C-REACTIVE PROTEIN  It has highest affinity for  Scavenging Action

- Phosphocholine on bacteria CRP DOES NOT BIND TO NORMAL CELL

KEY FACTS: - Mixture of sphingomyelin and MEMBRANE
phosphatidylcholine in - Bind avidly to cells that are
 The higher the CRP level, the more eukaryotic membranes undergoing apoptosis or
inflammation in your body necrosis
 CRP can recognize self ligands
 CRP is not very specific; it isn’t unique - Plasma lipoproteins - Activates complement
to one disease - Damaged cell membrane - Initiating an inflammatory
 CRP tests can help monitor disease - Several phospholipids reaction
progress and flares - Small nuclear ribonucleoprotein - Attracts neutrophils and
 Measures of CRP add to the diagnostic components monocytes to the site
procedure in selected cases (e.g. in the - Apoptotic Cells
differentiation between a bacterial and PROCESSES INDUCED BY CRP
 CRP also bind to some extrinsic ligands
a viral infection) - Phospholipid  ACTIVATION OF COMPLEMENT
 An extremely elevated CRP is suggestive - Capsular/Cell body components CASCADE
of a possible bacterial infection of bacteria, fungi, and parasite  RAAS ACTIVATION
 The CRP level may be useful also for
 VASCULAR WALL DAMAGE
monitoring the effect of treatment and FUNCTIONS OF CRP
- Wall gets infiltrated by
for detection of postoperative
 Anti infective inflammatory cells
complications or intercurrent infections.
- Opsonize particles for - Smooth muscle proliferates and
C-reactive protein (CRP) phagocytosis migrates to intima
- Activate complement via - Extracellular matrix is synthesized
 A blood test marker for inflammation in classical pathway - Sensibility to proatherogenic factors
the body  Anti inflammatory actions is increased
 Produced in the liver and its level is - CRP helps in preventing  PROTHROMBOTIC STATE
measure by testing the blood systemic inflammation - activation of complement cascade
 Classified as an acute phase reactant, - CRP aids in the release of - faster thrombin formation
which means that its levels will rise in neutrophils from blood vessels, - release of tissue factor
response to inflammation. while preventing white cell - diminished fibrolysis
 CRP Gene – chromosome 1, short arm adhesion to vessel in non – - increased formation of adhesion
 Few cytokines especially, IL-6 and IL-1 inflamed tissue molecules
regulate CRP at transcriptional level - stimulates the release of anti – - increased thrombocyte
 Normal range: Less than 10mg/L inflammatory molecules from adhesiveness
monocytes
  Endothelial dysfunction CLINICAL IMPORTANCE OF CRP  Pancreatitis
- decreased nitrogen oxide - Level peaks 3 days after onset of
production  Elevated CRP levels pain
- vasodilation impairment - Osteoarthritis - Level of 150 mg/L distinguishes mild
- glycocalyx damage - Predictive coronary events (esp. in from sever disease
stable angina)
 Opsonization of oxidized LDL
- easier uptake by macrophages
- Proinflammatory or prothrombotic HS-CRP
effects
- formation of foam cells  High sensitivity C – reactive protein
 Mild elevation of CRP levels
(hs-CRP)
FACTORS AFFECTING CRP LEVELS - SLE
 Similar to CRP, it is also an Acute Phase
- Scleroderma
Factor Effect - Sjorgen Syndrome
Reactant
Gender Women have  More sensitive than CRP especially for
- Dermatomyositis/ Polymyositis
higher levels than cardiovascular injury
 Normalization of CRP levels
men  Normal range: <0.3 mg/dL
- helpful tool in determining the
Body mass effect Weight loss- response to antibiotic therapy and HS – CRP Uses
decrease duration of treatment
Ethnicity Blacks have higher  Transplant cases  Performing risk assessment for
levels than whites - Elevated levels were seen in cardiovascular diseases
Exercise After exercise CRP majority of kidney or heart - taken as an independent risk factor
levels decrease transplant for CVD, Stroke and Peripheral
Alcohol Decrease - Highly elevated GVHD vascular disease
consumption - Changes in levels are not organ - it also adds to the predictive value
specific, like other inflammatory of total cholesterol and HDL
conditions cholesterol for future events
METHODS FOR DETECTION OF CRP  Determining risk of hypotension
 Cerebral vein or sinus thrombosis
 ELISA - An increase CRP is associated with a - hs-CRP has been reported as a risk
poorer short term prognosis factor for hypotension
 Immunoturbidimetry
 Rapid immunodiffusion  Giant cell arteritis
- Thrombocystosis with platelet
 Visual Agglutination
counts >400,00/uL and CRP levels
>2.45 mg/dl have been found to be
the strongest laboratory predictors
of a positive temporal artery biopsy
ANTI-STREPTOLYSIN O (ASO) for weeks or months after the primary  Principle: In the presence of ASO
source of infection has eradicated. antibody, a visible agglutination
 Streptolysin O isa a hemolytic factor  Incidence decreases as the time reaction will be exhibited when a serum
produced by most strains of Group A increases. specimen combine with latex particle
beta-hemolytic streptococci (S.  The antibody levels begin to rise after 1 coated with streptolysin O antigen
pyogenes) to 3 weeks of strep infection, peaks in 3  Specimen should be Serum that is clear
 Streptococci are gram-positive cocci in to 5 weeks and falls back to insignificant and hemolysis free
chain, non-motile, facultative levels in 6 months. Values need to be
anaerobes correlated with a clinical diagnosis. If REAGENT STORAGE AND STABILITY
 It produce toxin like streptolysin O and the titer doesn’t decrease with time;  Reagents are stable until stated
streptolysin S as well as enzymes like this means that a recurrent or chronic expiration date
DNAase and streptokinase. infection may exist.  Must be refrigerated (2-8◦C)
 The toxin is called streptolysin O, the O
KEY PRINCIPLES  DO NOT FREEZE
stands for oxygen- labile; theother toxin
 The ASO Latex Reagent, once shaken
that secreted is an oxygen-stable “  Anti-streptolysin O can react specifically must be uniform without visible
streptolysin S ”. with SLO and inhibits the hemolytic clumping. When stored refrigerated, a
- Both toxins are involved in activity. slight sedimentation may occur and
producing hemolysis, in particular,  The amount of ASO can be estimated by should be considered normal.
Beta-hemolysis. dilution of patient’s serum in the  Do not use the latex reagent or controls
 It is a specific neutralizing antibody presence of constant amount of SLO to if contaminated.
produced after infection with these the point where there is still complete
organisms and it appears in serum from prevention of hemolysis. SPECIMEN COLLECTION AND STORAGE
1 week – 1 month after the onset of a  The occurrence of ASO depends on the
streptococcal infection.  Use fresh serum collected by
production of SLO by streptococci in the centrifuging clotted blood.
 It combines and neutralizes the infected host.
hemolytic activity of streptolysin O.  If the test cannot be carried out on the
same day, store the specimen for 7 days
ASO Uses: at 2-8 degree Celsius. If it will not be
COMERCIALLY AVAILABLE TESTS used for 3 months or more, store at -20
 Anti-streptolysin O test is used to
degree Celsius.
diagnose conditions from a  ASO latex slide test
 For longer periods the sample must be
streptococcal infection especially in - used for screening a significant raise
FROZEN
- Rheumatic fever in ASO titer
 As in all serological test, hemolytic or
- Glomerulonephritis  ASO titration test
contaminated serum must not be used.
 Antibodies ( IgG ) begin to appear in - used to determine the titer of ASO
 DO NOT USE PLASMA
patient serum days after infection. The antibody
antibody may be detected in the blood
Rapid ASO latex agglutination test
 worldwide. HIV-2 is limited primarily to host cells, appear about 1 year after
HUMAN West Africa. infection. Although these
IMMUNODEFICIENCY  HIV-1 has three subtypes: M, N, and O.
M is the major subtype.
neutralizing antibodies can interfere
with viral replication, they do not
VIRUS (HIV) B. HIV Replication
seem to play a major role in
protection.
Basic differentiation between AIDS and HIV  HIV binds to the CD4 molecule on T - HIV is able to escape the immune
helper cells, monocytes, macrophages, response by undergoing antigenic
HIV AIDS and other cells. Secondary receptors variation.
HIV is the virus that AIDS is the last stage  Effect on T cells
(co-receptors) are also important in
causes infection. of HIV infection. - As the disease progresses, there is a
viral binding. T helper cells are the
HIV damages the As HIV infection depletion of CD4+ T helper cells.
primary target.
immune system by advances to AIDS, the
 HIV penetrates the plasma membrane The immune deficiency worsens as
killing the CD4 cells. amount of HIV in the
of the cell, and the viral RNA is released. more T helper cells are killed by the
body increases and
 The RNA is transcribed to DNA by the virus.
the number of CD4
CD4 Cells cells decreases. activity of the viral enzyme reverse - HIV compromises the immune
CD4 cells are part of HIV medicines can transcriptase. Viral DNA is then inserted response by destroying T helper
the immune system. stop HIV infection into the host cell's DNA by viral cells. These cells are key players in
from advancing to integrase. both humoral and cellular immune
AIDS.  The viral DNA is transcribed into mRNA, responses.
HIV attacks and kills Without HIV which is then translated into viral - The ratio of CD4 to CD8 cells is
CD4 cells. medicines, HIV proteins. Mature viruses leave the host reduced from 2:1 (normal).
advances to AIDS in  Additional effects
cell by budding.
about 10 years. - Decreased natural killer cell activity
 The replication process kills the infected
Loss of CD4 cells - Defective chemotaxis in monocytes
cell and leads to a diminishing number
makes it hard for the and macrophages
body to fight off of T helper cells.
Enhanced release of interleukin-1
infections. C. Immune Response and HIV and cachectin by monocytes

 Serologic effects D. Epidemiology

A. Human Immunodeficiency Virus (HIV)
- Antibodies to HIV generally appear
1. HIV-1 is transmitted by unprotected sex,
 Member of the family Retroviridae about 12 weeks after infection.
contaminated blood or blood products,
 HIV causes acquired immunodeficiency These are the first antibodies
contaminated needles, or perinatally.
syndrome (AIDS). detected by ELISA and Western blot
 There are two serogroups. HIV-1 is the assays. 2. In the U.S., AIDS is the number one cause of
predominant strain, and it is found - Neutralizing antibodies, antibodies death for people between 20 and 35 years of
able to interfere with infection of age.
E. Symptoms Two of the three bands must appear for - Virus infects the very cells of the
a Western blot to be considered immune system that any vaccine is
 Initially, infected persons (acute phase) positive: p24, gp41,orgp!20/160. supposed to induce
will be asymptomatic or can have minor  Genetic probes can detect replicating
symptoms resembling IM (infectious viruses.
mononucleosis)  Reverse transcriptase—polymerase
 The virus continues to replicate rapidly chain reaction assays detect nucleic acid
in the lymphoid tissue. This stage is gene sequences in HIV-1 and HIV-2.
referred to as clinical latency.
 The indirect immunofluorescence assay
 As the number of T cells begins to is used to detect HIV antigen in infected
decrease, the patient develops a cells. This can also be used as a
number of infections caused by confirmatory test.
opportunistic pathogens: Candida,
herpes simplex virus, cytomegalovirus, G. Treatment
etc. This stage has been referred to as
 Retrovir (Zidovudine) provides hope:
AIDS-related complex (ARC).
o Increases survival time
 Final stage (full-blown AIDS) includes T
o Decrease mortality
cell depletion resulting in severe
opportunistic infections and cancers, H. Prevention
such as esophageal candidiasis,
cryptococcosis, systemic  Modification of sexual behavior
cytomegalovirus and herpes simplex  Measures to protect infection of blood
virus infections, Pneumocystis jiroveci and blood products
pneumonia, and Kaposi's sarcoma. - self – referral among high risk
 CD4+ T cell counts and presence of a groups
variety of opportunistic infections are - screening of blood donors
used to stage the severity of the - heating blood plasma at 68 degree
disease. Celsius for 24 hours
 Search for effective vaccine is still on
F. Laboratory Tests - HIV mutates rapidly, it’s extremely
 ELISA tests are used to detect challenging to develop a single
antibodies to HIV and HIV antigen. vaccine to target all the strains and
Repeatedly positive samples must be mutations. HIV is also unique in
confirmed by a Western blot or how it hides from the immune
immunofluorescent test. system, so even if you eradicate the
 The Western blot assay is the circulating virus, the hidden HIV can
confirmatory serological test for HIV. spread the infection.
 c) Syphilitic aortitis, aortic valve
SYPHILIS SEROLOGY  Secondary syphilis
a) Symptoms include skin rash, low- insufficiency, and thoracic
grade fever, malaise, pharyngitis, aneurysm are possible.
A. Causative Agent
weight loss, arthralgia, and d) Neurosyphilis can cause blindness
 Treponema pallidum subsp. pallidum, a lymphadenopathy. Symptoms last and senility
spirochete 4-6 weeks.
GUMMAS – most common complication of
 Transmitted by direct contact (including b) Spirochetes are present throughout
late syphilis. May be single or multiple. They
sexual contact) and across the placenta the body during this stage.
are ordinarily indolent, slowly progressive,
c) Ulcers develop on mucous
B. Disease Stages and indurated granulomata, with central
membranes.
healing and atrophic scar surrounded by
 Incubation period: T. pallidum enters d) Serologic tests are positive.
hyperpigmented borders. Destructive but
the body, reaches the bloodstream, and responds rapidly to treatment.
Condyloma lata – formed by coalescence of
is disseminated to all organs. This early
asymptomatic phase lasts 10 days to 10 large, pale, flat – topped papules. Occur in
 Congenital syphilis
weeks. warm, moist areas such as the perianal area a) Treponema pallidum can cross the
 Primary syphilis and are highly infectious. placenta during any stage of the
a) The initial lesion is a painless, disease.
nonbleeding ulcer called a b) Infection of the fetus causes late
 Latency
chancre. abortion, stillbirth, neonatal death,
a) Stage of syphilis with no signs or
b) The chancre appears, on neonatal disease, or latent
symptoms
average, 2-3 weeks after the infection.
b) Nontreponemal and treponemal
initial infection. c) The outcome depends on the stage
serologic tests are positive.
c) Within 1 week after the chancre of the mother's disease—primary or
c) Early latency: One in four
appears, lymph nodes enlarge. secondary syphilis causing the
individuals relapses into secondary
d) Antibodies are produced 1-4 worst outcome—and the age of the
syphilis.
weeks after the chancre fetus at infection.
d) Late latency: The patient is resistant
appears. d) If the mother receives treatment
to reinfection and to relapses.
e) Darkfield analysis of lesion during the first 4 months of
 Tertiary syphilis
demonstrates spirochetes. pregnancy, congenital syphilis is
a) Symptoms occur 2-40 years after
usually avoided.
CHANCRE – sores that are mostly initial infection.
e) Congenital syphilis presents in the
painless, “punched out” appearance with b) Gummas (syphilis lesions due to
neonate as diffuse maculopapular
hypersensitivity reaction to
a red and smooth based and visible scant desquamatous rash (particularly
treponemal antigens) are found
serous secretions. around the mouth and on the palms
throughout the body.
and soles), hemolytic anemia,
jaundice, hepatosplenomegaly,
 abnormal cartilage and bone - Examples of nontreponemal antigen USR
involvement, and mental tests include Venereal Disease Research
 This test is a modified VDRL test in
retardation. Laboratory (VDRL), unheated serum
which choline-chloride EDTA is added to
 Diagnosis: reagin (USR), and rapid plasma reagin
the VDRL antigen. The addition of this
a) Signs and symptoms, detection of (RPR) assays.
compound allows serum that has not
spirochetes in lesion, and positive - The percentage of false positives in
been heat inactivated to be tested.
syphilis serology these tests is high (30^0%), so all
reactive results must be confirmed RPR test
C. Direct Detection using a test that detects antibodies
specifically directed at T. pallidum, so-  Macroscopic flocculation
 Definitive diagnosis of syphilis is made
called treponemal antigen tests.  The assay uses VDRL antigen with
by detection of T. pallidum in CSF,
c. Treponemal antigen tests use T. charcoal particles. The antigen is not
umbilical cord, or skin or mucous
pallidum cells as the antigen source. attached to the charcoal as in latex
membrane lesions—depending on the
These assays are highly specific and agglutination assays. The charcoal is
stage of the disease.
include the fluorescent treponemal trapped in the flocculation reaction,
 Treponema pallidum is detected using
antibody absorption (FTA-ABS), T. which allows the reaction to be seen
darkfield microscopy or silver stain. 3.
pallidum-particulate agglutination (TP- macroscopically.
Direct fluorescent antibody-Z pallidum
PA), and microhemagglutination T.  The test can be qualitative or
(DFA-TP) test: A fluorescence labeled
pallidum tests. semiquantitative. Dilutions are made to
antibody is used to detect T. pallidum in
semi quantify the amount of antibody
lesions. VDRL test present.
D. Serological Tests  This test measures the antibody (reagin) TP-PA test
General principles a patient has formed against cardiolipin,
cholesterol, and lecithin.  Treponemal antigen is combined with
a. Treponema pallidum infection causes  Tests are read microscopically for liposomes. If antibodies are present, a
the host to produce nonspecific flocculation. Results are reported as NR mat of agglutination forms in wells of a
antibody, reagin, and specific (nonreactive), WR (weak reactive), or R microtiter plate.
treponemal antibodies. (reactive).
b. The nontreponemal antigen tests detect  The VDRL test is positive 1-3 weeks
reagin and are only used for screening after the chancre appears. d. Mainly
because this antibody will cross react limited to use on CSF now, this is the
with similar antigens present in SLE, only serologic test approved for testing
autoimmune disease, pregnancy, and CSF.
some chronic infections such as
hepatitis. These conditions can result in
biologic false positives.
FTA-ABS test

 Principle: Indirect antibody test

 Nichol's strain of T. pallidum subsp.
pallidum is affixed into wells of
microscope slides.
 Patient serum is heat inactivated.
 Nontreponemal antibody is absorbed
from patient serum with a sorbent of
Reiter's strain of nonpathogenic
treponeme.
 Sera are placed in the wells of the
microscope slide.
 FITC-labeled antihuman antibody is
added.
 Fluorescent reactions are graded 1 to
4+.
  Laboratory tests through transfusion of
VIRAL HEPATITIS - Aspartate aminotransferase (AST) contaminated blood products,
SEROLOGY and especially alanine
aminotransferase (ALT) levels are
hemodialysis, intravenous drug
use, contaminated needle
A. Hepatitis Testing increased and peak before jaundice sticks, tattooing, acupuncture,
occurs. or ear piercing.
 Testing for antibodies and antigens in - Other findings include - High-risk groups for acquiring
patient sera can determine the hyperbilirubinemia, decreased HBV infection include
responsible virus, stage of infection, and albumin, tea-colored urine, and intravenous drug users, men
immune status of patient. pale-colored stools. who have sex with men,
 The most widely used test method is - Paired sera (acute collected at hemodialysis patients, and
ELISA. onset of symptoms and healthcare workers.
convalescent 3-4 weeks later) are  Clinical manifestations
B. Hepatitis A
analyzed for an increase in anti-HAV - Incubation period is 50-180
 Hepatitis A virus (HAV): Member of the antibodies. Alternatively, a single days.
family Picornaviridae acute sample with a higher titer of - Symptoms develop abruptly
 Epidemiology IgM compared to IgG is considered and include fever, anorexia,
- Transmission by fecal-oral route diagnostic of an acute infection. vomiting, fatigue, malaise,
- Epidemics occur through fecal - Anti-HAV antibodies are present at jaundice, and arthralgia.
contamination of food or water. onset of symptoms and for years - Long clinical course: Acute
 Clinical manifestations afterward. infection can last up to 6
- Infections may be asymptomatic or months. Most patients recover
symptomatic; infections in children
C. Hepatitis B within 6 months.
are usually asymptomatic.  Hepatitis B virus (HBV) - Approximately 5% of infected
- Incubation period is 10-50 days. - Partially double-stranded DNA patients develop a chronic
- Symptomatic infections - Member of the family infection, in which the patient
 Symptoms include fever, anorexia, Hepadnaviridae remains hepatitis B surface
vomiting, fatigue, abdominal pain, and - Dane particle: Complete HBV antigen (HBsAg) positive.
malaise. Patient may become jaundiced. virus (42 nm) that causes - If chronic infections are active,
Symptoms are more severe in pregnant infection severe damage to the liver
women.  Epidemiology occurs, which can result in liver
 Recovery occurs in 2-4 weeks. - The virus is transmitted via cirrhosis or hepatocellular
 Mortality rate is 0.1 %, and chronic mucous membranes (e.g., carcinoma.
disease rarely occurs. sexual contact) or wounds - All chronic carriers shed virus.
 Inactivated vaccines, first developed in contacting contaminated blood - A recombinant HBV vaccine is
1995, are recommended for travelers, and body fluids, or parenterally. recommended for healthcare
drug abusers, and children. Parenteral infection occurs workers. The Advisory
 Committee for Immunization during recovery. Anti-HBc IgG  Symptoms
Practices now recommends will persist for several decades. - Causes either acute or chronic
routine vaccination for all - At the end of the acute stage, disease
children in the U.S anti-HBe begins to rise and - The incubation period is 2-26
 Laboratory tests peaks about 2-16 weeks later. weeks.
- The first marker that appears at The concentration of this - Acute infections are asymptomatic
the end of the incubation antibody decreases slightly or mild—nausea, vomiting,
period is HBsAg. The during a person's lifetime but abdominal pain, fatigue, malaise,
concentration of the surface never disappears. and jaundice.
antigen continues to rise and - The last marker to appear is - Approximately 50-80% of cases
peaks about midway through anti-HBs. It appears at the end become chronic, with 25% leading
the acute infection. Presence of of the acute stage and the to cirrhosis.
this antigen indicates infectivity. beginning of the recovery stage. - About 20% of cirrhosis cases lead to
- Soon after HBsAg is detected in Its concentration peaks, then cancer.
the blood, hepatitis Be antigen plateaus during recovery and  Laboratory tests
(HBeAg) appears. HBeAg peaks never disappears. Presence of - Anti-HCV is diagnostic of HCV
at about the same time as the this antibody indicates infection.
surface antigen. HBeAg immunity. - Anti-HCV IgM does not distinguish
disappears about two-thirds of - In chronic infections, patients between acute and chronic disease
the way through the acute do not produce detectable because both IgM and IgG
infection phase. levels of anti-HBs, and HBsAg antibodies are detectable for years.
- The next marker to appear is persists. These patients become - ELISA tests have false positive
antibody to hepatitis B core chronic carriers of the virus and results, so the best test to use for
(anti-HBc), which begins to rise are at risk for cirrhosis and diagnosis is an immunoblot assay.
a couple weeks into the acute hepatocellular carcinoma.
infection. Anti-HBc peaks at the E. Delta Hepatitis
end of the acute infection stage D. Hepatitis C
 Hepatitis D virus (HDV)
after HBsAg is no longer  Hepatitis C virus (HCV) - Unclassified, single-stranded RNA
detectable and before antibody - Single-stranded RNA virus virus
to hepatitis B surface antigen - Member of the family Hepacivirus - Requires HBsAg from HBV infection
(anti-HBs) can be detected. This  Epidemiology to replicate and infect host
period is referred to as the - Parenteral transmission is most  Epidemiology
"core window." common. - Occurs worldwide
- The anti-HBc IgM antibody - Sexual and perinatal transmission of - Transmission is via the parenteral
peaks a few weeks after the the virus is less common. and transmucosal routes.
acute infection stage, then
disappears in about 6 months
  Symptoms HEPATITIS
- Coinfection occurs when patients
acquire HBV and HDV infections (Inflammation of the Liver)
simultaneously.
- Superinfection occurs in patients
with an established HBV infection
who acquire HDV infection;
superinfections can occur and
progress to chronic HBV/HDV
infection.
- Patients with chronic HBV/HDV
infection have poor prognoses
because of severe liver damage,
inflammation, and cirrhosis.
- Vaccination against HBV also
prevents HDV.
 Laboratory Tests
- Only HBsAg positive patients are
tested for HDV.
- HDV-Ag is the first marker to
appear, detectable about 1-4 days
before symptoms start.
- IgM anti-HDV appears next followed
by low levels of IgG anti-HDV.
- The switch to high levels of IgG anti-
HDV indicates past HDV infection.

Jaundice- condition in which the skin, whites

of the eyes and mucous membranes turn
yellow because of a high level of bilirubin, a
yellow-orange bile pigment.

Liver cirrhosis - condition in which your

liver is scarred and permanently
damaged.
 TYPES OF HEPATITIS

TRANSMISSION PREVENTION TREATMENT

Hepatitis A Eating contaminated food or drinking contaminated *Practicing good hygiene No treatment
water *Vaccine

Hepatitis B Through contact with the blood or bodily fluids of an *Practicing good hygiene Alphainterferon
infected person *Vaccine Peginterferon
*Blood screening

Hepatitis C Blood-to-blood contact *Practicing good hygiene Direct-acting antiviral drugs

*Avoid sharing needles, toothbrushes, razors
or nail scissors

Hepatitis D Contact with infected blood (only occurs in people *Hepatitis B vaccine Interferon
already infected with hepatitis B) *Avoid sharing needles, toothbrushes, razors
or nail scissors

Hepatitis E Eating contaminated food or drinking *Practicing good hygiene No treatment

contaminated water *Avoid drinking water that has come
from a potentially unsafe source