Gastrointestinal Microbiology: Gastritis & Helicobacter

• The topic is a theoretical revision of microbiology of the gastrointestinal system

Gastritis

• Helicobacter pylori is the most important pathogen

Helicobacter Pylori Characteristics

• Helicobacters are motile, curved, Gram-negative bacilli
• Virulence factors include urease, cytotoxin-associated antigen (CagA), and vacuolating toxin (VacA)
• Urease generates ammonia from urea to neutralize stomach acid, allowing the organism to survive
• Cytotoxin-associated antigen (CagA) is associated with increased risk of both peptic ulcer and gastric malignancy
• Vacuolating toxin (VacA) forms pores in host cell membranes

Helicobacter Pylori Diagnosis and Clinical Manifestations

• Diagnosis includes clinical manifestation and laboratory diagnosis
• Patients with gastritis may experience dyspepsia (epigastric pain, burning), nausea, and vomiting; some may be asymptomatic
• Patients with peptic ulcer experience epigastric pain, which may be alleviated by food, especially in duodenal ulcers; a complication is gastrointestinal bleeding
• Laboratory diagnosis includes the urea breath test, stool antigen test, and urease test on biopsy specimen
• The urea breath test involves ingesting radiolabeled urea; if the organism is present, urease will cleave the urea, radiolabeled CO₂ is evolved, and radioactivity is detected in the breath
• Stool antigen test is used for diagnosis and follow-up of successful treatment
• Urease test is performed on the biopsy specimen
• Upper endoscopy with gastric biopsy is the definitive diagnostic strategy

Acute Diarrhea Mechanisms

• Acute diarrhea can be caused by disruption of normal absorption and secretory processes in the small intestine by either:
  • Preformed exotoxins in food such as Staph. Aureus and Bacillus cereus
  • Infectious agents in the intestinal tract, such as mucosal invasion, or production of enterotoxin or cytotoxin

Characteristics of Watery Diarrhea vs. Bloody Diarrhea

• Watery diarrhea is characterized by the absence of red or white blood cells in stool (no inflammation), typically is afebrile, has large volume, and located in small intestine
• Bloody diarrhea typically contains both red and white blood cells in stool, is inflammatory, is often febrile, has small volume, and located in the colon

Organisms that cause diarrhea

• Organisms that cause watery non-inflammatory diarrhea:
  • Enterotoxigenic Escherichia coli
  • Vibrio cholerae
  • Staphylococcus aureus
  • Bacillus cereus
  • Clostridium perfringenes
• Organisms that cause bloody (inflammatory) diarrhea:
  • Shiga toxin-producing E. coli (STEC) (0157:H7 serotype)
  • Shigella species
  • Salmonella
  • Campylobacter jejuni
  • Clostridium difficile
  • Yersinia enterocolitica

Campylobacter jejuni

• Curved, Gram-negative bacilli (comma- or S-shaped), microaerophilic (5% oxygen), oxidase positive, motile with single polar flagellum
• Grows well at 42°C
• Is a frequent cause of enterocolitis, especially in children

Campylobacter jejuni: Transmission

• Campylobacter jejuni reservoirs include domestic animals e.g. cattle, chickens and dogs
• Mode of transmission includes fecal-oral, ingestion of contaminated food and water with animal feces
• Food commonly involved is undercooked poultry, meat and unpasteurized milk
• Human to Human transmission occurs but less frequent

Campylobacter jejuni: Clinical manifestations

• Inflammation of the intestinal mucosa often occurs, accompanied by blood in stools (Bloody diarrhea)
• Clinical manifestations include watery, foul-smelling diarrhea followed by bloody stools
• Fever and severe abdominal pain.
• Associated with Guillain-Barré syndrome, and Reactive arthritis and Reiter's syndrome

Escherichia coli in the GIT

• Major groups of diarrhea-causing Escherichia coli can be:
  • Enterotoxigenic E. coli (ETEC)
  • Enterohemorrhagic E. coli (EHEC)
  • Enteropathogenic E. Coli (EPEC)
  • Enteroinvasive E.Coli (EIEC)
  • Enteroaggregative E. coli (EAEC)
• ETEC produce enterotoxin LT/ST, are found in the small intestine, leads to watery diarrhea, is also referred to as travelers diarrhea
• EHEC produces shiga toxin, is found in the large intestine, leads to bloody diarrhea, and may cause hemolytic uremic syndrome
• EIEC involves invasion of epithelium in the large intestine and causes bloody diarrhea
• EPEC adhere to and eliminate surrounding microvilli, are found in the small intestine, leads to watery diarrhea, also referred to as infantile diarrhea
• EAEC adhere and produces an enterotoxin, are found in the small intestine, and lead to watery diarrhea also referred to as traveller's diarrhea

Enterotoxigenic E. coli (ETEC)

• Acquired by ingestion of food or water contaminated with human feces
• Produces enterotoxins (heat-labile toxin (LT), heat-stable toxin (ST)
• The heat-labile toxin (LT) stimulates adenylate cyclase, resulting in increase in intracellular (cAMP)
• The heat-stable toxin (ST) stimulates guanylate cyclase and leads to an increase of intracellular (cGMP)
• Both cAMP and cGMP causes loss of fluid and ions (potassium, chloride) from the enterocytes into the lumen of the gut, resulting in watery diarrhea

Enterohemorrhagic E. coli (EHEC)

• The main reservoir is cattle, and the organism is acquired in undercooked beef e.g., in hamburgers
• Shiga-toxin-producing E. coli (STEC) (0157:H7 serotype) produces Shiga toxin which acts by inhibiting protein synthesis
• Diarrhea caused by O157:H7 strains with antibiotics e.g., ciprofloxacin, increases the risk of hemolytic uremic syndrome in children (increase the amount of Shiga toxin released by the dying bacteria)
• Therefore, antibiotics should not be used to treat diarrhea caused by EНЕС

Food Poisoning: Organisms and Toxins

• Food poisoning can be caused by the following organisms and toxins
• S. aureus produces an enterotoxin, is a superantigen, onset is after 1-8 hours, causes vomiting which is more prominent than diarrhea
• C. perfringenes produces an enterotoxin, is a superantigen, onset is after 8-16 hours, causes watery diarrhea with cramps and little vomiting
• C. botulinum produces a toxin that blocks release of acetylcholine at nerve synapses onset is after 18-24 hours, causes descending weakness and paralysis and no vomiting or diarrhea
• B. cereus produces TWO enterotoxins:
  • emetic form with onset after 4 hours causes emetic form
  • diarrheal form with onset after 18 hours causes diarrheal form

staphylococcus aureus

• Ingestion of enterotoxin mostly formed in foods e.g. dairy products, carbohydrate foods
• Short incubation period (1-8hrs)
• Enterotoxin: acts as a superantigen and stimulates the Vomiting center in brain
• Vomiting is more prominent than diarrhea

staphylococcus aureus: Diagnosis

• Diagnosis involves clinical manifestations, vomiting, epigastric pain, diarrhea
• There are laboratory diagnosis methods like detecting the toxin in food and stool samples
• Treatment involves supportive care

Clostridium perfringenes characteristics

• Spores are widespread in soil and can contaminate food
• The heat-resistant spores survive cooking and germinate
• The organisms grow to large numbers in reheated foods (MEAT dishes)
• C. perfringenes enterotoxin (superantigen) cause diarrhea

Clostridium botulinum Botulism

• Ingestion of canned food (e.g. alkaline vegetables & smoked fish) containing the preformed Botulinum toxin
• Toxin blocks the release of acetylcholine at nerve synapses
• Botulism is a severe form of food poisoning characterized by neurotoxic effects

Clostridium botulinum Botulism: Diagnosis

• Symptoms begin 18–24 hrs after ingestion of the toxic food. -Descending weakness and paralysis
• (diplopia, dysphagia, and respiratory muscle failure).
• Botulinum toxin is demonstrable in uneaten food and the patient's serum by mouse protection tests, enzyme-linked immunoassay (EIA) tests or PCR.

Clostridium botulinum Botulism: Treatment and preventative measures:

• treatment,The heptavalent antitoxin containing all seven types (A to G) is preferred to the trivalent antitoxin containing types A, B, and E, -and also respiratory support is suggested
• As a preventative measure proper sterilization of all canned and vacuum-packed foods is needed
• Foor must be adequately cooked to inactivate toxin
• Swollen cans must be discarded

Clostridium difficile

• Anaerobic, spore forming Gram-positive bacilli that causes antibiotic-associated pseudomembranous and is most common cause of hospital-acquired diarrhea
• Organism is carried in gastrointestinal tract approximately 3% of general population, and up to 30% of hospitalized patients -C difficile releases toxins that damage the colon and may lead to pseudomembrane formation with Virulence Factor: Exotoxins A and B (Cytotoxin causes death of enterocytes)

Clostridium difficile: Diagnosis and Treatment

-Symptoms include diarrhea (usually not bloody, with neutrophils found in stool), fever and abdominal pain. -Pseudomembranes can be visualized by sigmoidoscopy. -Laboratory diagnosis involves detecting exotoxins in stool samples.

• Treatment and Prevention: Treatment includes stopping the causative antibiotic and potentially vancomycin. Monoclonal antibodies against exotoxin B are effective in preventing relapses. Prevention focuses on only prescribing antibiotics when needed and strict infection control procedures in hospitals

Shigella

• Has shiga toxin which inhibits proteins with hemolytic uremic symdrome
• Reservoir: human, and Transmitted thru Fecal route

Viral infections of GIT:

• Common modes of gastrointestinal infections: - salivary glands infection(Mumps virus), small intestinal infection(Reoviruses and Caliciviruses, and Liver infection(Hepatitis virus)

Infection of Salivary Glands(Mumps virus)

• Mumps, a disease characterized by salivary gland swelling, occurs in childhood
• Structure: the(MuV) is a member of Paramyxoviridae family a Ve sense SS RNA virus enveloped, with two spikes hemagglutinin HA, single serotype, and Respiratory droplets antibody against HA
• Mode of transmission : Respiratory droplets
• I P: 18-21 days.
• Clinical Features (C/P) of Mumps: Prodnormal stage with (Fever, malaise, anorexia), or Tender swelling of the salivary glands or (unilateral or bilateral) with a virus ➔ upper respiratory bloodstream-glands. (Parotid gland, Testes, Ovaries, Pancreas and Meninges).

Complications of Mumps

• Orchitis, is bilateral can result in Sterility
• Meningitis, where selflimited
• For a lab diagnosis, diagnosis is clinically (but lab tests are useful), PCR is also detectable to detect viral nucleic acid also specimen (Saliva, spinal fluid , and Urine and cell culture is used for isolation
  • Serologic tests like detection antibody(I gM or four fold rising titer of I gG
• Treatment can managed with Antiviral There is no anti viral therapy for mumps MMR VACCINATION Infection is one time in life, Active immunization:MMR vaccine that is live attenuated ,Trivalent vaccine : Measles + Mumps+ Rubella(MMR0 and two vaccine is done approximately at 1.3 years and 5 years and last is 10 yr dose

GASTROENTERITIS

Common in Viral

• Acute watery diarrhea can be due, viruses, and 2 to 3 viral cases (fever, vomiting, diarrhea with out blood or pus Common causes: Rota virus, Calci, adino ,astro

ROTA VIRUS

Member of Reovirrirdial family cause high infections in kids At least 6 serotypes of Rotavirus

• It is segmented virus that is surrounded by Double layer protein coat that has wheel shape (Ag that cause type specicfic Mode of transmission route (fecal route to get into human gut)

Rota features:

High Diarrheal with vomit and cause Nausa Imbalance electrolytes, with De hydration and high fevers PCR : Test with RNA to do Viral load, and if high then its high Viral presence. ELISA.

PREVENTION ROTA

-immunizations: and is is Live vaccine that is Two vaccinations: First shot Rotarix, 2 shot- Rotatega They cause a sickness called intussusception. Oral rehydration to treat dehydration and electrolyte imbalance

2- CALICIVIRUSES

Is called No virus the virus, and calici that attack family. Is just called one name the Norwalk virus name Structure for, RNA and is nonenveloped and Transmission is in the fecal contaminated gut to swallow. In other hands causes diarrhea without any signs and Pathogenesis.

Feature of calcic:

Diarrhea, low key feve,r belly ache and symptoms are usually asymptom and and is diagnosis is clinically with RTPCR and that is that Treatments are hygiene based hand and sewage ( There are no known antibiotics or vaccines)

• Hepatitis is high liver inflammatory that affect fecal

Types Of Hepatitis

A: picarnoviridae, Bhepatic and all have have symptoms: Loss appetite , Diarrhea, Nausea (sickness) Fatigue Jaundice (yellow skin which is the highest indicator and A is for 6 weeks of damage and cause liver cancer Hepatitis B is sexual and needle (Cirrhosis of Liver, and can it cause Liver Cancer? If its A symptomatic then cause Fulminant Liver Failure and pregnancy Hepatitis C that is the most blood type ,Liver Cirrhosis? cause Liver Cancer? Flu Like can cause more Fulmanant with progression to cirrhosis and is Contaminated Needles) and is higher if it has no Immune system. Medical and is Hepatitis D that has hepatitis B causes Liver failure, but Medical Hepatitis E feco route and High fatal for pregenency

Structure of Hepatitis A

• Fecal route due to contaminated food Incubations is asymptomatic and last weeks Liver damage is tested when test the enzyme To detect you can test ELISA or serum tests, that test antibodies and if its IgM is an acute cases Vaccine for HA is inactivated, and inactivated virus, two doses Indicated to for travler and II twin for HBV and and for HA immunogloben and proper Hygiene

Hepatitis E-type

Mot is Fecal

HBV Structure

• HBsAg Its is the vaccine presence that last 6 mnths
• HBcAg
• HBeAC Hbv happens when your body goes thru injuries or needles And is sexually by mother birth if trans placid Hepatitis D virus. HD v uses HBV to function properly and can be contracted by getting multiple shots without properly cleaning needle. Causes a coinfection and can cause infection.