Professional Documents
Culture Documents
Viral infections
comprehensive review 2 SEROTYPES
HSV 2 – genital organs
3 Distinct Times of
Epidemiology
Acquisition
• risk of transmission from pregnant women to
fetus/newborn
44% after primary infection Congenital
3% after recurrence
• neonatal disease more commonly acquired from
Perinatal
maternal GUT during parturition Postnatal
• HSV2 account >/ 75% neonatal infections
• majority of women w/ HSV infection are
asymptomatic
• genital lesions present at parturition <10%
of cases
1 | PEDIA-VIRO
CONGENITAL INFECTION PERINATAL INFECTION
• Very rare; 1 in 250,000 live births • acquired from primary or recurrent HSV
infected cervicovaginal secretions
• due to transplacental maternal viremia or as
• 1/2,000 births
ascending infection after rupture of
• presents either as:
membranes – Disseminated disease
• Classis TRIAD at birth: – Encephalitis
skin vesicles or scars – Skin,Eye,Mouth lesions
chorioretinitis/keratocojunctivitis,
hydranencephaly or microcephaly
• Poor neurodevelopmental outcome
2 | PEDIA-VIRO
POSTNATAL INFECTION *Primary Herpetic
Gingivostomatitis Gingivostomatitis
– most common form of primary infection
Herpes labialis(cold sores)
• Enanthem:
– painful vesicles on lips,
– Most common form of reactivation
gums, buccal mucosa,
Genital herpes
anterior tongue and hard palate
– Most common form in adolescent/adults
– Primary or recurrent – vesicles rapidly become
Eye Infection shallow tan‐yellow ulcers
– Primary or recurrent with erythematous halo
– Superficial conjunctivitis/chorioretinitis
Herpetic Whitlow – gingivitis
– Single/multiple vesicles on distal fingers
DIAGNOSIS TREATMENT
Based on any 2 of the following: Acyclovir
1)compatible clinical picture • Drug of choice
• Dose:15‐20 mg/k/dose q 8 hrs x14‐21days,IV
2)Isolation of the virus:vesicles,urine,stool,blood, csf,swabs
for all infants w/ neonatal infection irrespective of
3)Development of specific antibodies presentation, herpes encephalitis
4)Demonstration of characteristic cells, histologic changes, viral • Topical treatment for oral/genital herpes: decrease viral
antigens or HSV DNA in scrapings, CSF or biopsy shedding but not symptoms;not recommended
CSF PCR for HSV DNA: • Topical trifluorothymidine,vidarabine,idoxuridine for
‐ diagnostic method of choice for HSV encephalitis keratitis
‐ sensitivity:75% neonatal CNS infection; 95% beyond neonatal • Gingivostomatitis:15m/k/dose 5x/day, w/in
period 72 hr of onset x 7 days
Serology not useful for rapid dx in neonates • Genital infection:
1st episode: 40‐80 mkdy q6‐8 x 5‐10 days
Positive cultures beyond 48 hrs after birth indicate true infection
recurrence >/=12y : 1000‐1200mg/day q8 x3‐5 days
3 | PEDIA-VIRO
PREVENTION
• Stat CS delivery for a woman with ruptured membranes and
active genital lesions at term
• For exposed asymptomatic infants who were born vaginally
to mothers with active genital lesions (10, recurrent or
unknown status) CYTOMEGALOVIRUS
– Obtain cultures:eyes,mouth,urine,stool
– Empiric acyclovir therapy after cultures are done
– Acyclovir therapy after culture is POSITIVE
• Since infection rate for infants whose mothers have active
recurrent genital herpes infection is <5%, most experts do
not recommend empiric treatment. Family education about
s/sx
Cytomegalovirus Cytomegalovirus
• Source: • Incidence:
saliva • Worldwide distribution
breastmilk • Congenital infection: 0.2 – 2.4% of live births
cervical and vaginal secretions • Perinatal infection: 10‐60% by 6 months old
urine • After 1st year of life: 50‐80% infection rate
semen
blood
Cytomegalovirus Cytomegalovirus
• Mode of Transmission:
Predisposing factors:
Vertical
‐ In utero: transplacental passage
• immunocompromised patients
‐ At birth: passage through infected maternal genital tract • seronegative premature infants
‐ Postnatal: ingestion of CMV‐positive breastmilk • seronegative recipients of organs
Horizontal
‐ salivary contamination
‐ contact with infected urine
‐ sexual contact
‐ blood transfusion
‐ organ transplantation
4 | PEDIA-VIRO
Cytomegalovirus Clinical Manifestations
• Incubation Period: • Congenital
1. Asymptomatic infection
3- 12 weeks after blood transfusion ‐ 90% of cases
1-4 months after tissue transplantation ‐ 5 to 10% develop sensorineural hearing loss later
unknown for horizontal transmission
2. Cytomegalic inclusion disease
‐ 10% of cases
‐ IUGR, jaundice, purpura, hepato‐ splenomegaly,
microcephaly, intracerebral calcifications &/or chorioretinitis
Infection in
Immunocompromised Patient: DIAGNOSIS
‐increased risk of disease whether primary or recurrent • Active CMV infection
1. Viral isolation
1. pneumonitis 2. Rapid detection of CMV antigens
2. hepatitis 3. Detection of CMV antibodies
IgG- primary or recurrent
3. chorioretinitis
IgM-acute phase of symptomatic/
4. GIT disease asymptomatic patient, rare in recurrent
4. Examination of urine for intranuclear inclusions
5. fever with leucopenia 5. Detection of pp 65 antigen in WBC of
immunocompromised hosts
5 | PEDIA-VIRO
DIAGNOSIS Prevention
• Blood product, human milk, & transplant donor selection
• Congenital Infection • Passive immunoprophylaxis
1. Positive viral culture – usually urine; the use of IVIG/CMV IVIG for prophylaxis in solid
organ/BM transplant recipients reduces risk of
within 3 weeks of birth symptomatic disease not prevent infection
2. Strongly positive IgM anti- CMV • Prophylaxis and early preemptive therapy with antiviral
agents
antibody • Active immunization
Adult study:Towne strain vaccine doesn’t protect against
natural infection
• Behavioral strategies to prevent primary CMV infection
Treatment Prognosis
• Ganciclovir • 90% with congenital infection demonstrate CNS
-combined with IVIG or CMV IVIG for life-threatening infections in the
immunocompromised & hearing defects in later years
-not routine in congenital infections; insufficient efficacy data,with adverse 30% - death rate of symptomatic congenital
side effect cytomegalovirus infection
-Randomized phase III study for syptomatic congenital infection:
12 mg/k/dy x 6 wk; • infants with subclinical infection
prevents hearing deterioration, improves/maintains normal
hearing at 6 mos old, prevent hearing deterioration at 5-10% - sensorineural hearing loss
>/1 yr old
3-5% - chorioretinitis
• Alternative drugs: less frequent:developmental abnormalities,
– Foscarnet
– Cidofovir microcephaly,neurologic defects
– Fomivirsen
6 | PEDIA-VIRO
Epstein Barr Virus Clinical Manifestations
• Incidence: predominantly in children and young Infectious Mononucleosis:
adults – Prodromal period: 2‐5
days malaise, fatigue
• Period of communicability:
with or without fever
Indeterminate; may be months after infection
– Triad:
• Incubation Period: 30 to 50 day lymphadenopathy
• Majority of primary infections in infants and splenomegaly
young children are silent exudative pharyngitis
Diagnosis
• Other distinct disorders associated to EBV: Absolute lymphocytosis : total leukocytes > 5,000/mm3
‐ atypical lymphocytes >10% of total leukocytes
– Lymphoproliferative disorders
– Burkitt’s lymphoma Serologic Tests:
– Nasopharyngeal carcinoma 1. Paul‐Bunnel heterophil test and slide agglutination
reaction (Monospot test)
– Undifferentiated B‐cell lymphoma of the CNS ‐ negative in children <4 years old
2. EBV specific serological test
‐ eg. IgM anti‐ VCA (viral capsid antigen)
3. Viral isolation
7 | PEDIA-VIRO
Diagnosis Complications
Infection VCA IgG VCA EA (D) EBNA • Hematologic
IgM
No previous infection 1. Splenic rupture
- - - - 2. Thrombocytopenia, ITP
Acute infection + + +/- - 3. Agranulocytosis
Recent infection + +/- +/- +/-
4. Hemolytic anemia
5. Hemophagocytic syndrome
Past infection + - +/- +
Treatment
Treatment
3. Steroids (1 mkday; max 20 mg/day) x 7 days
1. Bed rest - rarely needed
- considered in the following conditions:
2. No contact sports or activities that can
cause rupture of spleen until it is not
1. marked tonsillar inflammation with
palpable impending airway obstruction
2. Massive splenomegaly
3. Myocarditis
4. Hemolytic anemia
5. Hemophagocytic syndrome
8 | PEDIA-VIRO
Enterovirus (Nonpoliovirus)
Infections
Enteroviruses • Epidemiology
(NonPoliovirus) Infections – Source: feces and oropharyngeal secretions
Group A&B – Mode of Transmission:
Coxsackieviruses,Echovirus person to person by fecal‐ oral route
and Numbered Enteroviruses possibly oral‐ oral (respiratory) route
• Incubation period: 3‐6 days except for acute
hemorrhagic conjunctivitis
9 | PEDIA-VIRO
Hand, Foot and Mouth Syndrome Clinical Syndromes
– Pleurodynia or Bornholm’s Disease
‐ sudden onset of fever and muscular pain
(chest or abdomen), spasmodic and
excruciatingly severe with profuse
sweating
‐ usually lasts 1‐2 days
‐ may be biphasic
Diagnosis Treatment
– Viral isolation: – No specific therapy
stool,throat,csf,blood,biopsy;
less specific in stool alone since viral
– Immune Globulin Intravenous (IgIV)
shedding x6‐ 12 wks in asypmtomatic ‐ may be beneficial for chronic
patients enteroviral meningoencephalitis
– PCR – for enterovirus RNA in CSF
– Rise in neutralizing antibody titer from an
acute and convalescent specimen
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Poliovirus Infections
• Epidemiology
WHO Polio Global Eradication Program
Poliovirus Infections ‐ launched in 1988 with the following
strategies:
(Poliomyelitis) 1. Routine immunization
2. National Immunization Days (NID)
3. Active Acute Flaccid Paralysis (AFP)
Surveillance
4. “Mopping Up”: extra immunization
rounds when a wild virus is found
11 | P E D I A - V I R O
Poliovirus Infections Poliovirus Infections
• Source • Period of Communicability
‐ feces and possibly, oropharyngeal secretions ‐ Patients are potentially contagious for as
of man long as fecal excretion persists
• Mode of Transmission: ‐ OPV recipient: virus persists in throat for 1‐2
‐ fecal to oral weeks and excreted in feces for several weeks
‐ possibly oral to oral (respiratory) routes • Incubation period:
3‐6 days – abortive poliomyelitis
7‐21 days – paralysis in paralytic poliomyelitis
Clinical Forms
Clinical Forms
Inapparent illness – account for 90- 95% of cases
Abortive Cases (4‐8%) Non paralytic or aseptic Paralytic (0.1‐ 2%)
meningitis (1‐5%) Post‐polio syndrome
Non specific febrile Signs & symptoms of Signs & symptoms of
illness minor illness non‐ paralytic illness
• Occurs 30‐40 years later as muscle pain,
Malaise + + & exacerbation of weakness or new weakness
Nausea/ vomiting Nuchal/ spinal skeletal Weakness of >1 muscle
rigidity Or cranial (spinal,
or paralysis among 30‐40% of
Headache
Sorethroat
+ bulbar, bulbospinal or
encephalitic)
• Patients w/ childhood poliomyelitis
Increase/ decrease in
Constipation superficial/ or deep
Diffuse abdominal pain tendon reflexes Flacid paralysis w/o
sensory loss (hallmark)
+
Absent DTRs
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Complications Diagnosis
• GIT: gastric dilatation, hemorrhage, melena, • Clinical
paralytic ileus • Laboratory
1. viral isolation from 2 stool specimen taken 24‐ 48 hours
• Hypertension, occ pulmonary edema apart within 14 days of onset of paralysis
• Skeletal decalcification 2º to immobilization 2. serology: acute & convalescent sera
leading to hypercalcemia, hypercalciuria, 3. with CNS involvement: CSF examination
nephrocalcinosis ‐ pleocytosis with 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: Influenza
• No specific treatment;symptomatic &
supportive ‐Types A,B and C
‐Epidemic disease: Type A and B
‐ Influenza A subclassified by 2 surface antigens:
Control Measures: Hemagglutinin (HA) & Neuraminidase (NA) ;
• OPV:vaccine of choice for global eradication in examples: H1N1, H1N2, & H3N2
areas w/ VDPV,developing countries where ‐Antigenic drift: minor variations in influenza B or A;
inadequate sanitation necessitates optimal seasonal epidemics
mucosal barrier ‐Antigenic shift: major variations in HA or NA; only w/
influenza A; pandemics
• IPV:areas not at risk to wild type,
immunodeficient patients
Influenza Influenza
‐predominantly respiratory Diagnosis:
‐abrupt onset of coryza,conjunctivitis.pharyngitis, dry cough viral culture, immunofluorescent, or rapid diagnostic tests
‐localize as URI, croup, bronchiolitis or pneumonia for antigens, direct fluorescent antibody(DFA) and indirect
‐commonly associated w/ high fever(2‐4 days), myalgia, immunofluorescent antibody(IFA) staining for
malaise & headache Influenza A and B antigens in NP specimens
‐close contacts often have similar illness
‐indistinguishable from RSV, parainfluenza viruses &
adenovirus
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Antiviral Drugs for Influenza * Influenza Vaccine
Admini- Treatment Prophylaxis Prophylaxis
Drug Virus stration Indications Indications Adverse Effects Recommended in:
Central nervous
system, • Children 6mos‐5 yo
Amantadine A Oral =1 y of age =1 y of age anxiety,
gastrointestinal • High‐risk children:chronic heart
Central nervous /lung/metabolic diseases,renal disorders
=13 y of system,
Rimantadine A Oral
age
=1 y of age
anxiety, &hemoglobinopathies
gastrointestinal
Zanamivir
A&B Inhalation =7 y of age =5 y of age Bronchospasm
• Children on long term aspirin tx
Oseltamivir A&B Oral =1 y of age =1 y of age Nausea, vomiting
14 | P E D I A - V I R O
Parainfluenza viruses Respiratory Syncitial Virus
Adenovirus Adenovirus
15 | P E D I A - V I R O
Adenovirus Adenovirus
Other manifestations: Infections in the Immunocompromised:
Follicular conjunctivitis Chronic meningoencephailtis in B‐cell deficiency
Myocarditis Prolonged diarrhea in T‐cell deficiency
GIT Infections‐ diarrhea, intussuception
Hemorrhagic cystitis‐ suden onset bacteriologically
sterile hematuria,dysuria, frequency & urgency x 1‐2 Diagnosis: immunohistology in biopsy ,viral culture
weeks; types 11 & 21 or PCR, serology
Reye Syndrome and Reye‐like Syndrome Treatment: posssible role of Cidofivir
Rotavirus Vaccine
Monovalent human RV: 2‐dose series
1st dose: 6 wks old, 4 weeks apart
2nd dose: not later than 24 weeks
Pentavalent human‐bovine reassortant RV:
THE END
1st dose:6‐12 weeks old, 4‐10 wk intervals
final dose :not later than 32 weeks •
May be given with OPV or 2 weeks apart
With a potentially higher risk of intussuception if 1st
"Lord, thank you for everything, I can’t name them all
dose given beyond recommended age but it all comes from You, everyday I am very grateful
for everything!"
16 | P E D I A - V I R O
RABIES
• Primarily a disease of animals
• Dogs account for >90% of reported human
RABIES & HIV cases
• 6‐10% ‐ cats, cattle, horse, sheep, bats, exotic
pets
• Small rodents, birds & reptiles are NOT
KNOWN to serve as reservoir of infections
Rabies • Variation:
Rabies
– Severity of the bite
• Transmission: bites of rabid animals or by – Site of bite in relation to nerve supply
licking of the mucosa or open wounds – Size of inoculum, protection offered by clothing & other
factors
• Period of communicability:
– Age and immune status of host
– Dogs & cats‐ 3‐5days before the onset of
• Incidence:
symptoms until the entire course of illness
WHO: 11th major killer diseases
– Person to person‐ NOT DOCUMENTED
60,000 deaths worldwide
• Incubation period: 1day to 5 years (8 WEEKS – >30,000 die yearly in Asia
average) about 10M exposed annually
DOH: 2006(219 cases)
2007(281 cases)
Rabies
• Infected patients go through 4 stages
– Incubation period
• Usually 20‐90 days
• >95% will present with s/sx within 6 months
• Virus remains at the site of the bite
• The only time when vaccination is effective
– Prodrome
• 2‐10 days
• Virus reaches the spinal cord
• 1st rabies specific sx‐pain or itching or paresthesia at
bite site
17 | P E D I A - V I R O
Rabies Rabies
Acute neurologic phase‐2‐7days
2 TYPES:
• Diagnosis
1. Encephalitic or furious rabies ‐80% – CBC‐ wbc 20,000‐30,000/mm3 with
– Hyperactive episodes(combative,bizarre behavior,apprehensive) polymorphonucleosis
– Hydrophobia( agitation,cringing,due to painful contractions of
laryngeal muscles upon drinking) – CSF‐ mononuclear cells may increase 100/mm3,
– aerophobia protein is slightly elevated
2. Paralytic or dumb rabies‐20%
– Paralysis of bitten area respiratory paralysis – PREMORTEM DIAGNOSIS
– Often missed;hydrophobia & aerophobia absent • Fluorescent microscopy of skin biopsies from nape
– Rabies suspected if with paralysis or encephalitis
• Isolation of virus
Coma ‐ 4‐10 days • Detection of antibody‐serum & CSF in unvaccinated
‐complications: myocarditis, diabetes insipidus,SIADH persons
‐outcome: death due to respiratory paralysis
• Detection of viral nucleic acid (PCR) in infected tissues
Rabies Rabies
• Diagnosis: • PROGNOSIS: fatal
– POSTMORTEM DIAGNOSIS‐ fluorescent • TREATMENT: intensive symptomatic or
microscopy of brain and salivary glands supportive care
– ANIMAL BRAIN
• ISOLATION: strict throughout the illness;
• Fluorescent antibody stain of brain tissue
caution against contamination of open wound
• Positive for negri bodies
or mucous membrane with patient’s saliva
• Anti‐tetanus prophylaxis should be initiated or boosted as indicated
• Antibiotics for all category III cat bites, category III dog bites that
are on the hand or deep,multiple & extensive
‐amoxycillin as propjylaxis
‐cloxacillin or amoxyclav if infected
• Antibiotics for category I & II only if wound is infected
18 | P E D I A - V I R O
Vaccination Vaccination
CARE OF EXPOSED PERSONS:
• ACTIVE IMMUNIZATION • STANDARD INTRAMUSCULAR SCHEDULE
– Purified vero cell rabies vaccine 0.5ml/vial
– Purified chick embryo cell vaccine 1ml/vial Day of PVRV PDEV/ Site of
• PASSIVE IMMUNIZATION immunization PCECV injection
‐ for all Category III exposures + anti‐rabies vaccine
‐RIG should be inflitrated around and into the wound as
Day 0 0.5ml 1ml One deltoid
anatomicaly feasible even if lesion has begun to heal, the Day 3 0.5ml 1ml One deltoid
rest IM Day 7 0.5ml 1ml One deltoid
‐may be given until 7days after the 1st dose
– Human rabies immune globulin (PREFERRED)
Day 14 0.5ml 1ml One deltoid
20IU/K Day 28 0.5ml 1ml One deltoid
– Hyper immune equine rabies immune globulin(Fab2):
40IU/K IM, needs skin testing
Category I Category I
• Feeding/touching an animal • Wash exposed skin immediately with soap
• Licking of intact skin (with reliable history and and water
thorough physical examination) • No vaccine or RIG needed
• Exposure to patient with S/Sx of rabies by • May opt to give pre‐exposure prophylaxis
sharing of eating or drinking utensils
• Casual contact to patient with signs and
symptoms of rabies
19 | P E D I A - V I R O
Category II Category II
• Nibbling of uncovered skin • Start vaccine immediately
• Complete vaccination regimen until day 28/30 if:
• Minor scratches/abrasions without bleeding*
– Animal is rabid, killed, had died or unavailable for 14‐day
• Licks on broken skin observation or examination
– Animal under observation died within 14 days and was
FAT‐positive or no FAT testing was done or had signs of
rabies
20 | P E D I A - V I R O
Category III Passive Immunization
• Complete vaccination regimen until day 7 if: • to neutralize rapidly the virus locally in the wound
– Animal is alive and remains healthy after 14‐day before it reaches the local nerve endings
observation period
– Animal under observation died within 14 days, • To provide the immediate availability of neutralizing
was FAT‐negative and without any signs of rabies Ab at the site of the exposure before it is
physiologically possible for the patient to begin
• Give anti‐tetanus prophylaxis producing his or her own Ab after vaccination
(usually 7 to 14 days later)
• 3 kinds: HRIG, ERIG, Fab2
OLD: Complete vaccination regimen until day 30
21 | P E D I A - V I R O
Guidelines for subsequent exposure following
primary immunization(PreXP :D0,7,28 0r
PEP:D0,3,7)
HIV
‐no RIG needed
• Broad spectrum of disease
‐any exposure,regardless of severity,after completion of the • Varied clinical course
primary immunization should be given as follows: • AIDS‐most severe end of the clinical spectrum
• Target cells
<1month no booster
1‐6 months 1 booster
– T‐helper CD 4+ lymphocyte
>6mos‐3 yrs 2 boosters on D0 & D3 – Monocytes
> 3 years repeat full course of vaccine without – Macrophages
RIG – CNS cells with CD4 + receptors
• Mother‐to‐Child Transmission(n=46)
‐25 M,21 F
‐1‐11 yo
‐30 asymptomatic
‐16 AIDS cases,7 deaths
‐last MTCT wasin FEB 2008
In 2007, 8 cases reported
4 –Region IV
3 –Region III
1 – Region I
22 | P E D I A - V I R O
Clinical manifestations Infections
• Vary widely 20% of AIDS‐defining illnesses recurrent bacterial infections
caused by encapsulated organisms(pneumococcus, salmonella)
• PE at birth may be normal Most common serious infections: bacteremia, sepsis,
• Initial symptoms may be subtle/ non‐specific pneumonia
Opportunistic infections with severe depression of CD4 count
• Symptoms more common in children than adults PCP pneumonia: most common opportunistic infection
– Recurrent bacterial infections children; peak: 3‐6 months;44‐47% mortality
– Chronic parotid swelling Tuberculosis‐higher prevalence of TB & HIV co‐infection in
– Lymphoproliferative interstitial pneumonitis developing countries
Oral candidiasis‐most common fungal infection in HIV infected
– Early onset of progressive neurologic disorder patients
Viral infections with Herpes viruses pose a significant problem
• GI
• CNS – Oral candidiasis, gingivitis, parotitis
– occurs in 50‐90 % of perinatally infected children in developing – Most common symptoms: chronic or recurrent
countries as progressive encephalopathy, loss of developmental diarrhea with malabsorption, abdominal pain,
milestone cognitive deterioration and impaired brain growth. dysphagia, failure to thrive, chronic hepatitis
• RESPIRATORY TRACT – Pathogens: salmonella, campylobacter,MAC, giardia,
– Recurrent otitis media and sinusitis are common
cryptosporidium, CMV, HSV, rotavirus, candida
– LIP – the most common chronic lower respiratory tract • Renal
abnormality; affects 30‐40% of HIV infected children; maybe an – uncommon
exaggerated response to EBV & HIV, non‐productive cough, • Skin
insidious hypoxia, bronchiectasis, pulmonary decompensation,
clubbing – Severe & unresponsive seborrheic dermatitis or
eczema
• CARDIOVASCULAR SYSTEM
• Hematologic
– Rhythm disturbances; dilated cardiomyopathy & LVH
– Anemia, leukopenia, thrombocytopenia
– Malignant diseases infrequent in children
– Common reported neoplasms: NHL, primary CNS
lymphoma, leiomyosarcoma
• Initial clues to consider possibility of HIV infection: A.Pre‐test Counseling
1. Having multiple sex partners(MSP) ‐important because of the profound psychosocial
2. Unprotected sex w/a person who has MSP impact of an HIV(+) antibody test
3. Hx of STI ‐assess person’s risk for HIV infection
4. Hx of IV drug use ‐provide adequate & correct info about HIV
5. Unprotected sex w/ an HIV infected person antibody test and HIV/AIDS
6. (+) clinical conditions suggestive of HIV infection not ‐assess how the person would cope with a (+) test
explaned by other causes ‐promote behaviors that will prevent transmission
7. Children below 13 years born to HIV infected
mothers
23 | P E D I A - V I R O
Steps to HIV Testing Steps to HIV Testing
B.Request for HIV Ab Test C.Post‐test Counseling
‐provide intitial emotional support in case of a (+)
‐informed CONSENT prior to test HIV antibody test
‐request for HIV Ab testing must be written on the ‐provide adequate medical info about HIV/AIDS
chart using a code name for the test ‐identify other medical and social support system
‐all hospital personnel with whom the patient may ‐re‐emphasize behaviors that will prevent HIV
interact for the conduct of HIV testing should act transmission to other people
professionally and responsibly to ensure ‐if (‐), explain the meaning of a (‐) test and re‐
CONFIDENTIALITY of the test emphasize prevention
24 | P E D I A - V I R O
Clinical Categories for Children with Human
Immunodeficiency Virus (HIV) Infection
CATEGORY N: NOT SYMPTOMATIC
• Children who have no signs or symptoms considered to be the result of
HIV infection or who h we only one of the conditions listed in Category A.
CATEGORY A: MILDLY SYMPTOMATIC
• Children with two or more of the conditions listed bel )W but none of the
conditions listed in Categories B and C.
• Lymphadenopathy (>0.5 cm at more than two sites; bilateral= one site)
• Hepatomegaly
• Splenomegaly
• Dermatitis
• Parotitis
• Recurrent or persistent upper respiratory infections, sinusitis, or otitis
media
• Herpes simplex virus (HSV) stomatitis, recurrent (more than two episodes
• Children who have symptomatic conditions other than those listed for within 1 year)
Category A or C that are attributed to HIV infection. Examples of conditions • HSV bronchitis, pneumonitis, or esophagitis with onset before 1 month of age
in clinical Category B include but are not limited to: • Herpes zoster (shingles) involving at least two distinct episodes or more than
• Anemia (<8 gm/dL), neutropenia (<1000/mm3), or thrombocytopenia one dermatome
(<100,000/mm3) persisting >30 days • Leiomyosarcoma
• Bacterial meningitis, pneumonia, or sepsis (single episode) • Lymphoid interstitial pneumonia (LIP) or pulmonary lymphoid hyperplasia
• Candidiasis, oropharyngeal (thrush), persisting (>2 months) in children >6 complex
months of age • Nephropathy
• Cardiomyopathy • Nocardiosis
• Cytomegalovirus infection, with onset before 1 month of age • Persistent fever (lasting >1 month)
• Diarrhea, recurrent or chronic • Toxoplasmosis, onset before 1 month of age
• Hepatitis • Varicella, disseminated (complicated chickenpox)
25 | P E D I A - V I R O
Management Treatment
Antiretroviral therapy Antiretroviral therapy does not eradicate
– Prevention of infection virus nor cure
• Prophylaxis against specific infections – Indicated for HIV‐infected children with
• Vaccination symptoms or immunosuppressed regardless of
• IVIg viral load
– Provision of psychosocial support – Triple drug therapy: 1 protease inhibitor
(Nelfinavir, ritonivir, indinavir) + 2 nucleoside
analogue reverse transcriptase inhibitors
(zidovudine + dideoxynosine or lamivudine)
• Early diagnosis/aggressive treatment of opportunistic • Early diagnosis/aggressive treatment of opportunistic
infections infections
• Prophylaxis • Prophylaxis
Tuberculosis
PPD (+) 5 mm induration or exposure to open case of – IVIG
TB • To prevent serious bacterial infection for HIV
Pneumocystis jiroveci pneumonia infected children with: at 2 lab documented serious
• Trimetoprim sulfa, aerosolized pentamidine, dapsone bacterial infections
‐at 4‐6wks‐1 yo unless hiv excluded • Lab‐documented inability to make antigen‐specific
‐CD4+T cell count <200 cells or (+) oral thrush or AIDS‐defining antibodies
conditions
MAC prophylaxis • Hypogammaglobulinemia
• Clarithromycin or azithromycin • 400mg/kg every 4 weeks
‐CD4 + T cel l <100 cells or clinical condition(marked wasting, alopecia,
skin dicoloration
26 | P E D I A - V I R O
Zidovudine Regimen for decreasing the Prevention of Mother-to-Child
rate of peri-natal transmission of HIV Transmission of HIV (PMTCT)
Period of time 1)Primary prevention of HIV‐infection among women
Route Dosage
of reproductive age(HIV info and voluntary
During pregnancy, initiate Oral 200 mg tid or counseling and testing(VCT) of ANC
anytime after 14 wk AOG
& throughout pregnancy 300 mg BID 2)Prevention of unintended pregnancies among HIV‐
infected women thru family planning
During labor and delivery IV 2mg 1st hr, 3)Prevention of vertical transmission thru ARV
1mg/k/hr until prophylaxis
delivery
4)Provision of Tx, care and support for HIV‐women and
For newborn, within 6-12 Oral 2mg’k qid, for
hr of birth children
1st 6 wk of life
THE END
•
"Lord, thank you for everything, I can’t name them all
but it all comes from You, everyday I am very grateful
for everything!"
27 | P E D I A - V I R O