HERPES SIMPLEX VIRUS

DESCRIPTION 2 SEROTYPES 2 TYPES OF INFECTION Epidemiology:

1) PRIMARY INFECTION - risk of transmission from pregnant women to
 HSV 1 – mouth and skin above - mostly subclinical fetus/newborn
the waist - otherwise,local superficial lesions w/ serious systemic  44% after primary infection
 HSV 2 – genital organs reaction w/o lesions in NB & severely malnourished
 3% after recurrence
- circulating antibodies and CMI response in non-fatal cases
2) RECURRENT INFECTION
- neonatal disease more commonly acquired from
- reactivation of latent infection in an immune host w/ maternal GUT during parturition
circulating antibodies - HSV2 account >/ 75% neonatal infections
- follows non-specific stimuli: cold, uv light, menstruation, - majority of women w/ HSV infection are asymptomatic
fever, emotional stress - genital lesions present at parturition <10%
- asymptomatic or localized lesions w/o systemic reactions of cases
DISTINCT TIMES CONGENITAL INFECTION PERINATAL INFECTION POSTNATAL INFECTION
- very rare; 1 in 250,000 live births - acquired from primary or recurrent HSV infected - acquired from close contact after birth
OF ACQUISITION - due to transplacental maternal viremia or as ascending cervicovaginal secretions - majority asymptomatic
infection after rupture of membranes - occurs~ 1/2,000 births - usually SEM, may progress to encephalitis or disseminate
- presents either as:
 disseminated disease
 encephalitis
 skin,eye,mouth lesions
CLINICAL Classic TRIAD at birth: A. DISSEMINATED PRIMARY HERPETIC GINGIVOSTOMATITIS
 skin vesicles or scar • ONSET :4-11 days of life * most common primary infection in childhood
MANIFESTATIONS - Enanthem
 Chorioretinitis/keratoconjunctivitis, • irritability,respiratory distress,jaundice,shock
: painful vesicles on lips, gums, buccal mucosa, anterior tongue, &
 hydranencephaly or microcephaly seizures, DI
hard palate
*Poor neurodevelopmental outcome • skin lesions-80% : vesicles rapidly become shallow tan-yellow ulcers w/
• meningoencephalitis-60-75% erythematous halo
• sepsis-like picture : gingivitis
• mortality:70=90 HERPES LABIALIS
B. ENCEPHALITIS - most common form of reactivation
- ONSET: 16-17 days of life GENITAL HERPES
- Fever,irritability,lethargy,focal/generalized - most common form in adolescent/adults
- primary or recurrent
seizures,poor feeding
: frequently subclinical but virus shed may infect sex partner or
- Suspect in any neonate w/ aseptic meningitis or focal infant during delivery
signs EYE INFECTION
- Isolated(30%), w/ skin lesions(60%),disseminated - primary or recurrent
- Mortality:15-50%, neurodevelopmental sequelae - superficial conjunctivitis/chorioretinitis
common : little discharge, tender preauricular lymphadenopathy, dendritic
C. SKIN, EYE, &/OR MOUTH (SEM) 40% keratitis is unique to HSV eye infection
- ONSET:10-11 days of life HERPETIC WHITLOW
- single/multiple vesicles on distal fingers
- discrete clusters of vesicles on skin/scalp
HERPETIC GLADIATORUM
- SEM alone ,part of encephalitis(30%) or disseminated - Herpetic infections of superficial abrasions in wrestlers, medical
disease personnel

VIRO1 Mary08AM
 - cutaneous recurrences during 1st yr of life MENINGOENCEPHALITIS
- mortality: rare - Predilection for frontal/ parietal lobes
- may progress to - unusual cause of aseptic meningitis
- most common cause of fatal focal encephalitis 75%
encephalitis,pneumonitis,dissemination
- acute onset of fever, HA, malaise, irritability & nonspecific
- suspect in neonate w/ rash,conjunctivitis,oral lesions, symptoms X 1-7 days w/ progression to s/sx of CNS involvement
unexplained stridor. (memory loss, personality changes, dysphasia, sz, focal signs) in 3-
Greatest opportunity for intervention 7 days
- acute, Fulminant course leading to coma & death if untreated
- EEG shows Paroxysmal lateral epileptiform discharges (PLED)
w/c are suggestive of HSE
- MRI: hypersensitivy on temporal areas
*most common cause of recurrent aseptic meningitis
(MOLLARET MENINGITIS)
ERYTHEMA MULTIFORME
- HSV implicated as the most common etiology of EM
- classic lesion
: TARGET or BULL’S EYE- LESION
(erythematous outer border, inner pale ring & dusky purple
center)
IMMUNOCOMPROMISED PATIENT
- severe local lesions/ disseminated
- most common : local or chronic oral or genital mucocutaneous
disease
- less common: mucositis, esophagitis, proctitis, pneumonitis
DIAGNOSIS Based on any 2 of the following: CSF PCR for HSV DNA:
1)compatible clinical picture - diagnostic method of choice for HSV encephalitis
2)isolation of the virus :vesicles,urine,stool,blood, csf,swabs - sensitivity:75% neonatal CNS infection;95% beyond
3)development of specific antibodies
4)demonstration of characteristic cells, histologic changes, viral antigens Meningoencephalitis
or HSV DNA in scrapings, CSF or biopsy EEG shows Paroxysmal lateral epileptiform discharges (PLED) w/c are suggestive of HSE
MRI: hypersensitivy on temporal areas
TREATMENT Acyclovir PREVENTION
Drug of choice • Stat CS delivery for a woman with ruptured membranes and active genital lesions at
- Dose:15-20 mg/k/dose q 8 hrs x14-21days, IV term
: for all infants w/ neonatal infection irrespective of presentation, herpes • For exposed asymptomatic infants who were born vaginally to mothers with active
0
encephalitis genital lesions (1 , recurrent or unknown status)
- Topical treatment for oral/genital herpes o Obtain cultures: eyes,mouth,urine,stool
: decrease viral shedding but not symptoms;not recommended o Empiric acyclovir therapy after cultures are done or
- Topical trifluorothymidine, vidarabine, idoxuridine for keratitis • Acyclovir therapy after culture is POSITIVE
- Gingivostomatitis:15m/k/dose 5x/day, w/in 72 hrs onset x 7 day • Since infection rate for infants whose mothers have active recurrent genital herpes
- Genital infection: infection is <5%, most experts do not recommend empiric treatment. Family
1st episode: 40-80 mkdy q6-8 x 5-10 days education about s/sx
recurrence >/=12y : 1000-1200mg/day q8 x3-5 days

VIRO2 Mary08AM
 CYTOMEGALOVIRUS
DESCRIPTION SOURCE MODE OF TRANSMISSION PREDISPOSING FACTORS
saliva • Vertical - Immunocompromised patients
breastmilk - In utero: transplacental passage - seronegative premature infants
cervical and vaginal secretions - At birth: passage through infected maternal genital - seronegative recipients of organs
urine tract
semen - Postnatal: ingestion of CMV-positive breastmilk INCUBATION PERIOD
blood • Horizontal - 3-12 weeks after blood transfusion
INCIDENCE - salivary contamination - 1-4 mos after tissue transplantation
• worldwide distribution - contact with infected urine - unknown for horizontal transmission
• congenital infection: 0.2 – 2.4% of live births - sexual contact
• perinatal infection: 10-60% by 6 months old - blood transfusion
• after 1st year of life: 50-80% infection rate - organ transplantation

CLINICAL CONGENITAL PERINATAL INFECTION INFECTION IN OLDER CHILDREN INFECTION IN IMMUNOCOMPROMISED

MANIFESTATIONS * most common
1. Asymptomatic infection
- 90% of cases
- 5 to 10% develop sensorineural
hearing loss later
2. Cytomegalic inclusion disease
- 10% of cases
- IUGR, jaundice, purpura,
hepatosplenomegaly, microcephaly,
intracerebral ,calcifications
&/or chorioretinitis
- majority are asymptomatic ADOLESCENT & ADULTS PATIENT
1. Mononucleosis- like syndrome: - increased risk of disease whether
- PRETERM INFANTS possible sequelae fatigue, malaise, myalgia, headache, primary or recurrent
: at greater risk of CMV illness & fever, hepatosplenomegaly, increased - especially among transplant recipients
liver enzymes and atypical lymphocytes; & AIDS patients
- in infants & young children milder 1. pneumonitis
: Pneumonitis, hepatomegaly, 2. Persistent fever 2. hepatitis
hepatitis,& petechial rashes 3. Hepatitis 3. chorioretinitis
: no risk of hearing loss, chorioretinitis & 4. Morbilliform rash 4. GIT disease
microcephaly 5. Combination of above conditions 5. fever with leucopenia

DIAGNOSIS ACTIVE CMV INFECTION SHELL VIRAL ASSAY OR EAD CONGENITAL INFECTION
1. Viral isolation- urine, leukocytes, tissues - Adaptation of tissue culture 1. Positive viral culture or EAD – usually urine
2. Rapid detection of CMV antigens - low speed centrifugation enhancement, monoclonal : w/n 3 weeks of birth
3. Detection of CMV antibodies antibody culture
IgG- primary or recurrent - inoculated culture cells in small vials are stained w/ 2. Strongly positive IgM anti-CMV antibody
IgM-acute phase of symptomatic/ fluorescein- conjugated monoclonal antibody to CMV
asymptomatic patient, rare in recurrent antigen
4. Examination of urine for intranuclear inclusions (+) fluorescence 18-72 hours
5. Detection of pp 65 antigen in WBC of - Reliable w/ urine & BAL
immunocompromised hosts - Maximum sensitivity & specificity as ADJUNCT, not in
place of standard culture

VIRO3 Mary08AM
TREATMENT GANCYCLOVIR
- combined with IVIG or CMV
IVIG for life-threatening
infections in the
immunocompromised
- not routine in congenital
infections; insufficient efficacy
data,with adverse side effect
-Randomized phase III study for
syptomatic congenital infection:
- 12 mg/k/dy x 6 wk;
- prevents hearing deterioration
-improves/maintains normal
hearing at 6 mos old, prevent
hearing deterioration at >/1 yr
old
A/E
: Neutropenia, gonadal toxicity,
carcinogenicity
Indications
: chorioretinitis, severe
pneumonitis, severe/ persistent
thrombocypenia, severe sepsis
 against natural infection
VIRO4 Mary08AM
VALGANCYCLOVIR
: phase I/II study on oral safety &
effective dose
Alternative drugs:
 Foscarnet
 Cidofovir
 Fomivirsen
PREVENTION
• Blood product, human milk,
& transplant donor selection
• Passive immunoprophylaxis
: the use of IVIG/CMV IVIG for
prophylaxis in solid organ/BM
transplant recipients reduces risk
of symptomatic disease not
prevent infection
• Prophylaxis and early
preemptive therapy with
antiviral agents
• Active immunization
• Adult study: Towne strain
vaccine doesn’t protect
• Behavioral strategies to
prevent primary CMV
infection
PROGNOSIS CARE OF EXPOSED PERSONS
• 90% with congenital - hand hygiene, especially after
infection demonstrate CNS & changing diapers
hearing defects in later years - pregnant personnel must be
• 30% - death rate of educated about the risk of
symptomatic congenital acquisition & practice standard
cytomegalovirus infection precautions
• infants with subclinical
infection
: 5-10% - sensorineural hearing
loss
: 3-5% - chorioretinitis
• less frequent
: developmental abnormalities
: microcephaly
: neurologic defects
• immunocompromised
patient w/ severe
pneumonitis may have high
fatality rate
 EPSTEIN BARR VIRUS
DESCRIPTION Causes 80 to 95% of mononucleosis syndrome • Incidence: predominantly in children and young adults
• Period of communicability:
Epidemiology: : Indeterminate
Source: Man – sole source : may be months after infection
• INCUBATION PERIOD: 30 to 50 days
Mode of transmission: • Majority of primary infections in infants and young children are silent
1. oral- salivary spread : >50% of cases in adolescents & adults present w/ fever, pharyngitis &
2. close intimate contact - kissing generalized lymphadenopathy
3. blood transfusion

CLINICAL INFECTIOUS MONONUCLEOSIS SIGNS & SYMPTOMS OCCASIONAL SIGNS & SYMPTOMS OTHER DISTINCT DSO ASSOC TO EBV
MANIFESTATIONS Prodromal period: 2-5 days malaise, Fever  Erythematous and maculopapular EBV * 1st assoc w/ malignancy
fatigue with or without fever :usually rises to 39◦C rash
Triad: :Adenopathy-90%  : 80% w/ ‘ampicillin rash’ if  Nasopharyngeal carcinoma
 lymphadenopathy : usually in the anterior , posterior treated w/ ampicillin or amoxicillin  Burkitt’s lymphoma
 splenomegaly cervical , & submandibular nodes  Enanthem  Hodgkin dse
 exudative pharyngitis : suggestive if epitrochlear  Edema of eyelids  X-linked lymphoproliferative
 Jaundice syndrome (DUNCAN
Palatal Petechiae  Guillain- Barre syndrome SYNDROME)
Splenomegaly – 50%  Myelitis  others
Hepatomegaly – 10%  Bell’s palsy
 Acute cerebellar ataxia
DIAGNOSIS CBC Infection VCA IgG VCA IgM EA (D) EBNA
: 90% W/ LEUCOCYTOSIS (10000-20000 cells/mm3)
: 2/3 are lymphocytes No previous infection - - - -
: 20-40% atypical lymphocytes (antigenetically stimulated mature
lymphocytes)
Acute infection + + +/- -
Serologic Tests
Heterophil Antibody Test (Monospot Test) Recent infection + +/- +/- +/-
: IgM antibodies detected by Paul Bunnel Davidson Test in sheep cell
agglutination Past infection + - +/- +
Specific EBV Antibodies
: IgM and IgG anti-VCA (Viral Capsid Antigen)
: IgG to EA (Early Antigen)
: Anti EBNA ( Ebstein Barr Nuclear Antigen) *most valuable & specific for
acute infection

VIRO5 Mary08AM
TREATMENT 1. Bed Rest
2. No contact sports or activities that can cause rupture of spleen until it is not palpable
3. Steroids (1 mk/day; max 20 mg/day) X 7days
: rarely needed
: considered in the following conditions
1) Marked tonsillar inflammation w/ impending airway obstruction
2) Massive Splenomegaly
3) Hemolytic anemia
4) Hemophagocytic syndrome
COMPLICATIONS HEMATOLOGIC CNS OTHER COMPLICATIONS
1. Splenic rupture 1. Aseptic meningitis  Pneumonia
2. Thrombocytopenia, ITP 2. Encephalitis  Orchitis
3. Agranulocytosis 3. Myelitis  Myocarditis
4. Hemolytic anemia 4. Optic neuritis
5. Hemophagocytic syndrome 5. Cranial nerve palsies
6. Transverse myelitis
7. Guillain- Barre syndrome

ENTEROVIRUSES (NONPOLIOVIRUS) INFECTION

Group A & B Coxsackiviruses, Echoviruses, & Numbered Enteroviruses
DESCRIPTION  Epidemiology
o Source: feces and oropharyngeal secretions
o Mode of Transmission:
 person to person by fecal- oral route
 possibly oral- oral (respiratory) route
 Incubation period: 3-6 days except for acute hemorrhagic conjunctivitis

CLINICAL ASYMTOMATIC INFECTIONS: large percentage of infection
are asymptomatic
MANIFESTATIONS : majority of those shedding the virus are asymptomatic
SOURCE OF SPREAD
NON-SPECIFIC FEBRILE ILLNESS >90% of cases
: discomfort, rash, sore throat, & respiratory symptoms
abrupt fever (38.5-40C)
: malaise, irritability, lethargy, anorexia, diarrhea, nausea,
vomiting
: abdominal discomfort, rash (macular, maculopapular,
utricarial, vesicular, petechial eruption)
MYOCARDITIS & PERICARDITIS NEONATAL INFECTIONS
: account for 25-35% of proven cases - frequently w/ coxsackie B2-B5, echo 6, 11, 19
: usually coxsackie B viruses - transmitted before, during or after delivery or horizontally
- asymptomatic (majority) to benign febrile illness to sever
NEUROLOGIC MANIFESTATIONS multisystem dse
- Viral Meningitis - affects healthy full term
* the most common cause (>90% of proven cases) (+) recent maternal viral illness
- In mump-immunized populations : fever abdominal pain
st
: COXSAKIE b2-5, ECHO 4, 6, 7, 9, 11, 16, 30, ENTERO 70& - severe disease usually w/n 1 2 weeks of life
71tis-like - frequent findings: fever, hypothermia, irritability, lethargy,
- Encephalitis anorexia, rash (maculopapular, occ petechial or
: accounts for 10-20% of proven cases papulovesicular), jaundice, respiratory symptoms, apnea,
- Poliomyelitis-like acute flaccid paralysis (entero 70 & 71, hepatomegaly, abd distention, emesis

VIRO6 Mary08AM
 RESPIRATORYaryngit
: common colds, ps, herpngina, stomatitis, pneumonia,
pleurodynia
GIT
: frequent but not dominant (vomiting, mild diarrhea,
abdominal pain)
SKIN
: Non- specific fbrile illness with rash
: Rubelliform or petechial rash fever usually
: Rash & fever usually at the same time
: may mimic meningococcemia (ECHOVIRUS 9)
coxA7, coxB)
-Chronic meningoencephalitis
: in patients w/ antibody deficiencies
: persistent CSF abnormalities, viral detection by culture or
PCR for years & recurrent encephalitis
: progressive neurologic deterioration
-Myositis & arthritis
:myalgia a common complaint but direct muscle involvement
only occasionally
- minority w/ severe disease
: any combination of sepsis, meningoencephalitis,
myocarditis, hepatitis, coagulopathy & pneumonitis
OCULAR MANIFESTATIONS
- acbute hemorrhagic conjunctivitis
: ENTROVIRUS 70, COXSACKI A24

CLINICAL HERPANGINA PLEURODYNIA OR BORNHOLM’S DISEASE

SYNDROMES - anorexia, dysphagia, salivation, sore throat - Sudden onset of fever & muscular pain (chest or abdomen), spasmodic &
- vesicles & anterior pillars * most common site excruciating severe w/ profuse sweating
- soft palate, uvula, tonsils, pharyngeal wall, posterior buccal surfaces - usually lasts 1-2 days
- Coxsackie A virus - may be biphasic

HAND, FOOT, & MOUTH SYNDROME

- COXSACKIE A16, ENTEROVIRUS 71, COXSACKIE A5, 7, 9, & 10, COXSACKIE B 2 & 5
DIAGNOSIS VIRAL ISOLATION
: stool, throat, CSF, blood, biopsy
: less specific in stool alone since viral shedding x 6-12 weeks in asymptomatic patients

PCR
: for enterovirus RNA in CSF

ANTIBODY TEST
: rise in neutralizing antibodies from an acute & convalescent specimen
TREATMENT - No specific therapy
-IVIg

VIRO7 Mary08AM
 POLIO VIRUS INFECTIONS
POLIOMYELITIS
DESCRIPTION EPIDEMIOLOGY SOURCE
WHO Polio Global Eradication Program - Feces & possibly, oropharyngeal secretions of man
- launched in 1988 with the following strategies:
1. Routine immunization MODE OF TRANSMISSION
2. National Immunization Days (NID) - fecal to oral
3. Active Acute Flaccid Paralysis (AFP) Surveillance - possibly oral to oral (respiratory) routes
4. “Mopping Up”: extra immunization rounds when a wild virus is found
PERIOD OF COMMUNICABILITY
Remaining Polio- endemic countries as of 2006: - px are potentially contagious for as long as fecal excretion persists
1. India - OPV recipient
2. Pakistan : virus persists in throat for 1-2 weeks & excreted in feces for several weeks
3. Afghanistan
4. Nigeria INCUBATION
3-6 days- abortive poliomyelitis
7-21 days- paralysis in paralytic poliomyelitis
CLINICAL INAPPARENT ILLNESS BULBAR POLIOMYELITIS CIRCULATING VACCINE DERIVED POLIOVIRUS (CVDPV)
: 90-95% : May occur w/o apparent spinal cord involvement - dependent of sabin virus
MANIFESTATIONS : a continuum - accumulation of small spot mutations over a period of > 6 months
ABORTIVE POLIOMYELITIS - dominance of dysfunction of cranial nerves & medullary resulting in virologically different strain
: 5% of cases center (paralysis of extraocular, facial, masticatory - recovers properties of wild virus like neurovirulence, recombination &
: Influenza-like syndrome muscles, nasal twang, inability to swallow, ineffective transmissibility
(fever, malaise, anorexia, headache, sorethroat, cough, nasal regurgitation, deviation of palate, - occurs only where there is no wild virus
abdominal/ muscular pain) involvement of vital centers, paralysis of vocal cords - with accumulation of susceptible
- Epidemiology
NONPARALYTIC POLIOMYELITIS POLIOENCEPHALITIS : in 2001
: 1% : rare : type 1 circulating vaccine-derived poliovirus (cVDPV) was isolated from
: more intense HA, NV, soreness, & stiffness of posterior : sz, coma, spastic paralysis 3 children in 3 places
muscles of neck, trunk, limbs, fleeting paralysis of  Cagayan De Oro
bladder, constipation POST-POLIO SYNDROME  Cavite
: PE- nuchal- spinal signs, abnormal superficial & deep : occurs 30-40 years as muscle pain  Laguna
reflexes : Exacerbation of weakness or new weakness or paralysis
PARALYTIC POLIOMYELITIS among 30-40% of persons who survived paralytic polio in Features Virus in VAPP VDPV
: 0.1% of cases childhood
SPINAL PARALYTIC POLIOMYELITIS Structure Identical to sabin >3% different from
: severe muscle pain  sensory & motor phenomena VACCINE-ASSOCIATED PARALYTIC POLIOMYELITIS vaccine virus sabin vaccine virus
(paresthesia, hyperesthesis, fasciculations, spasms) - VAPP (mutant)
: asymmetric flaccid paralysis or paresis usually of one - a paralytic dse in OPV recipient/ close contact Virus circulation in a None Circulates or is
leg followed by one arm - incidence: 1 case in > 3 million doses distributed community transmissible
: absent deep tendon reflexes, intact sensation Occurrence Wherever OPV is Occurs only where
used there is no wild
virus and there is an
accumulation of
susceptibles

VIRO8 Mary08AM
DIAGNOSIS CLINICAL
LABORATORY
1. Viral isolation from 2 stool specimens taken 24-48 hours apart w/n 14 days of onset of paralysis
2. SEROLOGY: acute & convalescent area
3. With CNS INVOLVEMENT: CSF examination
: pleocytosis w/ early PMN predominance followed by shift to mononuclears
: protein= normal or slightly elevated
: normal glucose
4. DNA sequence analysis- distinguish wild virus from vaccine virus

TREATMENT No specific treatment, symptomatic & supportive

CONTROL MEASURES
- OPV : vaccine of choice for global eradication in areas w/ VDPV, developing countries where inadequate sanitation necessitates optimal mucosal barrier
- IPV : areas not at risk to wild type, immunodeficient patients
COMPLICATION GIT: gastric dilation, hemorrhage, melena, paralytic ileus
Hypertension, OCC pulmonary edema
Skeletal decalcification 2: to immobilization leading to hypercalcemia, hypercalciuria, nephrocalcinosis

INFLUENZA PARAINFLUENZA VIRUSES

DESCRIPTION Types A,B & C members of paramyxoviridae family
Epidemic disease: Type A and B -types 1-4
Influenza A subclassified by 2 surface antigens:
Hemagglutinin (HA) & Neuraminidase (NA) ;
examples: H1N1, H1N2, & H3N2
-Antigenic drift: minor variations in influenza B or A; seasonal epidemics
-Antigenic shift: major variations in HA or NA; only w/ influenza A; pandemics

CLINICAL predominantly respiratory as URI, croup, bronchiolitis or pneumonia account for 50% of hospitalizations for croup, 15% of
MANIFESTATIONS -abrupt onset of coryza,conjunctivitis.pharyngitis, dry cough bronchiolitis and pneumonia
-commonly associated w/ high fever(2-4 days), myalgia, malaise & headache - respiratory tract infection
-close contacts often have similar illness -not associated with fever; systemic complaints rare
-indistinguishable from RSV, parainfluenza viruses & adenovirus
DIAGNOSIS viral culture, immunofluorescent, or rapid diagnostic tests diagnosis is based only clinical and epidemiologic criteria
for antigens, direct fluorescent antibody(DFA) and indirect immunofluorescent antibody(IFA) staining
for xray
Influenza A and B antigens in NP specimens -”Steeple sign” or progressive narrowing of the subglottic
region
: characteristic of parainfluenza virus

VIRO9 Mary08AM
TREATMENT DRUG VIRUS ADM TX IND PX AE
AMANTIDINE A ORAL >1YO > 1YO CNS,
ANXIETY,
GI
RIMANTIDINE A ORAL > 13 YO > 1 YO SAME
ZANAMIVIR A&B INHALANT > 7 YO > 5 YO BRONCHO-
SPASM
OSELTAMIVIR A & B ORAL > 1YO > 1 YO N,V
VACCINE Recommended in
 Children 6 mos- 5 yo
 High risk children: chronic heart/ lung/ metabolic dses, renal
dse&hemoglobinopathies
 Children on long term aspirin tx
Children 6mos-8yo: 2 doses, 4 weeks apart then yearly
Preferably given Feb to June
Healthy children>5 yo who want to be protected against influenza can be given the
vaccine
SOUTHERN HEMISPHERE SEASONAL FLU VACCINE 2011
- A/ California/ 72009 (H1N1)- like virus
- A/ Perth/ 16/ 2009 (H3N2)- like virus
- B/ Brisbane/ 60/ 2008-like virus

VIRO10 Mary08AM
 RESPIRATORY SYNCITIAL VIRUS ADENOVIRUS
(RSV)
DESCRIPTION major cause of bronchiolitis and pneumonia in most common manifestation in children & adults
children <1 yr old -not clinicaly distinctive; types 1-6
-the most important respiratory pathogen of early
childhood

- association of RSV bronchiolitis early in life and

reactive airway disease remains poorly understoood;
underlying predisposition to reactive airway disease
rather than a direct consequence of RSV infection
-almost all children infected once by 2 yrs old ;
reinfection common

CLINICAL -initially Primary infections w/ fever & respiratory symptoms Other manifestations:
MANIFESTATIONS :rhinorrhea and pharyngitis complicated by otitis media in > half of patients with Follicular conjunctivitis
: cough ,low grade fever diarrhea. Myocarditis GIT Infections- diarrhea,
wheezing Pharyngitis intussuception
Pneumonia: types 3,7,& 21 cause severe type w/ 10% Hemorrhagic cystitis- sudden onset
-if progressive mortality; residual airway damage: bronchiectasis; bacteriologically sterile hematuria,dysuria,
: cough and wheezing increase bronchiolitis obliterans, rarely pulmonary fibrosis frequency & urgency x 1-2 weeks; types 11 & 21
(+)air hunger Pertussis-like syndrome Reye Syndrome and Reye-like Syndrome
Tachypnea Pharyngoconjunctival fever-type 3; high fever x 4-5 days - also associated w/ influenza & varicella
Retractions  pharyngitis - acute encephalopathy & fatty degeneration of
hyperexpansion of chest  non-purulent conjunctivitis liver
restlessness  preauricular & cervical lymphadenopathies - occurs 4-12 years old
cyanosis  rhinitis - prodromal URI (90%) or chicken pox  apparent
 headache recovery  w/n 5-7 days, protracted vomiting,
 malaise & weakness delirium, combative behavior, stupor, coma,
INFECTIONS ON IMMUNOCOMPROMISED death
- Chronic meningoencephalitis in B cell deficiency (+) slight to moderate hepatomegaly & hepatic
- Prolonged diarrhea in T cell deficiency dysfunction, no jaundice, normal CSF
- generalized loss of mitochondrial fxn
(+) etiologic link b/w bacterial & viral infections

DIAGNOSIS CXR: normal(10%), air-trapping(50%), interstitial Immunohistology in biopsy, viral culture or PCR
pneumonia(50-80%), segmental cosolidation(10-25%)

detection of viral antigen by EIA ,

immunofluorescence,viral isolation

VIRO11 Mary08AM
TREATMENT Ribavirin aerosol treatment not routine Possible role of CIDOFOVIR
: small studies show↑O2 saturation
: consistent ↓ for mechanical ventilation
: ↓ length of PICU stay
: ↓ hospitalization days among recipients

PREVENTION Palivizumab, humanized mouse monoclonal antibody

given IM, reduces risk of RSV hospitalization in high-risk
children (chronic lung disease of prematurity,preterm,
CHD)
: q 30 days starting early november x 5 doses

VIRAL GASTROENTERITIS
ROTA VIRUS ASTRO VIRUS
*single most important cause of severe dehydration diarrhea in early childhood * 2ND most important agent of viral diarrhea in
- incubation period <48 hours (1-7 days) young children
- mild to moderate fever & vomiting followed by watery stools, vomiting & fever stop - milder, less significant dehydration
by D2, diarrhea for 5-7 days
ENTERIC ADENOVIRUS
DIAGNOSIS DIARLEX ROTA-ADENO - longer duration 10-14 days
- stool latex for rotavirus & adenovirus
- when a fecal exctract containing rota virus or adenovirus particles (antigen) is mixed CALICIVIRUSES
w/ the test latex reagent, an antigen-antibody reaction occurs visible agglutination * most common cause of gastroenteritis on older
(red color) of the latex particles children & adults
VACCINE Monovalent human RV: 2-dose series
1st dose: 6-14 wks & 6 days, 4 weeks apart
2nd dose: not later than 24 weeks

Pentavalent human-bovine reaasortant RV

1st dose: 6-14 weeks & 6 days
2nd dose: 4-10 week interval from dose 1
3rd dose: not later than 32 weeks
May be given w/ OPV or 2 weeks apart
W/ a potentially higher risk of intussuception if 1st dose given beyond recommended
age

VIRO12 Mary08AM
 RABIES
DESCRIPTION • Primarily a disease of animals • Transmission: bites of rabid animals or by licking Mode of Transmission
• Dogs account for >90% of reported human cases of the mucosa or open wounds - Infected animal saliva
• 6-10% - cats, cattle, horse, sheep, bats, exotic • Period of communicability:  Vehicle of virus transmission
pets  Dogs & cats- 3-5days before the onset of  Inoculated by a bite or scratch
• Small rodents, birds & reptiles are NOT KNOWN symptoms until the entire course of illness  Contact of infected saliva w/ human mucous
to serve as reservoir of infections  Person to person- NOT DOCUMENTED membranes can also transmit infection
• Incubation period: 1day to 5 years (8 WEEKS – - human- to- human transmissions have occurred after
average) transplantation to infected tissue
- Human rabies cases have also been observed secondary to
aerosol transmission of virus, as has occurred after exposure
in caves containing bats & from laboratory accidents
CLINICAL 4 STAGES 3) Acute neurologic phase-2-7days
1) Incubation period 2 TYPES:
MANIFESTATIONS
• Usually 20-90 days 1. Encephalitic or furious rabies -80%
• >95% will present with s/sx within 6 months • Hyperactive episodes(combative,bizarre behavior,apprehensive)
• Virus remains at the site of the bite • Hydrophobia( agitation,cringing,due to painful contractions of
• The only time when vaccination is effective laryngeal muscles upon drinking)
2) Prodrome • aerophobia
• 2-10 days 2. Paralytic or dumb rabies-20%
• Virus reaches the spinal cord • Paralysis of bitten area à respiratory paralysis
• 1st rabies specific sx-pain or itching or paresthesia at bite site • Often missed;hydrophobia & aerophobia absent
• Rabies suspected if with paralysis or encephalitis
4) Coma - 4-10 days
-complications: myocarditis, diabetes insipidus, SIADH
-outcome: death due to respiratory paralysis
DIAGNOSIS Usually made clinically
Presence of pathognomonic hydrophobie & aerophobia in a patient w/ history of exposure is enough to make a diagnosis

Laboratory Work Up
- RT- PCR of saliva ( & oral swab) for genomic detection
- Corneal imprint for rabies virus direct fluorescent antibody test (FAT)
- CSF examination- for those in whom the diagnosis is questionable
- CSF is examined by RT-PCR , IgG detection by ELISA or mouse inoculation test (MIT)
- Postmortem samples of brain tissue, R-PCR, FAT & MIT, (+) negri bodies
TREATMENT Isolation of Hospitalized Patient
- Standard precautions
- If bitten by rabid patient or the patient’s saliva has contaminated an open wound or mucous membrane  washed the involved area thoroughly & post-exposure
prophylaxis (PEP) should by administered

VIRO13 Mary08AM
PREVENTION Post Exposure Prophylaxis
- Anti-rabies prophylaxis administered after an
exposure ( such as bite, scratch or lick etc) to a
potentially rabid animal/ humans
- Includes local wound care, administration or rabies
vaccine with or without rabies IG (RIG) depending on
the category of exposure
Objectives
To minimize the virus at the site of inoculation
To develop a high titer of neutralizing antibody early
&maintain it for as long as possible
Local Wound Care
- Immediate vigorous washing & flushing w/ soap &
water preferable for 10 minutes
: Apply POVIDONE IODINE or ALCOHOL
: Avoid suturing of wounds since it may inoculate virus
deeper into the wound
- If suturing is unavoidable, it should be delayed for at
least 2 hours after administration of RIG to allow
diffusion of the antibody to occur through the tissues
- Avoid practices that may further exterminate the
wound
Rabies Vaccine
- given at the DELTOID AREA in adults
: ANTEROLATERAL ASPECT OF THE THIGH in infants
: never administered in the gluteal area
- ID injection should produce a 3mm wheal using a 1
ml syringe
Vaccines should be at 2-8 C in a refrigerator & used
w/n 8 hours
RABIES IMMUNOGLOBULIN
- skin test prior to ERIG administration
Infilitration of all category III wounds w/ RIG is
mandatory
A guage 23 or 24 needle, 1 inch length should be used
for infilitration
: multiple needle injections in the should be avoided
- If fingers or toes need to be infilitrated, care not to
impair blood circulation by injection of an excessive
amount leading to cyanosis, swelling & pain
- care needed to avoid RIG from seeping out of the
wound during infiltration
: if such loss occur, the volume should be estimated &
replaced
-RIG should not exceed the computed dose
: if total computed dose of RIG is inadequate to in
infiltrate in all wounds, it may be diluted 2-3 fold using
sterile saline solution
-Observe for at least an hour for allergic reactions
after ERIG administration

CATEGORY RABIES VACCINE RABIES IMMUNOGLOBULIN

CATEGORY I
a) touching/ feeding an animal Not recommended but PEP may be considered Not recommended
b) Licking of intact skin (w/ reliable history & thorough PE)
CATEGORY II
a) Superficial scratch/ abrasion w/o bleeding Recommended Not Recommended
b) superficial scratch/ abrasion that is induced to bleed
c) Nibbling of skin w/ bruising/hemstone
d) licks on broken skin
Category III
a) Transdermal bites or scratches w/ spontaneous bleeding (to Recommended Recommended
include puncture wound, laceration, avulsion)
b) licking of mucous membrane
c) all Category II exposure on head and neck areas
d) Handling of infected carcass or ingested of new infected areas

VIRO14 Mary08AM
 RABIES VACCINE B) Recommendations for antibiotic treatment
SCHEDULE OF ACTIVE IMMUNIZATION DESCRIPTION RECCOMENDED ALTERNATIVES
REGIMEN DOSE NO. OF DOSES ON SPECIFIED DAYS All frankly infected wounds Cloxacillin or Coamoxiclav Clindamycin
PVRV PCECV DAY 0 DAY 3 DAY 7 DAY 14 DAY All category III bites
(VERORUB) (RABIPUR) 28/30* Uninfected category III Amoxicillin
Modified 2 0.1 ml 0.1ml 2 2 2 0 2 wounds that are
site : inflicted by cat
Intradermal : inflicted by other animals
(ID) that are either deep,
Regimen penetrating, multiple or
o.5ml 1.0ml 1 1 1 1 1 extensive or located on the
hand/face/ genital area
* For category II and III
1) complete vaccination regimen until day 28/30 PRE-EXPOSURE PROPHYLAXIS (PrEP)
- Laboratory proven to have rabies OR Rabies vaccination administered before an exposure to potentially rabied animal/ human
- have s/sx of rabies OR BENEFITS
- is killed/ died without laboratory testing OR : the need for RIG is eliminated
2) May omit day 28/30 dose is biting animal : PEP vaccine is reduced from 5 to 2 doses
- is alive & remains healthy after 14 days observation : Protection against rabies is possible if PEP is delayed, especially in areas where access to
- is killed or died within 14 days of observation but was FAT ned and was confirmed without vaccine or RIG is limited
signs and symptoms of rabies : The cost of PEP is reduced
The Anti Rabies Act of 2007
POST-EXPOSURE PROPHYLAXIS : recommends pre-exposure prophylaxis for children aged 5-14 years who live in highly
- It is necessary to give PEP even if the dog vaccinated, because endemic areas
: animal vaccine failure may occur
: Only 20-25% is the current dog vaccination rates, so rabies virus continue to circulate in the RESPONSIBLE PET OWNERSHIP
dog population - Vaccinating pet dogs against rabies at 3 months of age and every year thereafter
: some owners may clain that their dogs are vaccinated - Providing clean, comfortable & proper shelter
- Bites by rodents (rats, mice, guinea pigs, hamsters & rabbits) do require rabies PEP - Providing enough exercise
Exposed persons who present for evaluation & treatment weeks or months after the bite, - Providing enough care and proper nutrition
should be treated as if the exposure occur recently - Keeping then within our own backyard, where they are free from contact with infected dogs
A) Anti-Tetanus Prophylaxis : keeping them on leash when we take them from walks or daily exercise
- bringing the pet for regular health consultation w/ the veterinarian

GUIDELINES FOR SUBSEQUENT EXPOSURE FF PRIMARY IMMUNIZATION

- Any exposure, regardless of the interval b/w re-exposure & last dose of the vaccine should
receive a BOOSTER on D0 and D3
- NO RIG needed
: booster doses will rapidly induce increased antibody production

VIRO15 Mary08AM
 HIV
DESCRIPTION -Broad spectrum of disease MODE OF TRANSMISSION MOTHER TO INFANT TRANSMISSION (VERTICAL)
- Varied clinical sourse - Sexual contact -Primary route of transmission
- AIDS * most severe end of clinical spectrum : Heterosexual contact -Rate: 12-30% in US & Europe
TARGET CELL : Homosexual contact -Time of transmission
: T- helper CD4+ lymphocyte : Bisexual contact • Before delivery
: Monocytes - Blood/ blood product • 30-40%, (+) PCR within 1st week
: Macrophages -Injecting drug use • Intra-partum transmission
: CNS cells w/ CD4+ receptors - Needle prick injury • 60-70%, no detectable virus before 1 week of age
- mother to child • Via breast feeding
- no data available • WHO recommend breastfeeding in developing
countries
• 14% risk of transmission in women with HIV
before pregnancy
• 29% risk in women with HIV postnatally
CLINICAL • Vary widely RESPIRATORY TRACT
MANIFESTATION • PE at birth may be normal • Recurrent otitis media and sinusitis are common
• Initial symptoms may be subtle/ non-specific • LIP – the most common chronic lower respiratory tract abnormality
• Symptoms more common in children than adults : affects 30-40% of HIV infected children; maybe an exaggerated response to
 Recurrent bacterial infections EBV & HIV, non-productive cough, insidious hypoxia, bronchiectasis, pulmonary
 Chronic parotid swelling decompensation, clubbing
 Lymphoproliferative interstitial pneumonitis
 Early onset of progressive neurologic disorder CARDIOVASCULAR SYSTEM
• Rhythm disturbances; dilated cardiomyopathy & LVH
INFECTIONS
• 20% of AIDS-defining illnesses recurrent bacterial infections caused by GI
encapsulated organisms(pneumococcus, salmonella) • Oral candidiasis, gingivitis, parotitis
• Most common serious infections: bacteremia, sepsis, pneumonia • Most common symptoms: chronic or recurrent diarrhea with malabsorption,
• Opportunistic infections with severe depression of CD4 count abdominal pain, dysphagia, failure to thrive, chronic hepatitis
• PCP pneumonia: most common opportunistic infection children; peak: 3-6 • Pathogens: salmonella, campylobacter,MAC, giardia, cryptosporidium, CMV,
months;44-47% mortality HSV, rotavirus, candida
• Tuberculosis- higher prevalence of TB & HIV co-infection in developing countries
• Oral candidiasis-most common fungal infection in HIV infected patients Renal
• Viral infections with Herpes viruses pose a significant problem • uncommon
• Skin
CNS • Severe & unresponsive seborrheic dermatitis or eczema
occurs in 50-90 % of perinatally infected children in developing countries as
progressive encephalopathy, loss of developmental milestone cognitive deterioration Hematologic
and impaired brain growth. • Anemia, leukopenia, thrombocytopenia
• Malignant diseases infrequent in children
• Common reported neoplasms: NHL, primary CNS lymphoma, leiomyosarcoma

VIRO16 Mary08AM
DIAGNOSIS INITIAL CLUES TO CONSIDER POSSIBILITY OF HIV
1. Having multiple sex partners (MSP)
2. Unprotected sex w/ a person who has MSP
3. Hx of STI
4. Hx of IV drug use
5. Unprotected sex, w/ an HIV infected person
6. (+) clinical conditions suggestive of HIV infection not
explained by other causes
7. Childrean below 13 years born to HIV infected
mothers
STEPS TO HIV TESTING
a. Pre test Counseling
- Important because of the profound psychosocial
iimpact of an HIV (+) antibody test
- assess person’s rick for HIV infection
- provide adequate & correct info about HIV antibody
test & HIV/AIDS
- assess how the person would cope w/ a (+) test
- promote behaviors that will prevent transmission
TREATMENT o Antiretroviral therapy
o Prevention of infection
 Prophylaxis against specific infections
 Vaccination
 IVIg
o Provision of psychosocial support
• Antiretroviral therapy does not eradicate virus nor
cure
• Indicated for HIV-infected children with symptoms
or immunosuppressed regardless of viral load
• Triple drug therapy: 1 protease inhibitor
(Nelfinavir, ritonivir, indinavir) + 2 nucleoside
analogue reverse transcriptase inhibitors
(zidovudine + dideoxynosine or lamivudine)
VIRO17 Mary08AM
B.Request for HIV Ab Test
-informed CONSENT prior to test
-request for HIV Ab testing must be written on the
chart using a code name for the test
-all hospital personnel with whom the patient may
interact for the conduct of HIV testing should act
professionally and responsibly to ensure
CONFIDENTIALITY of the test
C.Post-test Counseling
-provide intitial emotional support in case of a (+) HIV
antibody test
-provide adequate medical info about HIV/AIDS
-identify other medical and social support system
-re-emphasize behaviors that will prevent HIV
transmission to other people
-if (-), explain the meaning of a (-) test and re-
emphasize prevention
Early diagnosis/aggressive treatment of opportunistic
infections
Prophylaxis
• Tuberculosis
:PPD (+) 5 mm induration or exposure to open case
ofTB
• Pneumocystis jiroveci pneumonia
: Trimetoprim sulfa, aerosolized pentamidine, dapsone
: at 4-6wks-1 yo unless hiv excluded
:CD4+T cell count <200 cells or (+) oral thrush or AIDS-
defining conditions
• MAC prophylaxis
: Clarithromycin or azithromycin
: CD4 + T cel l <100 cells or clinical condition(marked
wasting, alopecia, skin dicoloration
DIAGNOSIS OF HIV INFECTION
• Serologic test
o ELISA
o Western blot assay
• Definitive virologic diagnosis
o Viral culture
o HIV DNA PCR
o HIV p24 antigen
CASE DEFINTION FOR HIV INFECTION AGE <18 MOS
 Positive result on 2 separate determination from 1
or more of the ff, HIV virologic test, HIV culture,
HIV PCR, HIV p24 antigen (definite)
 Positive result on only 1 specimen using any HIV
virologic test and no subsequent negative HIV
virologic or negative antibody test (presumptive)
 Any condition that meets criteria for AIDS (clinical)
CASE DEFINITION FOR HIV INFECTION AGE >18 MOS
 HIV antibody positive by repeatedly reactive EIA
and confirmatory test (western blot or IFA)
 Positive result on any HIV virologic test, HIV
culture, HIV PCR, HIV p24 antigen
 Any condition that meets criteria for AIDS
Early diagnosis/aggressive treatment of opportunistic
infections
Prophylaxis
• IVIG
• To prevent serious bacterial infection for HIV
infected children with: at 2 lab documented
serious bacterial infections
• Lab-documented inability to make antigen-specific
antibodies
• Hypogammaglobulinemia
• 400mg/kg every 4 weeks
CATEGORY N: NOT SYMPTOMATIC - cryptococcosis, extrapulmonary
- No signs or symptoms considered to be the result of HIV infection - cryptosporidiosis or isospriasis w/ diarrhea persistening >1 month
- cytomegalovirus disease w/ onset of symptoms after 1 month of age
CATEGORY A: MILDL SYMPTOMATIC - Lymphoma, small, noncleaved cell or immunoblastic or large cell lymphoma of b-cell or
- Children w/ 2 or more of the conditions listed but none f the conditions listed in categories unknown ummunologic type
B and C - mycobacterium tuberculosis, disseminated or extra pulmonary
: Lymphadenopathy (> or = 2 sites, bilateral at 1 site) - Mycobacterium, other species or unidentified species, disseminated
: hepatomegaly - pneumocystis pneumonia
: Splenomegaly - progressive multifocal leukoencephalopathy
: dermatitis - Salmonella (nonthyphoid) septicemia, recurrent
: parotitis - Toxoplasmosis of the brain w/ onset at after 1 month of age
: recurrent or persistent upper respiratory tract infection, sinusitis or otitis media - Wasting syndrome in the absence of a concurrent illness other than HIV infection that could
explain the following findings
CATEGORY B: MODERATELY SYMPTOMATIC : Peristent wt loss >10% of baseline
- Children w/ 2 or more of the conditions listed by none of the conditions listed in categories : Downward crossing of at least 2 of the following percentile lines on the weight for age chart
A and that are attributed to HIV infection in a child 1 year of age or older
th
: Anemia :<5 percentile on weight for height chart on 2 consecutive measurements
: Bacterial meningitis, pneumonia, or sepsis > 30 days apartch
: Candidiasis, oropharyngeal, persisting in children older than 6 mos : plus chronic diarrhea or documented fever
: Cardiomyopathy - Encephalopathy
- CMV, w/ onset before 1 mo of age - HSV infection causing mucocutaneous ulcer that persists for greater than 1 month or
- Diarrhea bronchitis
- hepatitis : pneumonitis or esophagitis for any duration affecting child older than 1 month of age
- HSV stomatitis, recurrent (>2 episodes w/n 1 yr) - Histoplasmosis, disseminated
- HSV bronchitis, pneumonia, esophagitis w/ onset before 1 month of age - Kaposi sarcoma
- Gerpes zoster, at least 2 distinct episode or more than 1 dermatomes -Lymphoma, primary in brain
- Leiyomyosarcoma
- Lymphoid interstitial pneumonia or pulmonary lymphoid hyperplasia complex MONITORING OF PEDIATRIC HIV INFECTION
-nephropathy Cd4+ Cell Count/ C4 + %
-Nocardiosis - Obtained once (+) virologic test for HIV, then every 3 months
- Persistent fever - Declines as HIV infection progresses
-Toxoplasmosis - Lower count associated w/ poorer prognosis
-Varicella, disseminated * CD$+ Cell count: identifies a specific level of immune suppression that changes w/ age
* CD4+%: not affected by age
CATEGORY C: SEVERELY SYMPTOMATIC : a better marker of disease progression
- Serious bacterial infections, multiple or recurrent, of the following types Quantitative RNA Asssay
: septicemia, pneumonia, meningitis, bone or joint infection, or abscess of an internal organ - Indicated viral burden in peripheral blood
or body cavity - Best single prognostic indicator
- candidiasis, esophageal or pulmonary - Higher level (>100,000 copies/m) associated w/ high risk for disease progression
- coccidiodomycosis, disseminated
& mortaliym particularly if also w/ CD4+ lymphocyte of <15%

VIRO18 Mary08AM