Infections of gastrointestinal tract

Done by : Walaa Alzatari

Supervised by : Hasan Adi
 Outlines
• Viral hepatitis
• Botulism
• Intraabdominal abscess
• Pseudomembranous colitis
VIRAL HEPATITS
 Hepatitis simply means inflammation of the liver.

 Infectious types hepatitis A, B, C, D, and E.

 Other viruses that can cause one form or another of hepatitis are EBV,
CMV, and HSV These are not commonly associated with hepatitis in
immunocompetent patients.

 Noninfectious types of hepatitis, such as alcoholic hepatitis, drug-induced

hepatitis, autoimmune hepatitis, and numerous hereditary diseases that
can cause hepatitis.
 Clinical features
 classified as acute(<6months of liver inflammation) or chronic (>6months of persistent
liver inflammation).

 Acute hepatitis has a wide spectrum of clinical presentations (asymptomatic to fulminant

liver failure)

 GENERAL CLINICAL FEATURES

1. Jaundice-look first in the sclera, because this may be the first place jaundice can be
detected, especially in black patients
2. Dark-colored urine may be present (due to conjugated hyperbilirubinemia)
3. RUQ pain
4. Nausea and vomiting
5. Fever and malaise
6. Hepatomegaly may also be present
 In severe cases, acute hepatitis may result in liver failure and its
complications. This is known as fulminant hepatitis (uncommon) and
may be life-threatening. It occurs more commonly in hepatitis B, D, and
E than in other types.

 COMPLICATIONS INCLUDE:
o Hepatic encephalopathy-Look for asterixis and palmar erythema
o Hepatorenal syndrome
o Bleeding diathesis-this occurs only when liver function is very
compromised

 Sometimes acute hepatitis may only present with transient flu-like

symptoms such as fever, myalgias, and malaise
 Acute HBV may also present with a serum sickness-like illness(rash,
fever and polyarthritis)
 Hepatitis C typically does not cause significant acute illness
 Chronic hepatitis also has a wide variety of presentations. Some patients are
asymptomatic ("chronic carriers") and may only present with late complications of
hepatitis, such as cirrhosis or hepatic cell carcinoma (HCC)
 Diagnosis
1. Serum serology-the presence of serum antigens and immunoglobulins is the
most important factor for diagnosing viral hepatitis. (acuity or chronicity) .
2. PCR is used to detect viral RNA to diagnose HCV.
3. LFTs-Elevation of serum transaminases is not diagnostic, but LFTs are helpful.
a. ALT (SGPn is typically elevated more than AST (SGOT) for all forms of viral
hepatitis (the opposite of alcoholic hepatitis).
4. In acute hepatitis, ALT is usually >1,000. It is generally not as high as in
druginduced hepatitis. c. In chronic HBV. ALT can also be >l,000, but this varies.
In chronic HCV, ALT is generally lower than this due to destruction of
hepatocytes from longevity of disease
5. AST:ALT ratio < 1 in acute infection ,AST:ALT ratio > 1 in chronic hepatitis may
be a sign of cirrhosis
6. Abdominal ultrasound (to evaluate liver parenchyma and biliary tract and screen
for fibrosis and/or HCC)
7. Liver biopsy
 Treatment
Active (vaccine) and passive (immunoglobulin)
immunization are available for both hepatitis A and
B. It is the standard of care for infants and
healthcare workers to be vaccinated for HBV .
Travelers often receive vaccinations for HAV.
Passive immunization can be given for people who
are exposed to the virus.
Treatment for hepatitis A and E is supportive.
 Hepatitis B Treatment
 All patients
1. Provide supportive care and patient education as needed.
2. Consider referral for liver transplantation in patients with:
• End-stage liver disease due to HBV
• Fulminant hepatic failure (emergency transplantation)
 Acute hepatitis B
• Antiviral therapy is generally not indicated.
 Chronic hepatitis B
• Assess the need for antiviral therapy.
 Indications for antiviral therapy for chronic HBV infection include:
1. Cirrhosis or advanced fibrosis
2. Acute liver failure
3. Immune active phase: ALT ≥ 2× ULN plus significantly
elevated HBV DNA levels with or without HBeAg
4. HBV reactivation
5. Coinfection with HCV or HIV

 Agents:
1. Nucleotide reverse transcriptase inhibitors (NtRTIs),
e.g., tenofovir disoproxil fumarate (TDF) or tenofovir
alafenamide (TAF)
2. Nucleoside reverse transcriptase inhibitors (NRTIs),
e.g., entecavir (ETV)
3. Pegylated interferon alfa (PEG-IFN-α)
 Hepatitis C Treatment
• HCV infection is always treated with a multidrug approach .
Example regimens(direct acting antiviral agent)
• Ledipasvir PLUS sofosbuvir .
• Interferon PLUS ribavirin (Was the preferred treatment before the
development of DAAs):
 Associated with severe adverse effects
(e.g., arthralgias, thrombocytopenia, leukopenia, depression, anemia)
and teratogenicity
 Contraindicated in patients with decompensated cirrhosis (high risk of
worsening cirrhosis decompensation)
 Hepatitis C is the most frequent indication for liver transplantation in the
United States
 Vaccination
• is an inactivated recombinant vaccine that
BOTULISM
 Results from ingestion of preformed toxins produced by spores of
Clostridium botulinum.
 Improperly stored food (e.g., home-canned foods) can be contaminated
with these spores. Toxins can be inactivated by cooking food at high
temperatures (e.g., 100°C [212°F] for 10 minutes).
 Wound contamination is another source.
 Inhalation botulism has been reported in laboratory workers but is not a
common occurrence. Could be a possible bioterrorism weapon.
 Clinical features
 The severity of illness ranges widely, from mild, self-limiting
symptoms to rapidly fatal disease.
 Abdominal cramps, nausea, vomiting, and diarrhea are common.
 The hallmark clinical manifestation is symmetric, descending flaccid
paralysis. It starts with dry mouth, diplopia, and/or dysarthria.
Paralysis of limb musculature occurs later.
 Diagnosis
 Initial diagnosis is based on clinical symptoms. Treatment should not
wait for laboratory confirmation.
 Laboratory confirmation is done by demonstrating the presence of
toxin in serum, stool, or food, or by culturing C. botulinum from stool, a
wound or food.
 Routine lab tests (CBC, electrolytes, LFTs, urinalysis) are generally not
helpful in diagnosis as these tests show no characteristic
abnormalities.
 Normal CTs and MRIs help to rule out CVA.
 Treatment
 Admit the patient and observe respiratory status closely Gastric
lavage is helpful only within several hours after ingestion of
suspected food.
 If suspicion of botulism is high, administer antitoxin (toxoid) as soon
as laboratory specimens are obtained (do not wait for the results).
 For contaminated wounds--(in addition to the above) wound
cleansing and penicillin.
INTRAABDOMINAL ABSCESS
 intra-abdominal abscess is a collection of pus or infected fluid that is surrounded by
inflamed tissue inside the belly., are classified as intraperitoneal, retroperitoneal, or
visceral
 CAUSES INCLUDE :
 spontaneous bacterial peritonitis, pelvic infection (e.g., tubo-ovarian abscess),
pancreatitis, perforation of the GI tract, and osteomyelitis of the vertebral bodies
with extension into the retroperitoneal cavity
 Abdominal surgery, particularly that involving the digestive or biliary tract, is a
significant risk factor.
 The infecting organisms typically reflect normal bowel flora and are a complex
mixture of anaerobic and aerobic bacteria. Most frequent isolates are:
• Aerobic gram-negative bacilli (eg, Escherichia coli and Klebsiella)
• Anaerobes (especially Bacteroides fragilis)

 Usually polymicrobial in origin.

 Clinical features
 most abscesses cause fever and abdominal discomfort ranging from
minimal to severe (usually near the abscess). Paralytic ileus, either
generalized or localized, may develop. Nausea, anorexia, and weight loss
are common.
 Subphrenic abscesses may cause chest symptoms such as nonproductive
cough, chest pain, dyspnea, hiccups, and shoulder pain. Rales, rhonchi, or
a friction rub may be audible.
 Generally, there is tenderness over the location of the abscess. Large
abscesses may be palpable as a mass.
 Complications of intra-abdominal
abscesses
 Undrained abscesses may extend to contiguous structures, erode into
adjacent vessels (causing hemorrhage or thrombosis), rupture into the
peritoneum or bowel, or form a cutaneous or genitourinary fistula.
 Subdiaphragmatic abscesses may extend into the thoracic cavity, causing
an empyema, lung abscess, or pneumonia.
 An abscess in the lower abdomen may track down into the thigh or
perirectal fossa.
 Splenic abscess is a rare cause of sustained bacteremia in endocarditis
that persists despite appropriate antimicrobial therapy.
 Diagnosis
 CT of the abdomen and pelvis with oral contrast is the preferred
diagnostic modality for suspected abscess.
 plain abdominal x-rays may reveal extraintestinal gas in the abscess,
displacement of adjacent organs, a soft-tissue density representing the
abscess, or loss of the psoas muscle shadow.
 A complete blood count and blood cultures should be done. Leukocytosis
occurs in most patients, and anemia is common
 Treatment
 Drainage: Percutaneous or surgical
 IV antibiotics (are not curative but may limit hematogenous
spread and should be given before and after intervention)
PSEUDOMEMBRANOUS COLITIS
 antibiotic-associated colitis because many patients do not have grossly
visible pseudomembranes.
 Antibiotic treatment kills organisms that normally inhibit growth of
Clostridium diffidle, leading to overgrowth of C. difficile and toxin
production.
 Almost all antibiotics have been associated, but the most frequently
implicated antibiotics are clindamycin, ampicillin, and cephalosporins.
 Symptoms usually begin during first week of antibiotic therapy. However,
up to 6 weeks may elapse after stopping antibiotics before clinical findings
become apparent.
 Clinical features
1. Profuse watery diarrhea, usually without blood or mucus
2. Crampy abdominal pain
3. Toxic megacolon (in severe cases) with risk of perforation

 Disease severity can be classified as mild-moderate, severe, or

fulminant depending on the WBC count, serum creatinine, and
presence of hypotension/shock, ileus, or megacolon.
 Diagnosis
 Demonstration of C. difficile toxins in stool is diagnostic, but results
take at least 24 hours (95% sensitivity).
 Flexible sigmoidoscopy is the most rapid test and is diagnostic, but
because of discomfort/expense, it is infrequently used (usually
reserved for special situations).
 Abdominal radiograph is used to rule out toxic megacolon and
perforation.
 Leukocytosis is very common.
 Treatment
 Discontinue the offending antibiotic, if possible.
 Initial episode
• if mild-moderate or severe: vancomycin or fidaxomicin.
• if fulminant: vancomycin. If ileus is present, add metronidazole.
Subtotal colectomy or diverting loop ileostomy with colonic lavage
may be necessary
 First recurrence: vancomycin or fi.daxomicin
 Second or subsequent recurrence: vancomycin, fidaxomicin, or fetal
microbiota transplantation
 Regardless of choice of antibiotic, 15% to 35% of successfully
treated patients will have recurrence may occur within 2 to 8 weeks
after stopping the antibiotic. This occurs in 15% to 35% of
successfully treated patients.