INFECTIOUS GASTROINTESTINAL

DISEASES
MICROBIOLOGY
 COMMON GI INFECTIOUS DISEASES

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 VIRAL HEPATITIS
• 5 Types of Viral Hepatitis:
1. Hepatitis Type A
2. Hepatitis Type B
3. Hepatitis Type C
4. Hepatitis Type D
5. Hepatitis Type E
 HEPATITIS A VIRUS (HAV)
• containing a linear single-stranded RNA genome.
• distinct member of Piconavirus, Hipatovirus.
• Stable to treatment with: - 20% ether
- acid (pH 1.0 for 2 hrs)
- heat (60◦C for 1 hr)
• Destroyed by: - autoclaving (121◦C for 20 min)
- boiling in water for 5 mn.
- dry heat (180◦C for 1 hr.)
- ultraviolet irradiation ( 1 min. at 1.1 watts)
- treatment with formalin (1:4000 for 3 days at 37◦C)
- treatment with chlorine (10115 ppm for 30 min)
• Heating food to above 85◦C (185◦C) for 1 min and disinfecting surfaces with sodium hypochlorite
(1:100 chlorine bleach) can inactivate the virus.
 HEPATITIS B VIRUS
• Classified as a Hepadnivirus.
• viral genome consists of partially double-stranded circular DNA.
• Consists of virus or serologic markers:
1. HBsAg
- the most numerous particles in the serum with several subtypes.
2. HBeAg
- indicates viral replication that circulates as soluble antigen in the serum.
3. HBcAg
- Hepatitis B core antigen
4. Anti-HBs (Antibody to HBsAg)
- indicates past infection with and immunity, presence of passive antibody from HBIG, or
immune response from HBV vaccine.
5. Anti-Hbe ( Antibody to HbeAg)
- presence in the serum of the carrier suggests lower titer of HBV
6. Anti-HBc (Antibody to HBcAg)
- indicates infection with HBV at some undefined time in the past.
 CONTINUATION

7. IgM anti-HBc (IgM class ntibody to HBcAg)

• Stability of HBsAg does not always follow with that of the HBV. However, both are stable at -
20◦C for more than 20 yrs. and to repeated freezing and thawing
• also is stable at 37°C for 60 minutes and remains viable after being dried and stored at 25°C
for at least 1 week.
• HBV (but not HBsAg) is sensitive to higher temperatures (100°C for 1 minute) or to longer
incubation periods (60°C for 10 hours).
REPLICATION OF HEPATITIS B VIRUS
 HEPATITIS C VIRUS (HCV)

• During a study and experiments, there were several non-A, non-B (NANB)
hepatitis agents that, based on serologic tests, were not related to HAV or
HBV. This was identified as HCV.
• is a positive stranded RNA virus,
• classified as family Flaviviridae, genus Hepacivirus.
• Common cause of posttransfusion hepatitis.
• majority (70–90%) develops chronic hepatitis, and many are at risk of
progressing to chronic active hepatitis and cirrhosis (10–20%).
• 1–5% of infected individuals, leads to hepatocellular carcinoma, which is
the fifth most common cause of cancer worldwide.
 HEPATITIS D VIRUS (HDV)

- HDV (delta agent) contains delta-Ag (HDAg) surrounded by an HBsAg envelope.

- No homology exists with the HBV genome.
- HDAg is the only protein coded for by HDV RNA and is distinct from the antigenic
determinants of HBV.
- is a defective virus that requires the HBsAg coat for transmission.
- is classified in the Deltavirus genus, which is not assigned to any virus family.
- The genome consists of single-stranded, circular, negative-sense RNA.
- is often associated with the most severe forms of hepatitis in HBsAg-positive
patients
 HEPATITIS E VIRUS (HEV)

• is transmitted enterically and occurs in epidemic form in developing

countries, where water or food supplies are sometimes fecally
contaminated.
• It was first documented in samples collected during the New Delhi outbreak
of 1955, after sewage contamination of the city’s drinking water supply.
• In 1978, an epidemic occurred in Kashmir India that resulted in an estimated
1700 deaths.
• the viral genome has been cloned and is a positive-sense, single-stranded
RNA.
• is classified in the virus family, Hepeviridae, in the genus Hepevirus.
• There is evidence of HEV or HEV-like infections in rodents, pigs, sheep, and
cattle in the United States, with occasional transmission to humans.
 HEPATITIS VIRUS INFECTION IN HUMANS

• These viruses attacks or infects the human liver thus named Viral Hepatitis.

• 8–10% of adult patients, viral hepatitis may persist or unresolved which is a

mild benign disease that may follow after acute hepatitis.
• 10 – 50% of chronic active hepatitis patients, HBV is detected.
• 1 – 2% of jaundiced patients with hepatitis B may have fulminant or
massive hepatocellular necrosis. It is 10 times more common in those
coinfected with HDV than in the absence of HDV.
• Both HBV and HCV have significant roles in the development of
hepatocellular carcinoma that may appear many years (15–60) after
establishment of chronic infection.
 CLINICAL FINDINGS

HEPATITIS A (also known as Infectious Hepatitis)

• Usual onset : abrupt; 2 – 4 weeks after infection.

• Duration: usually 8 weeks.
• Symptoms: nausea, vomiting, diarrhea, dark urine, fever, and abdominal pain (right upper
quadrant under the ribs).
• Route/Transmission: fecal-oral route; by eating food or drinking water contaminated with
HAV infected feces. Shellfish which have not been sufficiently cooked are relatively common
source.
• Relapses can occur 1–4 months after initial symptoms have resolved.
• Acute liver failure rarely occur and mostly in the elderly.
• Children often do not have symptoms when infected but they are still able to infect others.
• Complete recovery occurs in most hepatitis A cases.
• Fulminant hepatitis rarely occurs.
 CLINICAL FINDINGS
HEPATITIS B DISEASE (also known as Serum hepatitis)

* Is a potentially life-threatening liver infection caused by the Hepatitis B virus (HBV).

• A major global health problem.
• Onset: Insiduous.
• Transmission/Route: Parenteral by needlestick injury, tattoing, piercing and exposure to
infected blood and body fluids, such as saliva, menstrual, vaginal and seminal fluids. Sexual
transmission also, particularly in unvaccinated men who have sex with men and heterosexual
persons with multiple sex partners or contact with sex workers.
• Can be transmitted also from infected mother to child at birth or delivery (perinatal
transmission). Transmission may occur through the reuse of needles and syringes either in
healthcare settings or among persons who inject drugs. It can spread also during medical,
surgical and dental procedures.
• Extrahepatic manifestations include a transient serum sickness-like prodrome consisting of
fever, skin rash, and polyarthritis; necrotizing vasculitis (polyarteritis nodosa); and
glomerulonephritis.
• The outcome after infection with HBV varies, ranging from complete
recovery to progression to chronic hepatitis and, rarely, death from fulminant
disease.
• 65-85% in adults are inapparent. 90–95% of all patients
• recovering completely.
• 80–95% of infants and young children infected with HBV become chronic
carriers.
• Chronic carriers are at high risk of developing hepatocellular carcinoma.
• Fulminant hepatitis occasionally develops during acute viral hepatitis, within
the first 8 weeks of disease in patients without preexisting liver disease.
• 70-90% of cases is fatal especially after age 40.
• About 95% of newborns infected at birth become chronic carriers of the
virus, often for life
HEPATITIS C DISEASE (Posttransfusion Hepatitis)

• Onset : Insiduous
• Transmission/Route: Parenteral and mostly transfusion of contaminated blood.
• is usually clinically mild, with only minimal to moderate elevation of liver enzymes.
• Hospitalization is unusual, and jaundice occurs in fewer than 25% of patients.
• 70-90% 0f cases progress to chronic liver disease despite the mild nature of the disease.
• Most patients are asymptomatic, but histologic evaluation often reveals evidence of chronic
active hepatitis, especially in those whose disease is acquired after transfusion.
• 20-50% develop cirrhosis and are at high risk for hepatocellular carcinoma.
• End-stage liver disease associated with HCV is the most frequent indication for adult liver
transplants.
• Acute symptoms appear one to three months after exposure and last 2 weeks to 3 months.
• Born between 1945 and 1965, the age group with the highest incidence of hepatitis C
infection.
• Hepatocellular carcinoma is most likely to occur in adults who experienced HBV infection at a
very early age and became carriers. Therefore, for vaccination to be maximally effective
against the carrier state, cirrhosis, and hepatoma, it must be carried out during the first week
of life.
 LABORATORY FEATURES
• Liver biopsy permits a tissue diagnosis of hepatitis
• Liver Function Tests such as serum alanine aminotransferase (ALT), aspartate
aminotransferase (AST) and bilirubin, supplement the clinical, pathologic, and
• epidemiologic findings.

HEPATITIS A

• HAV can be detected in the liver, stool, bile, and blood of naturally infected humans
by immunoassays, nucleic acid hybridization assays, or PCR.
• Virus is detected in the stool from about 2 weeks before the onset of jaundice up to
2 weeks after.
• detection of IgM-specific antiHAV in the blood of an acutely infected patient
confirms the diagnosis of hepatitis A.
• Anti-HAV appears in the immunoglobulin M (IgM) fraction during the acute phase,
peaking about 2 weeks after elevation of liver enzymes and Anti-HAV IgM
 usually declines to nondetectable levels within 3–6 months.
• Anti-HAV IgG appears soon after the onset of disease and persists for decades.
• Enzyme-linked immunosorbent assay is the method of choice for measuring HAV antibodies.

HEPATITIS B

• High concentrations of HBV particles and highest communicability during the initial phase of
infection.
• HBsAg is usually detectable 2–6 weeks in advance of clinical and biochemical evidence of
hepatitis and persists throughout the active course of the disease.
• Appearance of High levels of IgM-specific anti-HBc in the serum is indicative of viral
replication.
• Antibody to HBsAg is first detected after the disappearance of HBsAg.
• HBeAg is replaced by anti-HBe, signaling the start of resolution of the disease.
• HBV chronic carriers are those in whom HBsAg persists for more than 6 months in the presence
of HBeAg or anti-HBe.
• Low titers of IgM anti-HBc in chronic HBsAg carriers.
• The most useful detection methods are enzyme-linked immunosorbent assay for HBV antigens
and antibodies and PCR for viral DNA.
 HEPATITIS C
* Enzyme immunoassays detect antibodies to HCV but do not distinguish
among acute, chronic, or resolved infection.
• 50-70% of patients, Anti-HCV antibodies can be detected at the onset of
symptoms
• Nucleic acid-based assays (eg, reverse transcription PCR) detect the
presence of circulating HCV RNA and are useful for diagnosis of acute
infection soon after exposure and for monitoring patients on antiviral
therapy.
• Because HDV depends on a coexistent HBV infection, acute type D infection
occurs either as a simultaneous infection (coinfection) with HBV or as a
superinfection of a person chronically infected with HBV.
• Because HDV depends on a coexistent HBV infection, acute type D infection
occurs either as a simultaneous infection (coinfection) with HBV or as a
superinfection of a person chronically infected with HBV.
• HDV superinfections may be associated with fulminant hepatitis.
 EPIDEMIOLOGY
Hepatitis A

• HAV is widespread throughout the world.

• Outbreaks of type A hepatitis are common in families and institutions, summer
camps, day care centers, neonatal intensive care units, and among military troops.
• HAV infections occur at an early age; most children in such circumstances become
immune by age 10 years. Clinical illness is uncommon in infants and children; disease
is most often manifest in children and adolescents, with the highest rates in those
between 5 and 14 years of age.
• Hemodialysis plays no role in the spread of hepatitis A infections to either patients
or staff.
 Hepatitis B

• HBV is worldwide in distribution.

• Health care personnel (medical and dental surgeons, pathologists, other physicians,
nurses, laboratory technicians, and blood bank personnel) have a higher incidence
of hepatitis and prevalence of detectable HBsAg or anti-HBs than those who have
no occupational exposure to patients or blood products.
• Hepatitis B infections are common among patients and staff of hemodialysis units.
• As many as 50% of the renal dialysis patients who contract hepatitis B may become
chronic carriers of HBsAg
 Hepatitis C

• Infections by HCV are extensive throughout the world.

• Other high-prevalence areas are found in South America and Asia. It is estimated
that there are more than 170 million chronic carriers worldwide who are at risk of
developing liver cirrhosis, liver cancer, or both—and that more than 3 million of them
are in the United States.
• Estimates of mother-to-child vertical transmission vary from 3% to 10%. Mothers with
higher HCV viral loads or coinfection with HIV more frequently transmit HCV. No risk
of transmission has been associated with breastfeeding.
• HCV was found in saliva from more than one-third of patients with HCV and HIV
coinfections.
• HCV has been transmitted by commercial intravenous immune globulin (IG)
preparations, including an outbreak in the United States in 1994.
• HCV can be transmitted to an organ transplant recipient from an HCV positive-
donor.
 Hepatitis D

• HDV infects all age groups. Persons who have received multiple transfusions,
intravenous drug abusers, and their close contacts are at high risk.
• Two epidemiologic patterns of delta infection have been identified.
• A. In Mediterranean countries, delta infection is endemic among persons
with hepatitis B, and most infections are thought to be transmitted by
intimate contact.
• B. In nonendemic areas, such as the United States and northern Europe,
delta infection is confined to persons exposed frequently to blood and blood
products, primarily intravenous drug users and individuals with hemophilia.
 TREATMENT
• Treatment of patients with hepatitis A, D, and E is supportive and directed at allowing
hepatocellular damage to resolve and repair itself.
• HBV and HCV have specific treatments, with some patients achieving viral clearance,
known as sustained virologic response.

A. Hepatitis B Treatment
- recommended for patients with chronic active hepatitis to prevent progression of liver
fibrosis and development of hepatocellular carcinoma.

I. First Line Therapy:

a. Pegylated Interferon alfa-2a
- can lead to approximately 25% rate of loss of HBV DNA

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 CONTINUATION
B. Entecavir
-is a guanosine analogue inhibitor of HBV polymerase, with treatment leading to 67%
undetectable HBV DNA in HBeAg-positive patients and 90% undetectable HBV DNA in HBeAg-
negative patients.

C. Tenofovir
-in a nucleotide analogue inhibitor of HBV reverse transcriptase and polymerase,
with response rates of 76% and 93% in HBeAg- positive and HBeAg-negative patients,
respectively.

II. Second-line Therapy

Telbivudine
- is a cytosine nucleoside analogue and inhibitor of HBV DNA polymerase.

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 CONTINUATION
III. Third-line agent
a. Lamivudine, also known as 3TC
b. Adefovir
- are nucleoside analog viral polymerase inhibitors.

B. Hepatitis C Treatment
• a. Pegylated interferon combined with ribavirin
- has been the standard treatment for chronic hepatitis C.
- Therapy is given for 24 or 48 weeks, depending on the viral genotype, with
cessation of therapy if sustained virologic response is unlikely to be achieved.
- This classical therapy leads to sustained virologic response in 30–35% of HCV
genotype 1 patients and 75–80% of genotype 2 or 3 patients.

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 CONTINUATION
b. First generation protease inhibitor drugs
1. telaprevir
2. boceprevir.

- These target the viral protease, which cleaves the translated viral polypeptide into functional
proteins.
- are given for HCV genotype 1 infections in combination with interferon and ribavirin, and
showed approximately 60–80% sustained virologic response rates, even in patients who failed prior
treatment.
-these drugs are quite toxic and selected viral resistance is a concern.

c. Second-generation HCV antivirals

- recently been approved for use based on clinical trials showing more than 90% sustained
virologic response.

1. Sofosbuvir - is a nucleotide analog HCV viral RNA polymerase inhibitor

2. Simepravir - is an HCV protease inhibitor.
-These drugs have less toxicity than first-generation antivirals, and greater efficacy.

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 CONTINUATION
d. Orthotopic liver transplantation - is a treatment for chronic hepatitis B and C end-stage
liver damage.
- Because donor livers are in such short supply, HBV- or HCV-positive livers may be
transplanted into seropositive recipients with end-stage liver disease.

PREVENTION AND CONTROL

- Viral vaccines and protective IG preparation are available against HAV and HBV.

A. Standard Precaution
- Include:

a. Maintaining personal hygiene like proper hand washing.

b. Using personal protective equipment (PPE)such as disposable gloves and mask,
nonporous protective gowns, goggles or face shield.
c. Work practice controls among others
d.Engineering controls such as isolating people from the hazard by providing sharps
containers for workers to immediately place needles after use or/and use of needles with safety
devices to help prevent needlestick injury.
 Hand washing

• Is one of the best ways to get rid or prevent the

spread of microorganisms in most situation.
• In hand washing with soap and water one should
rub the hands for at least 20 seconds or
equivalent to singing or humming the “Happy
Birthday” song from beginning to end twice.
• If soap and water are not readily available, you
can use alcohol-based hand sanitizer that
contains at least 60% alcohol. Although hand
sanitizers might not be effective when hands are
visibly dirty or greasy.

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 PREVENTION AND
CONTROL
Personal Protective Equipment

* Gloves should be used when handling all potentially infectious

materials and dispose properly of gloves to biohazard containers
and change gloves in between patients.
• Protective garments such as gowns should be worn and
removed before leaving the work area
• Masks and eye protection/face shield should be worn whenever
splashes or droplets from infectious material pose a risk
 PREVENTION AND CONTROL
Work practice controls among
others
• only disposable needles should be used;
• Change the way people work by creating a
culture of safety like avoiding recapping or
bending needles that may be
contaminated and promptly dispose used
needles in a sharp container
• work surfaces should be decontaminated
using a bleach solution;
• laboratory personnel should refrain from
mouth pipetting, eating, drinking, and
smoking in the work area.
 PREVENTION AND CONTROL
B. Hepatitis A

• HAV vaccine available is Formalin-inactivated HAV vaccines made from cell

culture-adapted virus provide prevention. These are safe, effective, and
recommended for use in persons more than 1 year of age.
• Routine vaccination of all children is now recommended, as is vaccination of
persons at increased risk, including international travelers, men who have sex with
men, and drug users.
• Immune (γ) globulin (IG) is prepared from large pools of normal adult plasma and
confers passive protection in about 90% of those exposed when given within 1–2
weeks after exposure to hepatitis A. Its prophylactic value decreases with time, and
its administration more than 2 weeks after exposure or after onset of clinical
symptoms is not indicated. This IG does not prevent infection but rather makes the
infection mild or subclinical and permits active immunity to develop.
• HAV vaccine has a more enduring immunity and should replace the use of Ig.
 PREVENTION AND CONTROL
C. Hepatitis B

• Available vaccine for HBV is the Recombinant DNA-derived vaccines which

currently used in the United States and locally also. Although some other
countries are still using plasma-derived vaccine.
• Recombinant DNA-derived vaccines consist of HBsAg produced by a
recombinant DNA in yeast cells or in continuous mammalian cell lines.
• Preexposure prophylaxis with hepatitis B vaccine currently is recommended
by the World Health Organization, the Centers for Disease Control and
Prevention, and the Advisory Committee on Immunization Practices for all
susceptible, at-risk groups.
• vaccine is recommended for all children as part of their regular immunization
schedule.
 PREVENTION AND CONTROL
• Hepatitis B vaccination is the most effective measure to prevent HBV and its
consequences. A comprehensive public health strategy exists to eliminate HBV
transmission. It involves universal vaccination of infants, routine screening of all
pregnant women for HBsAg, postexposure immunoprophylaxis of infants born to
HBsAg-positive mothers, vaccination of children and adolescents not previously
vaccinated, and vaccination of unvaccinated adults at increased risk for infection.
• hepatitis B immune globulin (HBIG)
• is not recommended for preexposure prophylaxis because the HBV
• vaccine is available and effective.
• Persons exposed to HBV percutaneously or by contamination of mucosal surfaces
should immediately receive both HBIG and HBsAg vaccine administered
simultaneously at different sites to provide immediate protection with passively
acquired antibody followed by active immunity generated by the vaccine.
• HBIG in preventing hepatitis B in infants born to HBV-positive mothers has been
recommended.
 PREVENTION AND CONTROL
Hepatitis C

• There’s no vaccine available.

• Control measures include screening and testing blood, plasma, organ, tissue,
and semen donors; virus inactivation of plasma-derived products; counseling
of persons with high-risk drug or sexual practices; implementation of infection
control practices in health care and other settings; and professional and
public education.

Hepatitis D

• Delta hepatitis can be prevented by vaccinating HBV- susceptible persons

with hepatitis B vaccine. However, vaccination does not protect hepatitis B
carriers from superinfection by HDV.
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