SHANZ – MED II 2.

02
COMMON CHILDHOD VIRAL AND PARASITIC INFECTIONS
KEY POINTS IN EXANTHEMATOUS DISEASES: Exposure history, season, age. Previous history, relation of rash to fever, adenopathy, enanthem, aseptic meningitis, rash distribution
VIRAL INFECTIONS
RUBEOLA RUBELLA (german measles) ROSEOLA
Etiology • Measles virus: ssRNA, lipid enveloped, Paramyxoviridae, Morbillivirus • Rubella virus; ssRNA, Togaviridae, Rubivirus • HHV 6
• Airborne droplet transmission via URT (small size virus) • VIA respiratory and transplacental route • Baby measles
• Highly contagious: 90% secondary attack rate • Droplet (within 3 feet) infection • Exanthema subitem
• Young children • Moderately contagious • Common childhood disease
• Viremia: 5-7 days after exposure
Clinical • Incubation: 10-12 days • Incubation: 14 days (12-23 days) • Classic: 9-12 mon with acute
Course • Prodromal: 2-4 days • Prodrome: rare in children, low grade fever in adults high grade fever and febrile
o Cough: dry, hacking, barking (bronchitic: halak) • Pathognomonic: lymphadenopathy seizure
o Coryza: nasal mucous membrane inflammation o Retroauricular, post cervical and post occipital • Fever lyses once rashes
o Conjunctivitis o Evident 24 hr before rash, remain for 1 week appear
o Koplik spots (rash on mucous membranes) • Enanthem: FORSCHEIMER SPOTS: discrete rose spots on soft palate • After 3 days: rapid
• Enanthem: KOPLIK spots (whitish grayish rashes in buccal mucosa) 1- coalesce = red blush extension defervesence + morbilliform
2 days after symptoms • Exanthem: erythematous, maculopapular, discreet, pinpoint rash
• Exanthem: MACULOPAPULAR MORBILIFORM CONFLUENT RASHES o Starts centrally, spreads centrifugally • can be around 6-8 years
o 2-4 days after prodrome, 14 days after exposure o 2nd day: pinpoint on the trunk old with history of previous
o Persists 5-6 days o 3rd day: eruption clears exanthem
o Begins on face and upper neck (back of ear or hairline, downward) o Pruritic rash, esp. in adults • maculopapular confluent
o Fades in order of appearance o 14-17 days after exposure rash from trunk and neck
o Red à brown à desquamations • Communicability: 7 days before to 5-7 days after rash onset spreading to face and
o Hyperpigmentation (brownish à desquamates) • Infants with CRS: shed virus in urine for up to 1 year extremities
• Communicability: 4 days before to 4 days after rash onset
Complications • Bacterial complications is probable if: • 70% Arthralgia/ arthritis: adolescent/adult female
o Rashes 5 days, rashes on soles of feet, high fever • Arthralgia: spontaneous resolution or severe and debilitating
o Pneumonia > otitis media > laryngitis > laryngotracheobronchitis > • Encephalitis 1/6k cases
bacterial pharyngitis • Hemorrhagic manifestation 1/3k
• Potential complications: • Orchitis, neuritis (progressive)
o Diarrhea 8% (most common), otitis media 7% (children), pneumonia • Congenital rubella syndrome classic triad:
6%, encephalitis 0.1%, SSPE 0.01% o Sensorineural hearing loss (most common, 58% patients)
• Persistent diarrhea, deafness, blindness (malnutrition, vit A def) o Ocular abnormalities (cataract, infantile glaucoma, pigmentary
• Pneumonia retinopathy in 43%)
o S.aureus, 60% deaths o CHD (PDA, pulmonary artery stenosis in 50% in infants infected during
o 6-21% of acute LRTI 2 mon AOG)
o Mortality factors: cyanosis, RR > 60/min, very severe pneumonia • Common disabilities
• Most common cause of death: o Intellectual disabilities, liver & spleen damage, LBW, skin rash at birth
• Children: Pneumonia, Adult : acute encephalitis • Less common: glaucoma, brain damage, thyroid problem, lung inflamm
Diagnosis • CLINICAL • Isolation from clinical specimen: nasopharynx, urine
o Typical febrile prodrome: 3 C + Koplik’s • (+) IgM and IgG
o Characteristic rash • Inspect for exanthema, enanthem, lymph node palpation, Sx
o Branny desquamation
• LABORATORY
o Isolation from urine, nasopharynx, blood, throat
o Significant IgG rise in EIA, HemaggInhibition
o IgG: past. Acute = 4x rise, IgM: current/ acute
Prevention • Vaccine: live attenuated virus • Primary aim: prevent congenital rubella in females
o 95% efficacy at 12 months, 98% efficacy at 15 months • MMR VACCINE 2 DOSES
o Lifelong immunity • 1st dose: 12 mon
o 1 single antigen: early 2 dose measles (6 mon, 12 mon: booster) • 2nd dose: 4-6 yo
o MMR/MMRV: 1st dose at 12-15mon, 2nd dose at 4-6 yo • Women childbearing age: within 28 days before conception
o FILIPINO: (interval: 4 weeks) • ADR: fever, lymphadenopathy, arthralgia, arthritis, arthropathy
§ 1st single dose (6-9mo)
§ 2nd dose (MMR 12-15 mo)
§ 3rd dose (MMR 4-6 yo)
• Post-Exposure prophylaxis
o Active: live, attenuated vaccine (within 3 days of exposure)
o Passive: Ig (cannot receive active vaccine, less than 6 mo,
immunocompromised)
§ Child with definite exposure, within 6 days: 0.25 mL/kg for
normal, 0.5mL/kg for immunocompromised
§ Child with contraindication during outbreak: 0.5mL/kg
Treatment • None specific • Supportive treatment
• Supportive for fever and hydration
• Vitamin A: 100,000 IU PO (6 mo- 1yo), 200,000 IU (>1 yo)

CONGENITAL RUBELLA SYNDROME

INFECTION TIME RISK OF CONGENITAL ABNORMALITIES MOST COMMON ABNORMALITIES
< 8 WEEKS 40-60% Multiple congenital defects, spontaneous abortion
9 – 12 WEEKS 30-35% Single defect: CHD, deafness
12 – 16 WEEKS 10% Single defect: deafness

VARICELLA ERYTHEMA INFECTIOSUM MUMPS HAND FOOT MOUTH

Etiology • VZV: dsDNA • Parvovirus B19 • Mumps virus (rubula virus); • Enterovirus:
• CONTAGIOUS: rubella < varicella < measles • Children 4-10 yo ssRNA, paramyxoviridae • coxsackievirus A16 (more
• Direct contact with vesicular skin, infected • Direct contact or respiratory common and benign)
respiratory tract, transplacental droplets • EV-71 more severe
• Replication: nasopharynx, regional • Children <5 yo
LN
• Contagiousness: measles & varicella
> mumps > rubella
• Children age 5-9 yo
Clinical • Mild infection • Incubation: 7 days • Swelling at the back of ear going • Mouth: vesicles on buccal
Course • Generalized vesicular rash + few systemic • Prodrome: influenza like (fever, coryza, downward to mandible mucosa
• Incubation: 14-16 days headache, nausea) • Incubation: 12-25 days • Palms and soles:
• Prodrome: 1-2 days fever malaise (adult only) • Well being: 7 days • Classic: flu like, parotid salivary gl papulovesicular (knees, elbow,
• 1st : EXANTHEM • Rash: after well being swelling, earache or tenderness buttocks)
• Communicability: 1-2 days before rash, 5 days after • Communicability: before illness onset • Parotitis: acute, bilateral/ unilateral • Discrete erythematous based
rash, longer in immunocompromised • Erythema infectiosum rash: tenderness, self limited > 2 days macules (evolves into papules
LESION: • 1st stage: slapped cheek with circumoral • Non specific prodrome: low grade and vesciculate and ulcerate
• Macules à maculopapular à vesicular à crusting à pallor 1-4 days fever, myalgia, headache, anorexia, centrally: ERYTHEMATOUS
scab formation • 2nd stage: maculopapular rash of extremities malaise HALO)
• Hallmark: vesicular lesion (contagious) 200-500 and trunk (central clearing with lacy reticular • Most commonly affected:
lesions in 2-4 crops pattern 1-6 weeks) anterior fauces pillar, soft palate,
 • Intensely pruritic • 3rd stage: rash varies with exposure to heat or uvula, tonsils, posterior
• 1st on the scalp, face, trunk (most concentrated) sunlight, spontaneous resolution, no pharyngeal wall
• Healing: crust permanent sequelae for 1-3 weeks • Difficulty in eating
Complications • Scratching: staph or strep • Fetal hydrops • Aseptic meningitis: 50-60% •
• Pneumonia (viral, bacterial): most common mode • Aplastic anemia • Symptomatic meningitis: <15%
of exit • Chronic anemia • Orchitis in post pubertal males 20-
• CNS • Intra uterine fetal deaths 66%
• Reye syndrome • Oophoritis in post pubertal females
• Congenital varicella syndrome 5%
• Neonatal varicella • Pancreatitis 2-5 %
• Increased risk for complication: >15 yo, <1 yo, • Encephalitis
immunocompromised, newborn of women with rash • Deafness
onset within 5-2 days before/after delivery.
Diagnosis • Isolation • Clinical diagnosis • rRT-PCR •
• Real time PCR or DFA • Culture
• IgG rise in standard assay • serology
Prevention • Post exposure prophylaxis: vaccine • • DOH EPI: MR, MMR •
o Healthy ppl: within 3-5 days of exposure • 1st dose: 12 mon
o Immunocompromised: VZIG within 96hr • 2nd dose: 4-6 yo
o IVIG: 400 mg/kg
o Chemoprophylaxis: Acyclovir 80 mg/kg/day
4x/day for 7 days (active replication is required for
effectivity, don’t give too early)
VACCINATION:
• For children: 12-15mon, 2nd: 4-6 yr
• Monovalent single antigen 2 doses:
o <13 yo = 3 mo interval
o >13 yo = 4 weeks interval
• Quadrivalent + MMRV (< 12 yo)
Treatment • DOC: Acyclovir, for >13 yo • No specific antiviral • None specific • Non specific
• For chronic cutaneous or pulmonary disorder, long • IVIG: chronic infection in immunodeficient • Supportive: anti pyretics, pain • Supportive: control fever and
term salicylate therapy, steroid therapy patients management mouthwashes or spray to
• IV in immunocompromised children and adults with numb mouth pain
viral mediated complications.

INFLUENZA CHIKUNGUNYA
Etiology • SsRNA, Orthomyxoviridae, A subtype: hemagglutinin and neuraminidase • Mosquito borne viral disease: ssRNA, alphavirus, togaviridae
• School age children, highest attack rate during community outbreaks • Primary vectors: aedes aegypti, aedes albopictus
• Pathology: • Primary host @ epidemic period: humans
• Viral shedding in respiratory secretion for 5-10 days • At risk: neonates exposed intrapartum, >65 yo, w/ comorbidities
Clinical • Antigenic drift: minor change, same subtype, point mutation, epidemic, annual • Incubation 3-7 days
Course • Antigenic shift: major change, new subtype, gene exchange, pandemic • Other: headache, myalgia, arthritis, conjunctivitis, N/V, maculopapular rash’
• Incubation: 2 days • Joint: Acute onset of fever and severe polyarthralgia (hands, feet, severe, recurring, morning)
• 50% develop classic symptoms: abrupt onset of fever, headache, myalgia, sore throat, • Pain: remit in saddle back pattern
non productive cough • Migratory polyarthritis with effusion in 70% cases
• Worst: ankles, wrists, small joitns of hands
• COMMON SX: fever, arthralgia, backache, headache
Complications • Secondary bacterial pneumonia: S.aureus •
 Diagnosis • Clinical and epidemiological • Most common: lymphopenia, thrombocytopenia, elevated creatinine, elevated ALT/AST
• Isolation from specimen • Viral culture: 1st 3 days
• IgG rise • RT-PCR: first 8 days
• Serology: IgM, IgG, neutralizing Ab
Prevention • Vaccine: inactivated IV (intramuscular or intradermal) à PH quadrivalent • Mosquito control
• Live attenuated vaccine intranasal (Not in PH)
• Inactivated vaccine: > 6 mon
• Recommended for vaccine: > 50 yo, 6mon-4 year, chronic dse, immunosuppressed,
pregnant women during influenza season, children with long term aspirin therapy,
nursing homes, healthcare personnel, household contacts
Treatment • PCN, Vancomycin • Symptomatic
• DOC: paracetamol
• Physiotherapy, exercise
• Mosquito nets

ETIOLOGY
• Arbovirus, flavivirus
• Mosquito vectors: aedes aegypti (daytime feeder)
o Produce larvae in artificial containers
o <25 m flight range
o 30-50 m dispersay per day
o Infective during lifetime
o Longer survival in humidity
o Average 8-15 days of lifespan
• Newly evolved: dirty water, whole year round
esp.rainy season, night biting 6-8pm and 11pm-1am
• 4 serotypes DEN 1 2 3 4
• Most common in PH: DEN 1 , 2
• Lifetime immunity, short term cross immunity (6 mo)
DENGUE
RISK FACTORS
• Virus strain (genotype): epidemic,
viremia level, infectivity
• Virus serotype: DHF: DEN 2 > DEN 3
> DEN 4 > DEN 1
• Pre existing anti dengue Ab:
maternal Ab, previous infection
• Race: blacks are less susceptible to
shock
• Nutritional status (malnutrition is
protective, suppresses cellular
immune response)
PATHOGENESIS
• Antibody dependent enhancement theory
• DHF Hypothesis:
• First infection:
o Neutralizing Ab and homologous non infectious complexes
o Non neutralizing Ab
• Subsequent infection:
o Heterologous infectious complexes
o Prevents body from creating antibodies against second infection
• Antibody dependent enhancement
o Viral strain complexed with non neutralizing Ab = greater cell proportion of mononuclear lineage
o Heterologous complexes enter more Monocytes, virus replicates
o Secondary infection is more severe and fatal due to non neutralizing Ag-Ab complex
• Infected monoctes release vasoactive mediators à INC vascular permeability à hemorrhagic

CRITERIA FOR DHF DIAGNOSTICS

• Fever or recent acute fever 2-7 days • CBC: WBC, Hct, PLT
• Hemorrhagic manifestation (nosebleed, gumbleed, (+) • Dengue NS1 RDT (day 1-5)
tourniquet, inc. menstrual flow, GI bleeding) • Dengue Ab test (day 6-10)
• Low platelet < 100k • Dengue PCR
• Leaky capillaries: INC Hct >20% from baseline, Hct >40%, drop •
>20% after volume replacement, low albumin, pleural effusion

UNDIFFERENTIATED FEVER
• Most common manifestation
• All age group demonstrate silent
transmission
CLASSIC DENGUE FEVER
• Fever, headache,
muscle/joint pain, N/V, rash,
hemorrhagic manifestation
CLINICAL SYNDROMES
DENGUE HEMORRHAGIC FEVER DENGUE SHOCK SYNDROME
• Skin hemorrhages (+) tourniquet test petechiae, purpura, • 4 criteria for DHF + Circulatory failure:
ecchymoses Rapid & weak pulse, narrow pulse pressure < 20 mmHg or
• Bleeding: gingival, nasal, GIT (hematemesis, melena, hypotension (SBP < 80 in < 5yo, and < 90 in >5 yo)
hematochezia), hematuria Cold, clammy skin, MSA
• Inc. menstrual flow Frank shock: direct evidence of circulatory failure

PHASES
 FEBRILE CRITICAL RECOVERY
• 2-7 days • Patient improve or deteriorate • In the next 48-72 hr
• Mild hemorrhagic manifestation: petechiae, mucosal membrane • Defervescence : 3-7 days of illness • Boy fluids go back to normal
bleeding • When fever abates: critical phase • Improvement of well being
• Monitor warning sign • WBC rise soon after defervescence

PREVENTION MANAGEMENT STEP 1 MANAGEMENT STEP 2 MANAGEMENT STEP 3

• Insect repellents • Overall assessment • Diagnosis, assessment • Disease notification
• Duration of protection • FBC • Determine, check for warning signs, • GROUP A: Send home
• Dengue diagnostic test hydration and hemodynamic status • GROUP B: In hospital management
TREATMENT • Culture isolation/PCR: confirm • GROUP C: Emergency
• Focus ON fluids and paracetamol
• hypoOsm fluids: best!
• NSAIDS will trigger bleeding

ACTION PLAN
GROUP A GROUP B GROUP C
• Can tolerate adequate volumes of oral fluids • Social circumstances • Severe dengue
• Pass urine at least every 6 hr • With warning signs • Require emergency treatment
• No warning signs • Coexisting conditions
• Stable Hct
• Daily monitoring
• Return immediately if shows warning signs
• ORS: reduced osmolarity, (plain water: electrolyte imbalance), no sport drinks NO warning signs + NO shock • Judicious IVF resuscitation
• Paracetamol: < 4 g for adults, don’t give aspirin, ibuprofen/nsaid • IVF: D5LRS, D5NSS • Improve central and peripheral circulation: decreasing
• TSB • Periodic assessment tachycardia, improving BP, pulse volume, warm and pink
• Antibiotics are not necessary YES warning signs + NO shock extremities, CRT < 2 sec
• Aspirin >39C • Baseline HCT • Improve end organ perfusion
• Home care card and avice: bed rest, fluid, fever management • Isotonic crystalloid 5-7 ml/kg/hr in 1-2 hr
• Reduce to 3-5 ml/kg/hr for 2-4 hr
• Reduce to 2-3 ml/kg/hr or less

SOIL TRANSMITTED HELMINTHES
• HOOKWORMS (N.americanus, A.duodenale)
• ASCARIS LUMBRICOIDES (Roundworm)
• TRICHURIS TRICHIURA (WHIPWORM)
PARASITIC INFECTIONS
LIFE CYCLE: CHILDREN
• CHILDREN: Largest reservoir, most affected
o Poor personal hygiene, poor eating habits, frequent outdoor exposure
• SCHOOL CHILDREN: high risk group:
o Intense physical growth, rapid metabolism, increase nutritional needs
NOTES
• Ascariasis: causes intestinal obstruction
• Trichuriasis: causes rectal prolapsed
• Mixed infection: cognitive symptoms (reduced memory and
fluency)
 ASCARIASIS TRICHURIASIS HOOKWORM
Etiology • Eggs in domestic and public sites • • Necator americanus (PH) and Ancylostoma duodenale
• Moist, warm climate, agricultural areas, barefoot
Clinical • Mild: asymptomatic • Asymptomatic mostly • SKIN: erythema, macules, papules (ground itch)
Course • Moderate to heavy: malnutrition, non specific GIT Sx, acute • No pulmonary migration o Cutaneous invasion, subcutaneous larval migration
intestinal obstruction • Nocturnal loose stools • PULMO: verminous pneumonia
• Very heavy: ball of worms • Dysentery if worms are >200 o Larval migration thru lung, bronchi, trachea
• Larval migratory phase: acute transient pneumonitis (Loeffler • Rectal prolapse • GIT: Mid epigastric pain, N/V, diarrhea/constipation, bloody
syndrome) + fever and marked eosinophilia • Failure to thrive, stunted growth dysentery
• Worm migration: peritonitis secondary to intestinal wall • Weight loss, anemia (massive infection) o Adult worms attached to upper intestinal mucosa
perforation, CBD obstruction (biliary colic, cholangitis, • Vague abdominal discomfort • HEMA: weight loss, anemia micro/hypo
pancreatitis) o Loss of nutrients and blood
• Most common : passing out of worm per rectum (spaghetti like)
• Most frequent CC: Vague abdominal pain
Complications • Intestinal obstruction 63%: predominate in young children • PREVENTION:
• Bile duct obstruction 23% • Sanitary disposal of feces, bots, mass chemo in >50%
• Perforation, peritonitis, Volvulus, Hepatic abscess, Appendicitis, incidence, correct anemia
Pancreatitis, Cerebral encephalitis, intussusception
Treatment • ALBENDAZOLE: 400 mg oral OD • ALBENDAZOLE: 400 mg oral OD for 3 days • ALBENDAZOLE: 400 mg oral OD
• MEBENDAZOLE: 100 mg oral BID for 3 days or 500 mg orally OD • MEBENDAZOLE: 100 mg oral BID for 3 days • MEBENDAZOLE: 100 mg oral BID for 3 days or 500mg OD
• Ivermectin 150-200 mcg/kg orally OD (weight at least 15 kg) • Ivermectin 200 mcg/kg orally OD • Pyrantel pamoate: 11 mg/kg (max 1 g), oral OD for 3 days

WHO: DEWORMING FOR PREVENTIVE CHEMOTHERAPY

WHO: CHILDREN
• Single dose ALBENDAZOLE 400 mg or
MEBENDAZOLE 500mg
• Public health intervention for all young children
12-23 mo, preschool 24-59 mo, school age
children
• Baseline prevalence of 20% or higher
• Biannual for area with baseline prevalence >50%
• ½ dose ALBENDAZOLE for children < 24 mo
WHO: NON PREGNANT ADOLESCENT GIRLS & REPRODUCTIVE WOMEN DOH: STH CONTROL
• Annual/ biannual single dose ALBENDAZOLE 400 mg or MEBENDAZOLE 500 mg • Chemotherapy
• Pubhealth intervention for all non pregnant adolescent (10-19), non pregnant women • Water, sanitation, hygiene WASH: cornerstone
reproductive age (15-49) • Promotion of desired behaviors
• Areas with baseline prevalence 20% • Children 1-24mo: ALBENDAZOLE 200mg/Mebendazole
• Reduce worm burden of STH infection 500 mg every 6mo (endemic country)
• Children >24mo: albendazole 400mg every 6mo or
mebendazole 500 mg every 6 mo
• All adolescent females: albendazole 400 mg annually, or
mebendazole 500 mg annually

ENTEROBIASIS FILARIASIS SCHISTOSOMIASIS

Etiology • Eggs • 2nd leading cause of permanent and long term • Snail: oncomelania quadrasi, biommphalaria, bulinus
• Via mouth, respiratory, anus, Familial disability • S.japonicum and s.mansoni: GIT
• Enterobius vermicularis: cannot be controlled by • S.haematobium: Urinary tract (bladder)
proper feces disposal
Clinical • Perianal pruritus (itching, irritation) • Mostly asymptomatic EARLY PHASE/ ACUTE INFECTION
Course • Nocturnal migration • Immunologic response: dying adult worms • Cercariae penetrates skin = RASH (schistosome or swimmer’s itch)
• Heavy: restlessness, sleeplessness, anorexia, weight • Subclinical lymphatic dilatation and dysfunction • Eggs Laid in organs, release antigen = KATAYAMA FEVER (fever,
loss, teeth grinding, nervousness, irritability, • Filarial lymphadenopathy: in children (UTZ of urticaria, malaise, diarrhea)
abdominal pain, vomiting inguinal, crural, axillary LN) LATE PHASE/CHRONIC INFECTION
• Filarial lymphangitis: acute inflammatory response, • Immune mechanism: granulomatous
retrograde progression along lymphatic vessels, • Eggs trapped in host tissue, secrete Ag
systemic Sx: fever, headache • Granulomas: macrophages surrounded by lymphocytes
• Fibroblast cells at site of infection’

Complications • Migrate to female reproductive tract: vaginitis,
endometritis, granuloma in uterus and fallopian
tube
Diagnosis • Perianal swab with cellophane (graham scoth)
tape: morning before defecation and washing
Prevention • Personal hygiene, Short fingernails
• Handwashing, Shower instead of bathtubs
• Sleep alone, Treat entire family
Treatment • Albendazole, mebendazole, pyrantel pamoate
• Major problem: reinfection
• Principle: retreatment after 2 weeks for radical
cure
• Post pubertal males: adult w.bancrofti in intrascrotal
lymphatic vessels (UTZ), funiculitis, epididymitis,
orchitis, tender granulomatous nodule palpable
• Chronic: lymphedema, hydrocele
• Lymphedema (LEGS, arms breasts, genitalia)
• RECURRENT: severe pain, fever, chills, hasten
lymphedema progression to elephantiasis
• CNS complication:
• Microfilariae in blood smear: 10PM-2AM with giemsa
or H&E
• IgG1 and IgG4 (EIA) Antifilarial
• • Don’t wade into bodies of water with snails
• Selective treatment: DEC 6mg/kg in 3 doses for 12
days after meal
• Mass treatment: DEC + albendazole 400 mg annually
• Disability prevention: home based or community
based (lymphedema and elephantiasis)
• Surgical management for hydrocele patients
• Collagen deposition in granuloma = fibrosis
HEPATOSPLENIC SCHISTOSOMIASIS
• Eggs meet liver/spleen thru portal circulation
• Granulomatous response
• Portal hypertension, esophageal varices, splenomegaly
CARDIAC
• Eggs Meet the heart, lodge in pulmo arteriole
• blood shunted to the heart, bypass the liver,
• RV strain and CVS collapse
GU
• Eggs lodge in bladder wall, polyps, erode or ulcerate = HEMATURIA
• Eggs lodge in ureter & urethra, lumps lesion = KIDNEY FAILURE
• Eggs lodge in ovaries, uterus, cervix, FT, LUMPS, = Infertility
• Men: lodges in testes and prostrate
• S.haematobium and S.mansoni migrate to spine
• S.japonicum = encephalopathy
• Microscopic detection of ova:
o S.haematobium: oval, spike at tip
o S. japonicum: small, spike at tip
o S. mansoni: spike on side
• Ab testing: COPT
o Earlier, more sensitive
o Ab detection test: COPT = Method of choice
o Cross react with other infection
o Cant differentiate current and old infection
o Can’t tell overall worm burden
• Ag detection test: in blood with immunoelectrophoresis
• Molecular detection: S. mansoni DNA
• Don’t swim in fresh stagnant water
• Harder in endemic areas
• Education
• Eliminate snail nesting grounds, use molluscicides
• Irrigation and engineering and canalization
• Chemotherapy: treatment of choice
• Praziquantel: most widely used drug
• Swimmer’s itch and katayama fever: symptomatic treatment
• S.mansoni, S.haematobium, S.intercalatum: 40mg/kg/day in 2 doses
• S.japonicum, S. mekongi: 60 mg/kg orally in 3 doses