COMMUNICABLE DISEASES: FINALS

LEPTOSPIROSIS o IP of up to 1 month was documented

Source: HPIM 19th ed + Baby HPIM 18thed, samplex  Leptospirosis classically described as biphasic
 globally important zoonotic disease caused by pathogenic Leptospiremic Phase Immune Phase
Leptospira species  After entry, the  Resolution of sx and
 Asymptomatic infection to fulminant, fatal disease organisms (+) antibodies
o Mild form nonspecific: fever, headache and proliferate, cross disappearance of
tissue barriers, and leptospires from the
myalgia.
disseminate blood
o Severe leptospirosis aka Weil’s syndrome hematogenously to  Bacteria persist in
jaundice, renal dysfunction, and hemorrhagic all organs various organs,
diathesis  Leptospires can be including liver, lung,
o Important presentation of severe disease isolated from the kidney, heart, and
Severe pulmonary hemorrhage (Immunoglobulin bloodstream brain  culture
and complement deposition) culture blood, CFS urine (2nd week of
(first 7-10 days) illness – months or
Leptospires  fever 3–10 days years)
 coiled, thin, highly motile organisms, (+) hooked ends and 2  Responsive to
periplasmic flagella(motility) antibiotics
 6–20 μm long and ~0.1 μm wide  Mild Vs Severe Leptospirosis
 stain poorly but can be seen microscopically by dark-field Mild Leptospirosis Severe Leptospirosis
examination Asymptomatic or mildly ill; do Rapidly progressive
 may take weeks to months for cultures to become positive not always include 2nd phase
 establish a symbiotic relationship with their host and can (+) serologic evidence Case–fatality rate ranging from
persist in the urogenital tract for years 1 to 50%
Flu-like illnesssudden onset, Higher mortality rates >40y/o
Epidemiology with fever, chills, headache, altered mental status, acute
 worldwide distribution, MC in the tropics and subtropics nausea, vomiting, abdominal renal failure, respiratory
o climate and poor hygienic conditions favor the pain, conjunctival suffusion insufficiency, hypotension, and
pathogen’s survival and distribution (redness without exudates) arrhythmias.
 Most cases occur in men, with a peak incidence Myalgia intense, esp affects Classic presentation Weil's
o Summer and fall in  Northern and Southern calves back and abdomen || syndrome
Headache intense, localized  hemorrhage,
Hemispheres
to the frontal or retroorbital jaundice, and acute
o Rainy season Tropics region (dengue) + kidney injury
 Appx 1 million severe cases occur per year photophobia, Pharyngeal
o mean case–fatality rate of nearly 10%. injection, lymphadenopathy, May be monophasic and
 Rodents, especially rats, are the most important reservoir meningismus, crackles, mild fulminant
 Presents as both an endemic and an epidemic disease jaundice, hepatomegaly,
splenomegaly; ±Aseptic
PATHOGENESIS
meningitis ( more common in
 Primary Mechanism Vasculitis children); ±Rash  often
 MOT: direct contact with urine, blood, or tissue from an transient, macular,
infected animal or, more commonly, exposure to maculopapular,
environmental contamination through cuts, abraded skin, or erythematousor hemorrhagic
mucous membranes, esp the conjunctival and oral mucosa Resolves in 7-10 days
 Platelet consumption plays an important role in  Death: septic shock with multiorgan failure and/or severe
hemorrhage. bleeding complications MC pulmonary hemorrhage
 Consumptive coagulopathy o widespread public health problem cough,
o Inc thrombin–antithrombin complexes, chest pain, respiratory distress, and hemoptysis
prothrombin fragments 1 and 2, d-dimer),  Jaundice occurs in 5–10%  orange skin
o Dec antithrombin & protein C o usually not associated with fulminant hepatic
o Deregulated fibrinolytic activity. necrosis.
 Elevated plasma E-selectin and von Willebrand   Cardiac involvement
endothelial cell activation disrupts endothelial-cell o nonspecific ST- and T-wave changes.
barrier function dissemination. o Repolarization abnormalities and arrhythmias 
 Lipopolysaccharide (LPS) in the outer membrane  poor prognostic factors.
relatively low endotoxic potency  Myocarditis, Hypotension, hemolysis, TTP, HUS
 OMPs for motility and cell and tissue adhesion and  Recognized sequel Autoimmune-associated uveitis
invasion (potential virulence factors)  loa22 o potentially chronic condition
 Immunity to Leptospira production of circulating Diagnosis
antibodies to serovar-specific LPS  exposure history combined + any of the protean
 Innate-immune TLR2 and TLR4 activation pathway manifestations of the disease.
controlling infection  Laboratory results:
Clinical Manifestations o leukocytosis with a left shift
 Clinical Hallmarks: Bleeding and multiorgan failure o elevated ESR & CRP
 Incubation period o Thrombocytopenia (≤100 × 109/L)
o usu 1–2 weeks  common & assoc with bleeding and RF
o ranges 1 to 30 days  Severe disease
o (+) coagulation activation DIC
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 COMMUNICABLE DISEASES: FINALS
 Kidneys
o Urinary sediment changes
 leukocytes, erythrocytes, and hyaline
or granular casts
o mild proteinuria, RF, Azotemia
o Characteristic of early leptospirosis
Nonoliguric hypokalemic renal insufficiency
 High Serum bilirubin, Aminotransferase and alkaline
phosphatase levels usually moderate, Amylase levels are
often elevated.
 Aseptic meningitis
o CSF pleocytosis few cells to >1000 cells/μL
o Polymorphonuclear cell predominance
o Elevated protein
o Glucose levels are normal
 Most common radiographic finding
o patchy bilateral alveolar pattern that
corresponds to scattered alveolar hemorrhage
 predominantly in lower lobes
 Definitive diagnosis of leptospirosis
o Culture Isolation
o (+) PCR
 high degree of accuracy during the first
5 days of illness
o seroconversion or rise in antibody titer (4x?)
 Serrologic Assay Mainstay of Diagnosis
 Microscopic agglutination test (MAT)
o Gold standard
o fourfold or greater rise in titer is detected bet
acute and convalescent-phase serum specimens.
 Antibodies generally do not reach detectable levels until
the second week of illness.
 Serologic testing lacks sensitivity in the early acute phase
of the disease (up to day 5) not used as basis for a
timely decision for tx initiation
Treatment
 Severe leptospirosis  treated with IV penicillin as soon
as the diagnosis is considered.
o Alternative: Ceftriaxone, cefotaxime, or
doxycycline
 Organism is highly susceptible to a broad range of
antibiotics and early intervention may prevent the
development of major organ system failure or lessenits
severity.
 Antibiotics are less likely to benefit patients in whom
organ damage has already occurred
 Mild cases, oral treatment
o Doxycycline(DOC) , azithromycin, ampicillin, or
amoxicillin
o In regions where rickettsial diseases are
coendemic
 DOC : doxycycline or azithromycin
 WOF Jarisch-Herxheimer reaction within hours after the
initiation of antimicrobial therapy
 Aggressive supportive care for leptospirosis is essential
and can be life-saving.
 Nonoliguric renal dysfunction:
o aggressive fluid and electrolyte resuscitation to
prevent dehydration and precipitation of oliguric
renal failure.
 Oliguric RF Peritoneal dialysis or hemodialysis
 Renal Failure is d/t Hypotension
 Patients with pulmonary hemorrhage
o Mech vent
Page 2 of 9
 All regimens are given for 7 days
 Do not give Doxycycline to pregnant women and children
TYPHOID
Source: HPIM 19th ed
Enteric (Typhoid) Fever
 systemic disease characterized by fever and abdominal pain
and caused by dissemination of S. typhi or S. paratyphi.
 enlarged Peyer’s patches and mesenteric lymph nodes
Epidemiology
 Etiologic agents:
o S. typhi and S. paratyphi serotypes A, B, and C
 no known hosts other than humans
 MOT:
o Food-borne or waterborne transmission results from
fecal contamination by ill or asymptomatic chronic
carriers.
o Sexual transmission between male partners
o Health care workers after exposure to infected patients
or during processing of clinical specimens and cultures
 High incidence of enteric fever
o poor sanitation and lack of access to clean drinking
water.
 In endemic regions
o more common in urban than rural areas; and among
young children and adolescents
 Risk factors
o contaminated water or ice, flooding, food and drinks
purchased from street vendors, raw fruits and vegetables
grown in fields fertilized with sewage, ill household
contacts, lack of hand washing and toilet access, and
evidence of prior Helicobacter pylori infection
Clinical Course
 Hallmark features:Fever (75%) and abd pain(30-40%)
 High index of suspicion is necessary
o (+) fever and a history of recent travel to a
developing country.
 IP of S. typhi  10–14 days but ranges from 5 to 21 days
o Det by inoculum size and indivudual's health
status and immune system
 Headache (80%), chills, cough, sweating, myalgias, malaise
and arthralgia
 GI: anorexia (55%), abdominal pain, nausea, vomiting, and
diarrhea , also less commonly, constipation
 Physical findings: coated tongue (51–56%), splenomegaly
and abdominal tenderness
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o Early findings  rose spots,
hepatosplenomegaly epistaxis, and relative
bradycardia at the peak of high fever
 Rose spots  faint, salmon-colored,
blanching, maculopapular rash located
primarily on the trunk and chest.
 Evident at the end of the first week
and resolves without a trace after 2–5
days.
 Salmonella can be cultured from punch
biopsies of these lesions
 Most prominent symptom  prolonged fever (38.8°–
40.5°C) up to 4 weeks, if untreated
 S. paratyphi A is thought to cause milder disease than S.
typhi, with predominantly gastrointestinal symptoms.
 The development of severe disease (10–15) depends on:
o Host factors (immunosuppression, antacid
therapy, previous exposure, and vaccination)
o Strain virulence and inoculum, and choice of
antibiotic therapy.
 Complications:
rd
o GI bleeding and intestinal perforation on the 3
or 4 week of illness d/t hyperplasia,
th
ulceration, and necrosis of the ileocecal Peyer’s
patches at the initial site of Salmonella
infiltration
 life-threatening and needs immediate
fluid resuscitation and surgical
intervention, + broad spectrum
antiobiotics for polymicrobial
peritonitis and bowel resection for GI
haemorrhages
o Neuro Meningitis, Guillain-Barre syndrome,
neuritis, and neuropsychiatric(“muttering
delirium” or “coma vigil”), with picking at
bedclothes or imaginary objects
o Rare complications  DIC, hematophagocytic
syndrome, pancreatitis, hepatic and splenic
abscesses and granulomas, endocarditis,
pericarditis, myocarditis, orchitis, hepatitis,
glomerulonephritis, pyelonephritis and
hemolytic-uremic syndrome, severe pneumonia,
arthritis, osteomyelitis, endophthalmitis, and
parotitis
 Up to 10% mild relapse, usually within 2–3 weeks of
fever resolution
 Up to 10% of untreated patients with typhoid fever
excrete S. typhi in the feces for up to 3 months
 1–4% develop chronic asymptomatic carriage, shedding S.
typhi in either urine or stool for >1 year.
o More common among women, infants, biliary
 Travelers to developing countries should be advised to monitor
abnormalities or concurrent bladder infection
with Schistosoma haematobium.
Diagnosis
 Dx is considered considered in any febrile traveller
returning from a developing region, especially the Indian
subcontinent, the Philippines, or Latin America.
 DDx
o malaria, hepatitis, bacterial enteritis, dengue
fever, rickettsial infections, leptospirosis, amebic
liver abscesses, and acute HIV infection
Page 3 of 9
 Labs
o 15-25%  Leukopenia & Neutropenia
 Definitive diagnosis  isolation of S. typhi or S. paratyphi
from blood, bone marrow, other sterile sites, rose spots,
stool, or intestinal secretions.
o sensitivity of blood culture is only 40–80%
o Bone marrow culture is 55–90% sensitive, and
yield is not reduced by up to 5 days of prior
antibiotic therapy
o Culture of intestinal secretions (best obtained by
noninvasive duodenal string test) can be positive
despite a negative bone marrow culture.
o Stool cultures
 negative in 60–70%
rd
 positive during the 3 week in
untreated patients.
 Serologic tests
o Classic Widal test for “febrile agglutinins,”
o Rapid tests to detect antibodies to
outermembrane proteins or O:9 antigen
 lower positive predictive values than
blood culture.
Treatment
 Prompt administration of appropriate antibiotic therapy
prevents severe complications of enteric fever and results
in a case-fatality rate of <1%
 Drug-susceptible typhoid fever Fluoroquinolones
(Ciprofloxacin)
 Patients infected with DCS S. typhi strains, give
o Ceftriaxone, azithromycin, or high-dose
ciprofloxacin
 DCS strains, a 10-14 day course of
high-dose ciprofloxacin is preferred.
 MDR enteric fever, caused by DCS and fluoroquinolone-
resistant strains, give
o Ceftriaxone, cefotaxime, and (oral) cefixime are
effective for treatment
 Azithromycin is associated with lower rates of treatment
failure and shorter durations of hospitalization than are
fluoroquinolones.
 Uncomplicated enteric fever
o managed at home with oral antibiotics and
antipyretics
 Severe enteric fever Glucocorticoid
 Chronic carriage of Salmonella
o treated for 4–6 weeks with oral amoxicillin,
TMP-SMX, ciprofloxacin, or norfloxacin + biliary
or kidney stones eradication
 DOC here in Philippines Chloramphenicol
Prevention and Control
their food and water intake carefully and to strongly consider
immunization against S. Typhi; Chronic carriers too.
o Ty21a, an oral live attenuated vaccine
 S. typhi vaccine given on days 1, 3, 5, and 7, with a
booster every 5 years
 Minimum age is 6y/o
o Vi CPS, a parenteral vaccine
 purified Vi polysaccharide from the bacterial
capsule, given in a single dose, with a booster every
2 years
 minimum age 2y/o
 poorly immunogenic in children <5y/o bec of T cell–
independent properties
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HEPATITIS
Source: Baby HPIM 18th ed + HPIM 19th ed, Previous reports, samplex
 Systemic infection predominantly affecting the liver.
 Malaise, nausea, vomiting, diarrhea, and low-grade fever
followed by dark urine, jaundice, and tender
hepatomegaly
 Subclinical and detected on basis of elevated AST and ALT
 Hepatitis-like illnesses may be caused not only by
hepatotropic viruses (A, B, C, D, E) , also by:
o Alcohol, drugs, Epstein-Barr,
coxsackievirus, etc.
Hepatitis A
 27-nm picornavirus (hepatovirus)
 single-stranded RNA genome.
 Recovery within 6–12 months,
o usually no clinical sequelae
o small proportion will have one or two apparent clinical
and serologic relapses
 Some cases (+) pronounced cholestasis  suggests biliary
obstruction
 Rare fatalities  fulminant hepatitis
 No chronic carrier state.
Dx:
 (+) IgM anti-HAV in acute or early convalescent serum sample
Epidemiology:
 MOT: Fecal-oral
 Endemic in underdeveloped countries
 Food-borne and waterborne epidemics
 Outbreaks in day-care centers, residential institutions.
Prevention
 After exposure:
o immune globulin 0.02 mL/kg IM within 2 weeks to
household and institutional contacts
 Before exposure:
o inactivated HAV vaccine 1 mL IM
 Half dose to children
 Repeat at 6–12 months;
 target travelers, military recruits, animal handlers, day-care
personnel, laboratory workers, and pts with chronic liver
disease (especially hepatitis C)
Hepatitis B
 42-nm hepadnavirus
o outer surface coat (HBsAg)
o inner nucleocapsid core (HBcAg)
o DNA polymerase, and partially double stranded
DNA genome of 3200 nucleotides.
 Marker of viral replication and infectivity HBcAg is
HBeAg
 Hepatitis B may be associated with immune-complex
phenomena
Page 4 of 9
o arthritis, serum sickness-like illness,
glomerulonephritis, and a polyarteritis nodosa–
like vasculitis.
Outcome
 Recovery >90%,
 Fulminant hepatitis (<1%)
 Chronic hepatitis or carrier state (only 1–2% of
immunocompetent adults; higher in neonates, elderly,
CMV, immunocompromised),
 Cirrhosis, and hepatocellular carcinoma (especially
following chronic infection beginning in infancy or early
childhood)
 Reactivation of HBV has been observed with
immunosuppression, particularly with rituximab
Diagnosis
 HBsAg in serumacute or chronic infection)
 IgM anti-HBc  early anti-HBc indicative of acute or
recent infection
 Most sensitive test is detection of HBV DNA in serum
o not generally required for routine diagnosis.
Epidemiology
 Percutaneous (needle stick), sexual, or perinatal
transmission
Prevention
 After exposure in unvaccinated persons
o hepatitis B immune globulin (HBIg) 0.06 mL/kg
IM immediately after needle stick to within 14
days of sexual exposure in combination with
vaccine series.
 For perinatal exposure (HbsAg+ mother)
o HBIg 0.05 mL in the thigh immediately after
birth with the vaccine series started within the
first 12 h of life.
 Before exposure
o Recombinant hepatitis B vaccine IM at 0, 1, and
6 months; deltoid, not gluteal injection.
 Targeted to high-risk groups
o health workers, persons with multiple sexual
partners, IV drug users, hemodialysis pts,
hemophiliacs, household and sexual contacts of
HBsAg carriers, persons travelling in endemic
areas, unvaccinated children <18
Hepatitis C
 Caused by flavi-like virus with RNA genome of >9000
nucleotides
o Similar to yellow fever virus dengue virus
o genetic heterogeneity
 Incubation period 7–8 weeks
Clinical Course
 Often clinically mild and marked by fluctuating elevations of
serum aminotransferase levels
 >50% likelihood of chronicity,
 leads to cirrhosis in >20%.
Diagnosis
 Anti-HCV in serum
 Current third-generation immunoassay incorporates proteins
from the core, NS3, and NS5 regions.
 The most sensitive indicator of HCV infection  HCV RNA
Epidemiology
 HCV accounts for >90% of transfusion-associated hepatitis
cases
 IV drug use accounts >50% of reported cases of hepatitis C.
 Little evidence for frequent sexual or perinatal transmission.
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 COMMUNICABLE DISEASES: FINALS
Prevention
 Exclusion of paid blood donors, testing of donated blood for
anti-HCV.
 Anti-HCV detected by enzyme immunoassay in blood donors
with normal ALT is often falsely positive (30%) result should
be confirmed by HCV RNA in serum.
Hepatitis D
 Defective 37-nm RNA virus that requires HBV for its replication
 either coinfects with HBV or superinfects a chronic HBV carrier
 Enhances severity of HBV infection
o acceleration of chronic hepatitis to cirrhosis, occasionally
fulminant acute hepatitis
o 
Diagnosis
 Anti-HDV in serum
o acute hepatitis D—often in low titer, is transient
o chronic hepatitis D—in higher titer, is sustained
Epidemiology
 Endemic among HBV carriers
o Spreads predominantly by nonpercutaneous means.
 In nonendemic areas
o HDV is spread percutaneously among HbsAg+ IV drug
users or by transfusion in hemophiliacs and to a lesser
extent among HbsAg+ men who have sex with men.
Prevention
 Noncarriers only Hepatitis B vaccine
Hepatitis E
 Caused by 29- to 32-nm agent thought to be related to
caliciviruses
 Enterically transmitted and responsible for waterborne
epidemics of hepatitis
 Self-limited illness with high (10–20%) mortality rate in
pregnant women.
Treatment for Viral Hepatitis:
 Activity as tolerated, high-calorie diet (often
tolerated best in morning)
 IV hydration for severe vomiting,
 cholestyramine up to 4 g PO four times daily for
severe pruritus
 avoid hepatically metabolized drugs
 no role for glucocorticoids
 Liver transplantation for fulminant hepatic
failure and grades III–IV encephalopathy
 In rare instances of severe acute HBV
lamivudine
 Treatment of acute HCV infection with
interferon α may be effective at reducing the
rate of chronicity
o treated with a 24-week course for HCV
Toxic and Drug Induced Hepatitis
 DOSE-DEPENDENT (DIRECT HEPATOTOXINS)
o Onset is within 48 h, predictable, necrosis
around terminal hepatic venule
o e.g., carbon tetrachloride, benzene derivatives,
mushroom poisoning, acetaminophen, or
microvesicular steatosis (e.g., tetracyclines,
valproic acid)
 IDIOSYNCRATIC
o Variable dose and time of onset
o small number of exposed persons affected
o may be associated with fever, rash, arthralgias,
eosinophilia.
Page 5 of 9
o Mechanism may actually involve toxic
metabolite, possibly determined on genetic basis
o e.g., isoniazid, halothane, phenytoin,
methyldopa, carbamazepine, diclofenac,
oxacillin, sulphonamides
TREATMENT
 Supportive as for viral hepatitis, withdraw suspected agent
and include use of gastric lavage and oral administration of
charcoal or cholestyramine.
 Liver transplantation if necessary
 acetaminophen overdose
o sulfhydryl compounds  N-acetylcysteine
provides a reservoir of sulfhydryl
groups to bind the toxic metabolites
 stimulating synthesis of hepatic
glutathione.
 Therapy within 8 h of ingestion but
may be effective even if given as late
as 24–36 h after overdose
Chronic Hepatitis
Chronic Hepatitis
 group of disorders characterized by a chronic
inflammatory reaction in the liver for at least 6 months.
ETIOLOGY
 Hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D
virus (HDV, delta agent), drugs (methyldopa,
nitrofurantoin, isoniazid, dantrolene), autoimmune
hepatitis, Wilson’s disease, hemochromatosis, α1-
antitrypsin deficiency.
HISTOLOGIC CLASSIFICATION
 Grade histologic assessment of necrosis and
inflammatory activity and is based on examination of the
liver biopsy.
 Stage  reflects the level of disease progression and is
based on the degree of fibrosis
PRESENTATION
 Asymptomatic serum aminotransferase elevations to
apparently acute, even fulminant, hepatitis
 Common symptoms include fatigue, malaise, anorexia,
low-grade fever
o jaundice isfrequent in severe disease.
 Some pts may present with complications of cirrhosis
o ascites, variceal bleeding, encephalopathy,
coagulopathy, and hypersplenism.
 Chronic HBV or HCV and autoimmune hepatitis
o extrahepatic features may predominate
CHRONIC HEPATITIS B
 up to 1–2% of cases of acute hepatitis B in
immunocompetent hosts
o more frequent in immunocompromised hosts.
 Spectrum of disease:
o asymptomatic antigenemia, chronic hepatitis,
cirrhosis, hepatocellular cancer
 Ultimately leads to cirrhosis in 25–40% of cases
o Particularly in pts with HDV superinfection or the
pre-C mutation and HCC particularly when
chronic infection is acquired early in life
 Early phase
o Continued symptoms of hepatitis
o Elevated aminotransferase levels
o (+)Serum HBeAg and HBV DNA,
o (+) Replicative form of HBV
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 COMMUNICABLE DISEASES: FINALS
 Later phase
o Clinical and biochemical improvement
o Disappearance of HBeAg and HBV DNA
o Appearance of anti-HBeAg in serum
o Integration of HBV DNA into host hepatocyte
genome.
 Extrahepatic S/Sx (Immune complex-mediated)
o Rash, urticaria, arthritis, polyarteritis nodosa–
like vasculitis, polyneuropathy,
glomerulonephritis
 Treatment
o interferon α (IFN-α), pegylated interferon (PEG
IFN), lamivudine, adefovir dipivoxil, entecavir,
telbivudine, and tenofovir
 Use of IFN-α has been supplanted by
PEG-IFN.
CHRONIC HEPATITIS C
 50–70% of cases of transfusion-associated and sporadic
hepatitis C
 Clinically mild, often waxing and waning aminotransferase
elevations; mild chronic hepatitis on liver biopsy.
 Extrahepatic manifestations
o cryoglobulinemia, porphyria cutanea tarda,
membranoproliferative glomerulonephritis, and
lymphocytic sialadenitis.
 Diagnosis confirmed by detecting anti-HCV in serum.
 May lead to cirrhosis in ≥20% of cases after 20 years.
 Treatment
o Considered in pts with detectable HCV RNA in
serum and biopsy evidence of at least moderate
chronic hepatitis (portal or bridging fibrosis).
o For pts with genotype 1
 PEG IFN/ ribavirin should be combined
with a protease inhibitor (boceprevir,
telaprevir) where available.
 Protease inhibitors should never be
used alone to prevent resistance
 Monitoring of HCV plasma RNA is useful in assessing
response to therapy.
 The goal of treatment is to eradicate HCV RNA predicted
by the absence of HCV RNA by polymerase chain reaction
6 months after stopping treatment (“sustained viral
response”).
o HCV RNA be measured at baseline and at weeks
4, 12, and 24 to assess response to treatment
and to aid in decisions regarding treatment
duration as well as after 12 weeks of therapy.
o Therapy can be stopped if an early virologic
response is not achieved.
HEPATITIS A
 No carrier state, chronic state and Oncogenic potential
 Rarely causes fulminant hepatic failure, it may do so more
frequently in pts with chronic liver disease—especially
those with chronic hepatitis B or C.
 The hepatitis A vaccine is immunogenic and well tolerated
in pts with chronic hepatitis.
o pts with chronic liver disease, especially those
with chronic hepatitis B or C, should be
vaccinated against hepatitis A
Page 6 of 9
HBV Serologic and Virologic Markers
th
Source: HPIM 19 ed
 HBsAg
o Most sensitive and First virologic marker of HBV
o detectable in serum within 1–12 weeks, usually
between 8 and 12 weeks,
o Precedes elevations of serum aminotransferase
activity and clinical symptoms by 2–6 weeks and
remains detectable during the entire icteric or
symptomatic phase of acute hepatitis B
o Undetectable 1–2 months after the onset of
jaundice and rarely persists beyond 6 months.
o Infrequently, in ≤1–5% , if levels of HBsAg are
too low to be detected
 presence of IgM anti-HBc establishes
the diagnosis of acute hepatitis B
 Anti-HBs
o Immune to Hepa B
o After HBsAg disappears
o detectable in the serum and remains detectable
indefinitely thereafter
o The protective antibody
 no clinical relevance and does not
signal imminent clearance of Hep B
 HBcAg
o intracellular and, when in the serum,
sequestered within an HBsAg coat naked core
particles do not circulate in serum not
detectable in the serum
 Anti-HBc
o readily demonstrable in serum beginning within
the first 1–2 weeks after the appearance of
HBsAg
o precedes detectable levels of anti-HBs by weeks
to months
o “gap” or “window” period (disappearance of
HBsAg and the appearance of anti-HBs)
o May represent the only serologic evidence of
current or recent HBV infection, and also in
transfusion-associated hepatitis B.
o Years after HBV infection, anti-HBc may persist
in the circulation longer than anti-HBs
isolated anti-HBc does not necessarily indicate
active virus replication
 most instances of isolated anti-HBc
represent hepatitis B infection in the
remote past
o Isolated anti-HBc represents low-level hepatitis B
viremia, and occassionally a cross-reacting or
false-positive immunologic specificity.
o Determines Recent and remote HBV infections
by the immunoglobulin class of anti-HBc.
 IgM anti-HBc  first 6 months after
acute infection
 IgG anti-HBc  beyond 6 months.
 HBeAg
o Readily detectable serologic marker of HBV
infection
o Appears concurrently with or shortly after HBsAg
o Coincides temporally with high levels of virus
replication and reflects the presence of
circulating intact virions and detectable HBV
DNA
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 COMMUNICABLE DISEASES: FINALS

o Becomes undetectable shortly after peak

elevations in aminotransferase activity, before
the disappearance of HBsAg,
 Anti-HBe
o Period of relatively lower infectivity

 Generally, in persons who have recovered from hepatitis B

o anti-HBs and anti-HBc persists

o (+) Chronic HBV infection.

 Markers of HBV replication appear transiently during acute

infection
o little clinical utility in typical cases of acute HBV
infection.
o Markers of HBV replication provide valuable
information in patients with protracted
infections.

 Chronic HBV infection

o HBsAg remains detectable beyond 6 months
o (+)HBsAg and nonneutralizing anti-HBs
 anti-HBs is either undetectable or at
low levels
o (+) IgG anti-HBc
Highly Replicative Nonreplicative
 Early HBV  (+) seroconversion from
DNA can be HBeAg to anti-HBe
detected both in  coincides with a transient,
serum and in usually mild, acute hepatitis-
hepatocyte like elevation in
nuclei aminotransferase activity
 Time of which reflects cell-mediated
maximal immune clearance of virus-
infectivity and infected hepatocytes.
liver injury  Only spherical and tubular
 HBeAg - forms of HBV, not intact
qualitative virions, circulate, and liver
marker injury tends to subside.
 HBV DNA-  Inactive HBV carriers
quantitative  But HBV replication can be
marker detected at levels of
approximately ≤103 virions
with highly sensitive PCR DENGUE
Source: HPIM 19th Ed, samplex, previous reports
 Non replicative may convert back to replicative infection Epidemiology
o reexpression of HBeAg and HBV DNA, and  Dengue fever epidemics
sometimes of IgM anti-HBc o Higher temperatures increase the rate of larval
o exacerbations of liver injury. development and accelerate the emergence of
 High-titer IgM anti-HBc can reappear during acute adult Aedes mosquitoes
exacerbations of chronic hepatitis B, o Temperatures <15°C or >36°C also substantially
o Relying on IgM anti-HBc versus IgG anti-HBc to reduce mosquito feeding
distinguish between acute and chronic hepatitis o Relative humidity is a strong predictor of dengue
B infection not always reliable outbreaks
o Patient history is invaluable in helping to o peak transmission at ~32°C, plus
distinguish de novo acute hepatitis B infection  shorter extrinsic incubation period
from acute exacerbation of chronic hepatitis B  higher feeding frequency
infection.  more rapid development of
mosquitoes
 >32–35°C  Viral replication can occur in as little as 7 days
o 30°C replication takes ≥12 days;
o 26°C replication does not reliably occur
 Rainfall established as a predictor of the seasonal timing
of dengue epidemics.
 Occurs in tropics and subtropics
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 COMMUNICABLE DISEASES: FINALS

 Most important arthropod-borne viral disease worldwide  Dengue Hemorrhagic Fever (DSS)
o Year-round transmission of dengue viruses 1–4 o Frank shock, low pulse pressure, cyanosis,
occurs between latitudes of 25°N and 25°S hepatomegaly, pleural effusion, ascites, severe
Etiologic Agent & Vector ecchymoses and GIT bleeding
 4 serotypes; flaviviruses o circulatory failure and profound shock with
o Most clinically imp: Dengue virus 1-4 undetectable BP and pulse
 Causes Fever and Myalgia o Main Criteria is Plasma leakage
 A. aegypti as their principal vector  period of clinically significant plasma
leakage lasts 24-48 hrs.
A. Aegypti (female) o First line mgt IVF resuscitation with isotonic
 typically breeds near human habitation, using relatively crystalloid solution
fresh water from sources such as water jars, vases,
discarded containers, coconut husks, and old tires.  Risk of Major bleeding
 usually inhabits dwellings and bites during the day o prolonged or refractory shock, hypotensive
 Closed habitations with air-conditioning may inhibit shock, renal or liver failure
transmission of dengue viruses 1–4. o severe and persistent metabolic acidosis
o given with NSAIDs, and with pre-existing peptic
ulcer disease,
Clinical Manifestations
o anticoagulant therapy, any form of trauma,
 Rash in 50% of cases initially diffuse flushing
including IM injection
o midway through illness, onset of maculopapular rash,
which begins on trunk and spreads centrifugally to
 Course of Dengue Illness
extremities and face
o Febrile Antigen detection for early det & mgt
 Often a transient macular rash appears on the first
o Recovery reabsorption of Extravascular fluids
day, as do adenopathy, palatal vesicles, and scleral
injection
o pruritus, hyperesthesia
o After defervescence(day 3-5) petechiae on extremities
and face
 Break-bone fever Sudden onset of fever, frontal headache,
retroorbital pain, and back pain along with severe myalgias.
 Occasionally biphasic (“saddleback”) fever
 Incubation period averaging 4–7 days,
 Illness may last a week with additional symptoms and clinical
signs
o anorexia, nausea or vomiting, and marked cutaneous
hypersensitivity
 Tourniquet Test
 Epistaxis and scattered petechiae are often noted in
o presumptive diagnosis
uncomplicated dengue, and preexisting gastrointestinal lesions
o applying an arm blood pressure cuff to the mean
may bleed during the acute illness.
arterial pressure for 5 min
 Laboratory findings
 A positive test is > 10 petechiae per 1
o leukopenia, thrombocytopenia, elevations of serum
square inch.
aminotransferase
 Cornerstone in Management of DHF Platelet transfusion
Diagnosis  Main pathophysiologic mechanism for the theory of a
 Viremia peaks at about 2-3 days after the onset of illness more severe dengue infection during a second infection
 Recovery IgM ELISA or paired serology TNF-a
 Acute phase Antigen-detection ELISA or RT PCR
o Virus is readily isolated from blood in the acute phase if
mosquito inoculation or mosquito cell culture is used.

WHO
Source: previous reports ( Buada et.al), Samplex
 Severe dengue
o SeverePlasma leakage
 may lead to DSS or fluid accumulation
with respiratory distress
o Severe bleeding
 As evaluated by physician
o Severe organ impairment
 liver enzyme ≥1000
 Impaired consciousness
 Heart and other organs

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 COMMUNICABLE DISEASES: FINALS

Dengue Case Management

Admission Criteria

Discharge Criteria

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