drinking, low socioeconomic status |
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| epidemiology: susceptible popoulations in which disease predominates - infants (1m-24m) young adults 14-24 yr families due to carriers and genetic predisposition -genetic predisposition, ie terminal complement deficiencies |
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| only agent of purulent meningitis capable of causing sporadic outbreaks and epidemics |
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| clinical manifestations: onset of mild sore thraot, slight fever and headache, then onset of classic clinical manifestations plus petchial rash on trunk and lower extremities which may progress to purpura (necrotic lesions; organism in lesion) course infection and disease can be fulminant - death within hours waterhouse-friderchsen syndrome: fulminant meningococcemia characterized by shock, DIC, hemorrhagic necrosis of adrenals purpura fulminans - symmetrical peripheral gangrene |
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| DIAGNOSIS gram stain of CSF or skin lesion rapid serological test available |
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| NEISSERIA MENINGITIDIS Meningococcal meningitis |
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| treatment: cefotaxime or ceftriaxone |
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| NEISSERIA MENINGITIDIS meningococcal meningitis |
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| prophylaxis: VACCINES tetravalent/quadrivalent polysaccharide vaccine; type 2 T-ind antigent vaccine limitations: only lasts 3-5 yr; poor immunogenicity in infants less than 2 yrs not efficacious againts b serotype tetravalent/quadrivalent diphtheria toxoid conjugate vaccine. t-dep vaccine, so should last more than eight years, and eliminate nasopharyngeal carriage, thus prevent transmission of infection; vaccine reduces prevalence by 75-90% eliminate carrier state by chemoprophylaxis with rifampin, ciprofloxacin or ceftriaxone within 24 hours of identification; no more than 14 days after onset of illness for small outbreaks, prophylaxis with antibiotics is effective for large outbreaks (countries, cities) vaccination and antibiotics is most effective vaccines for serotype B infecitons is in clinical trials eliminate nasopharyngeal carriage of N. meningitidis with ciprofloxacin, ceftriaxone, rifampin, or azithromycin unless fluoroquinolone-resistant strain is detected |
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| CRYPTOCOCCOSIS: FUNGAL MENINGITIS cryptococcus neoformans |
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| encapsulated yeast worldwide distribution, found in soil cryptococcus neoformans var grubii is MAJOR CAUSATIVE AGENT worldwide cryptococcus gattii is primary pathogen that infects immunocompetent persons; associated with eucalyptus trees infectious form is yeast; not thermally dimorphic; grows as yeast in humans virulence factor: capsule, multiple capsular serotypes in aids pt, c. neoformans var grubii capsule A predominates - antiphagocytic |
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| CRYPTOCOCCOSIS: FUNGAL MENINGITIS cryptococcus neoformans |
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| epidemiology: sporadic, world wide distribution risk factor: impaired CMI; rarely causes disease in immunocompetent pt aids: 3rd most common cause of CNS infection - HIV, toxomplasmosis aids: 4th most common opportunisitc infection - p. carinii, CMV, m. avium other impaired immunity: lymphoreticular malignancies immunosuppressive therapies |
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| CRYPTOCOCCOSIS: FUNGAL MENINGITIS cryptococcus neoformans |
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| clinical manifestations: enters RT, agent in monocytes disseminates through blood site of initial infection and disease is lungs; no symptoms in competent person but immunosuppresed have fever, cough, dyspnea, weight loss, headache. chest x ray reveals interstitial infiltrates meningoencephalitis: chronic, progressive disease which is fatal if not treated. insidious onset 2-4 weeks of headache, fever, lethargy, n/v, minimal nuchal rigidity progresses onto focal signs: personlity change; impairment of higher mental functions; ends with coma and death |
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| cryptococcus neoformans |
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| diagnosis: test CSF, blood, urine, respiratory samples, biopsied tissue by serologic tests - latex agglutination and ELISA; detect presence of capsular antigen microscopic exam of sedimented CSF with india ink; presence of small capsulated yeast forms and cells of monocyte lineage |
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| cryptococcus neoformans |
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| treatment high dose amphotericin B with 5-fluorocytosine (fluconazole), maybe itraconazolelater; drug resistance is rare prognosis is poor - some die initially, 30-60% die within a year |
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| aseptic viral meningitis |
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| human herpes virus HHV 6 and 7 and non-polio enteroviruses |
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| hhv6 and 7 |
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| major cause of acute febrile illness in young children hh6 infection in children 6-12m; accounts for many visits to ER many hospitalizations; many first time febrile seizures (CNS infection) among children less than 2yr |
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| HHV 6 AND 7 |
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| primary infection: manifestions- abrupt onset of high fever; lethargy, irritability, malaise, no rash take kid to ER, but no obvious cause so do spinal tap on kids; but tap is aseptic |
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| NON POLIO ENTEROVIRUSES |
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| meningitis or encephalitis, depending on serotype |
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| NON POLIO ENTEROVIRUSES |
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| etiology: echoviruses coxsackie virus enterovirus 68-71 non polio enterviruses are most common infection of CNS ECHO and coxsackie viruses are most common and important viral pathogens in humans; causes a nonspecific febrile illness with or without rash; initially replicate in small intestine |
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| NON POLIO ENTEROVIRUSES |
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| epidemiology most common cause of aseptic meningitis in countries that immunize against mumps humans are host summer and fall months - responsible for half febrile illness in infants and small children transmission: acid stable viruses acquired via fecal oral route; also transmitted via aerosols or passed in utero peak incidence: less than 9 yr old; highest attack rate under one yr; incidence and severity varies with age |
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| non POLIO ENTEROVIRUSES |
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| CLINICAL MANIFESTATIONS abrupt onset of fever, constitutional signs and symptoms -s ore throat, diarrhea, malaise; rash meningeal signs in neonate: fever, rash, vomiting, anorexia, nuchal rigidity; death due to destruction of liver or heart |
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| NON POLIO ENTEROVIRUSES |
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| diagnosis: PCR for enteroviral agents |
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| NON POLIO ENTEROVIRUSES |
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| symptomatic and supportive |
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| DIFFUSE ENCEPHALITIS |
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| arthropod-borne viruses -arboviruses |
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| diffuse encephalitis ARBOVIRUSES |
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| etiology: togaviridae group +ssRNA easter equine encephalitisEEE - worst mortality rate; survivors have severe problems; EEEV is unique in that infection often but not always leads to EEE. asymptomatic infeciton is NOT the norm western equine encephalitis - most benign form st. louis encephalitis - related to west nile; leading cause of epidemic arboviral encephalitis in us before west nile west nile encephalitis - like sLE, causes more severe disease in elderly; most COMMON ARBOVIRUS INFECTION in us today |
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| ARBOVIRUSES DIFFUSE ENCEPHALITIS |
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| etiology bunyaviridae group: california encephalitis - la cross virus -ssRNA most importatn cause of arboviral pediatric encephalitis in USA; seizures may occur during illness |
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| ARBOVIRUS DIFFUSE ENCEPHALITIS |
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| epidemiology - zoonosis survival of virus depends on alternating between vertebrate host (birds are reservoir) and arthropod host (mosquitos are vector); humans are infected tangentialy entire geographic distribution includes US primary cause of sporadic and epidemic meningoencephalitis in humans in summer months when reservoir (birds), vector and humans are outdoors |
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| ARBOVIRUS DIFFUSE ENCEPHALITIS |
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| clinical manifestations: asymptomatic infection is most common result abrupt onset of symptoms:mild flu like symptoms; mild, self limited aseptic meningitis; acute fulminant diffuse encephalitis, death west nile: note that focal symptoms seen with west nile are not common manifestations in diffuse encephalitis caused by other arbovirus agents; focal symptoms of muscle weakness, asymmetrical flacid paralysis; parkinson like tremors |
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| ARBOVIRUS DIFFUSE ENCEPHALITIS |
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| diagnosis: serologic diagnosis using specific ab tests performed on CSF or serum specimens eeg, CT scan, MRI |
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| ARBOVIRUS diffuse encephalitis |
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| Control/prevention: limit vector population avoid exposure no treatment for arbovirus - bening outcome |
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| FOCAL ENCEPHALITIS |
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| poliovirus rabies virus HSV |
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| POLIOVIRUS FOCAL ENCEPHALITIS |
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| acute systemic disease that results in viral destruction of motor neurons in spinal cord resulting in flaccid, ascending asymmetrical paralysis |
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| POLIO VIRUS FOCAL ENCEPH |
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| picornavirus +ssRNA acid stable 3 serotypes that dont cross |
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| POLIO VIRUS |
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| infection acquired by fecal oral route from infected person |
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| POLIO VIRUS |
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| virus replicates in small intestine; source of agent is shedding in feces viremia may occur; rarely, virus crosses bbb or travels neural routes along PNS via retrograde axoplasmic flow like polio and rabies) to the CNS virus infecs neurons esp anterior horn cells of spinal cord -- lYTIC VIRUS; destroys neurons |
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| POLIO VIRUS |
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| clinical manifestations ASYMPtomatic infection rarely, a flaccid ascending asymmetrical paralysis post polio syndrome - survivors of paralytic polio now have recurrent muslce weakness |
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| POLIO VIRUS |
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| diagnosis differential diagnosis acute flaccid paralysis ECHO, coxsackie and enterovirus 68-71 arbovirus tick paralysis guillian barre botulism dumb rabies myathenia gravis intoxication due ot poisons |
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| polio virus |
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| vaccine prophylaxis for polio prevents any cases of vaccine associated paralytic polio |
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| rabies virus FOCAL ENCEPHALITIS |
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| neurotrophic virus -ssRNA single serotype |
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| RABIES |
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| zoonosis incidence of rabies in humans is refleciton of both distribution of disease in animals, degree of human contact wiht animals, and extent of vaccination of animals rabies is zoonosis; transmissoin of rabies to humans by: animal bites, scratches, inhalation of aerosols all mammals are susceptible; domestic animals or wild animals rabies is epidemic, and worldwide control of human rabies primarily contingent on control of dog and cat rabies most common rabid dogs in us vaccination eliminates dog and cat bats are most common source of rabies today |
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| RABIES VIRUS |
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| pathogenesis: virus injected through epidermis at bite site; initially replicates in adjacent striated skeletal muscle when virus titer is high enough enters PNS, sequestered from immune system; travels slow up to CNS nerves virus predominates in grey matter but localizes in limbic region (focal sympotms) and infects neurons in almost all brain areas then travels back down autonomic nerves to salivary glands, bite site, others when it enters sensory terminals and nm junctions, pt will eventually die because virus is sequestered from rabies specific ab post exposure prophylaxis is imp! can prevent person from developing rabies |
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| RABIES VIRUS |
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| acute, fulminant fatal, focal encephalitis inc period 2-16 weeks prodome is flu like illness 2-4 days highly variable presentation: neurological phase / excitation/furious form: most common; aggressive sexual behavior; foaming at mouth; coma, death paralytic dumb rabies: less common; same as viral encephalitis; paralysis stating at extremities; hypoventialtion; resp paralysis; hypotension; coma death |
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| RABIES VIRUS |
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| lab diagnosis: provide health officials wiht animal demonstration of intracytoplasmic viral inclusion via fluorescent antibody testin (negri bodies) isolation of virus via mouse inoculaiton PCR; rabies ab in blood and CSF differential: non polio enterivrus; arbovirus, HSV1 |
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| RABIES VIRUS |
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| pre exposure management and prophylaxis: prevention is key; there is vaccination for vets, spelunkers, lab workers, animal handlers primes immune sys for response ; reduces number of doses of rabies vaccine for postexposure treatment |
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| RABIES VIRUS |
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| post exposure management: decision to do prophylaxis: know animals in which rabies is endemic (reservoir) and geographic distribution of rabies infection in each animal is imperative when considering initiation of prophylaxis in case of human exposure immediate and thorough cleansing of wound with soap and water vacccine and antirabies serum MUST DO BOHT HRIG; give with vaccine but diff site; half in gluteal half in wound site HDVC human diploid cell strain rabies vaccine; all are killed vaccines; NEVER ADMINISTER IN GLUTEAL - neuropathy; lower ab titers |
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| HERPES SIMPLEX VIRUS 1 AND 2 FOCAL ENCEPHALITIS |
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| ds DNA causes latent infections lytic virus |
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| HERPES SIMPLES VIRUS 1 AND 2 FOCAL ENCEPHALITIS |
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| transmission: direct contact with saliva, vaginal secretions, semen causes 20% of all cases of viral encephalitis in US and most common cause of non epidemic, sporadic, usually focal encephalitis (versus arbovirus diffifuse epidemic enceph) peak incidence in: neonates where infection occurs during natural birth with infected mother young adults and elderly via reactivation of latent infection in an adult primary genital herpes can result in bening, aseptic meningitis where there is urinary retentino, paresthesias, weakness of lower extremities |
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| HERPES SIMPLEX VIRUS 1 AND 2 focal enceph |
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| spread to CNS by hematogenous dissemination or neural routes of PNS via retrograde axoplasmic flow as per polio and rabies virus in adult, herpes in brain is usually focal encp with distinctive features because of location - usually one lobe; mostly cerebral cortex, localized lesions - inflammation, focal hemorrhage, necrosis with temporal lobe involvement, clinical manifestations occur which reflect areas of brain affected - memory defect, psychosis, slurred speech, personality changes fatality rate is high survivors have disability relapse is common |
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| HERPES SIMPLEX 1 ADN 2 |
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| in neonates: 3 possible presentations - HSV2 or 1, starts 9-14 d after birht: localized herpes disseminated disease CNS diagnosis in adult, primary genital herpes are benign, aspetic meningitis |
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| HERPES SIMPLEX 1 AND 2 |
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| diagnosis: lab tests - EEG, CT scan PCR of sedimented CSF differential diagnosis: any viral or bacerial agent capable of causing enceph, brain absceess, tumor, intracerebral hemorrhae, temporal lobe, epilepsy |
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| HERPES SIMPLEX1 AND 2 |
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| treatment: antiviral agents, nucleoside analogs- prodrugs NOT A CURE -inhibits HSV polymerase, acts as chain terminator acyclovir has selective toxicity vidarabine/adenosine arabinoside AraA, idoxuridine, trifluridine, famciclovir, valacyclovir cNS or disseminated disease in neonates: high dose acyclovir MUST Initiate treatment immediately after obtaining sample; if test results are negative, stop treatment. only treatment can decrease both fatality rate and neurological sequelae for management of pregnant mother with genital herpes, ACO recommendations for prophylaxis and C section - treat with suppressive therapy; acyclovir; use c section bc can pass on in utero |
