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Microbiology of the GIT Ziad Elnasser, MD, Ph.D


Introduction      

Food borne illnesses. Acute diarrhea, vomitting (food poisoning) Non food causes. GIT as a vehicle only. Fecal oral mode. Toxins of Microorganisms. ■ Enterotoxins. ■ Cytotoxins. ■ Neurotoxins.

Normal flora, bowel motility, immunity.


Types of foods associated with various pathogens that cause food poisoning.

TYPES OF FOODS ASSOCIATED WITH VARIOUS PATHOGENS THAT CAUSE FOOD POISONING

Pathogen

Foods

Staphylococcus aureus

Cream pastries, salads, meat products, cold foods

Bacillus cereus

Fried rice, vegetables, meat dishes, vanilla sauce

Clostridium perfringens

Cooked meats, gravies

Vibrio cholerae, Vibrio parahaemolyticus, Vibrio vulnificus

Shellfish, seafood

Campylobacter jejuni

Milk, poultry

Salmonella enteritidis

Eggs, poultry, other meats

Shigella spp.

Salads, milk, cold foods

Yersinia enterocolitica

Milk, pork products

Escherichia coli

Ground beef, milk, lettuce, unpasteurized cider

Listeria monocytogenes

Soft cheese, patĂŠ, milk, coleslaw

Clostridium botulinum

Meats, home-canned fruit and vegetables

Hepatitis A and enteric viruses

Shellfish, various foods


Micro-organisms associated with water-borne infections. MICRO-ORGANISMS ASSOCIATED WITH WATER-BORNE INFECTIONS

Bacteria

Vibrio cholerae Vibrio parahaemolyticus Campylobacter jejuni Shigella spp. Escherichia coli (especially enterotoxigenic Escherichia coli)

Viruses

Rotavirus Norwalk virus Small round-structured viruses Hepatitis A virus Hepatitis E virus

Protozoa

Giardia lamblia Entamoeba histolytica Cryptosporidium parvum Isospora belli Cyclospora cayetanensis Microsporidia spp. Dientamoeba fragilis Balantidium coli


Enterobacteriacae       

General properties. O, K, and H antigens. Toxins. Apportunistic infections. Intestinal infections: Salmonella, Shigella, Yersinia enterocolitica, and certain E. coli. Dysentry, watery diarrhea, and Enteric fever. Pathogenesis, Immunity, Diagnosis, and Treatment.




E. Coli intestinal infections 

Based on their virulence properties. ETEC.  EPEC.  EIEC.  EHEC.  EHEC. 





Shigella General properties.  Classification.  Epidemiology.  Pathogenesis.  Clinical presentation.  Diagnosis.  Treatment.  Prevention. 



Salmonella

Bacteriology.  Epidemiology  Pathogenesis.  Immunity.  Typhoid fever. 




Yersinia

Bacteriology  Epidemiology  Pathogenesis  Clinical manifestations 







Viruses of Diarrhoea Ziad Elnasser, MD, Ph.D


Viral Gastroenteritis   

It is thought that viruses are responsible for up to 3/4 of all infective diarrhoeas. Viral gastroenteritis is the second most common viral illness after upper respiratory tract infection. In developing countries, viral gastroenteritis is a major killer of infants who are undernourished. Rotaviruses are responsible for half a million deaths a year. Many different types of viruses are found in the gut but only some are associated with gastroenteritis


Viruses found in the gut (1) A. Associated with gastroenteritis  

     

Rotaviruses Adenoviruses 40 41 Caliciviruses Norwalk like viruses or SRSV (Small Round Structured Viruses) Astroviruses SRV (Small Round Viruses) Coronaviruses Toroviruses


Viruses found in the gut (2) B. Found in the gut, not normally associated with gastroenteritis  Polio  Coxsackie A  Coxsackie B  Echo  Enteroviruses 68-71  Hepatitis A  Hepatitis E  Adenoviruses 1-39  Reoviruses C. Found in the gut as opportunistic infection  CMV  HSV  VZV  HIV


Rotavirus Particle


Rotaviruses (1) 

Naked double stranded RNA viruses, 80 nm in diameter

also found in other mammals and birds, causing diarrhoea

account for 50-80% of all cases of viral gastroenteritis

usually endemic, but responsible for occasional outbreaks

causes disease in all age groups but most severe symptoms in neonates and young children. Asymptomatic infections common in adults and older children. Symptomatic infections again common in people over 60

up to 30% mortality rate in malnourished children, responsible for up to half a million deaths per year


Rotaviruses (2) 

80% of the population have antibody against rotavirus by the age of 3

more frequent during the winter

faecal-oral spread. ? respiratory droplets

24-48 hr incubation period followed by an abrupt onset of vomiting and diarrhoea, a low grade fever may be present.

diagnosed by electron microscopy or by the detection of rotavirus antigens in faeces by ELISA or other assays.

Live attenuated vaccines now available for use in children


Calicivirus Particles


Caliciviruses     

small RNA viruses, characteristic surface morphology consisting of hollows. particles 35 nm in diameter associated mainly with epidemic outbreaks of gastroenteritis, although occasionally responsible for endemic cases like Norwalk type viruses, vomiting is the prominent feature of disease majority of children have antibodies against caliciviruses by the age of three. diagnosed by electron microscopy only, often difficult to diagnose because of small size.


Norwalk-like Virus Particles


Norwalk-like Viruses   

 

small RNA viruses, with ragged surface, 35 nm in diameter, now classified as caliciviruses always associated with epidemic outbreaks of gastroenteritis, adults more commonly affected than children associated with consumption of shellfish and other contaminated foods. Aerosol spread possible as well as faecal-oral spread Also named "winter vomiting disease", with vomiting being the prominent symptom, diarrhoea usually mild Antibodies acquired later in life, in the US, only 50% of adults are seropositive by the age of 50. diagnosis is made by electron microscopy and by PCR.


Adenovirus Particle


Enteric Adenoviruses     

 

Naked DNA viruses, 75 nm in diameter. fastidious enteric adenovirus types 40 and 41 are associated with gastroenteritis associated with cases of endemic gastroenteritis, usually in young children and neonates. Can cause occasional outbreaks. possibly the second most common viral cause of gastroenteritis (715% of all endemic cases) similar disease to rotaviruses most people have antibodies against enteric adenoviruses by the age of three diagnosed by electron microscopy or by the detection of adenovirus antigens in faeces by ELISA or other assays.


Astrovirus Particles


Astroviruses 

Small RNA viruses, named because of star-shaped surface morphology, 28 nm in diameter associated with cases of endemic gastroenteritis, usually in young children and neonates. Can cause occasional outbreaks.

responsible for up to 10% of cases of gastroenteritis

similar disease to rota and adenoviruses

most people have antibodies by the age of three.

diagnosed by electron microscopy only, often very difficult because of small size


Other Possible Diarrhoeal Viruses Coronaviruses 

RNA viruses with a crown-like appearance

Not convincing associated with gastroenteritis at present

Small Round Viruses 

small virus-like particles with a smooth surface, 22-28nm in diameter

may possibly be parvoviruses, enteroviruses, or cubic bacteriophages

occasionally seen in the faeces of endemic or epidemic cases of gastroenteritis


Viral Hepatitis Ziad Elnasser MD, Ph.D















Schistosomiasis Ziad Elnasser, MD, Ph.D


Schistosoma hematobium




Schistosoma hematobium eggs


Schistosomiasis Blood flukes.

S. mansoni, S. hematobium, S. japonicum Worldwide. Cylindrical body, separate sexes, Ventral sucker anterior, gynecophoral canal, copulatory embrace.


Life cycle



Epidemiology ● >200 millions in 74 countries are infected. ● Urine into water, snails, human skin exposure. ● Agricultural areas in Africa and the middle east. ● Less than 10 pairs, more load more symptoms.


Pathogenesis and clinical manifestations Early stage: Schistosomiala penetration through the skin within few hours. Intermediate stage: 1 - 2 months after exposure, Oviposition, immune comlex disease, Katayama reaction. Chronic Schistosomiasis: Chronic inflamatory condition (Granuloma formation) due to eggs entrapment in the liver or the urinary bladder. Bladder symptoms. Malignancy.



Immunity Cell mediated immunity. HLA-A1, B5. Tolerance and disguise.

Protective IgE antibodies.


Diagnosis

Eggs in urine. Cystoscopy and bladder biobsy. Serology.


Treatment

Not that effective. Early stage corticosteroids and antihistamines alleviate inflammation. Drugs include praziqantel and metrifonate,


Control and prevention Interuption of the life cycle. – Proper sanitary conditions. – Snail controls. – Skin protection.

Vaccine.


Parasites of the GIT Ziad Elnasser, MD, Ph.D


Amebiasis


Amebiasis Entamoeba histolytica.  Acute and chronic diarrheas.  Pathogenic vs nonpathogenic amebas, adherence lectins, cystine proteases.  Enzymes analysis.  Ulcerative inflammatory lesions.  Extraintestinal sites. 


Entamoeba histolytica Rhizopoda.  Many spps. bases of.  Glucose phosphate isomerase, phosphoglucomutase, oxidoreductases (zymodemes).  10 – 60 μm, nucleus, cytoplasm, cysts and chromatoid bodies, glycogen. 



Life cycle and Epidemiology      

Cyst, exystation in small bowel, trophozoites in large bowel, cysts. Fecal contamination of water, vegetables and fruits. 10% of the world population are infected each year. Cultural habits, sanitation, crowding, socioeconomical status. Asymptomatic state. Male homosexuals, amebas carry HIV virus, children and nutrition.


Pathology and pathogenesis  

 

Lytic effect on tissues. Amorphus, granular, eosinophilic material surrounds trophozoites in tissues including neutrophiles → release toxic products → tissue distruction, overall protective role. Spectrum of colonic lesions ranges from non specific lesions to flask ulcers. Liver necrotic abscesses, periportal fibrosis. Adherence (lectin – mucin) → proteolytic effect → resistance to host effector mechanisms (C5b9).


Host immunity Immunity to recurrence.  High antibody titer following amebic liver abscess.  Comlement resistence.  sIgA protective effect, CMI and lectin Ag, role of corticosteroids.  Vaccine strategies.  Role of mucin in protection. 


Clinical Manifestations   

    

Non invasive manifestation vs invasive. Abdominal pain, tenderness, bloody stools Fever only in one third. Liver is enlarged if infected. All pts have heme positive stools, some as rectal bleeding without diarrhea. Fecal leukocytes might not be present. Fulminant colitis might need colectomy. Intestinal perforation, toxic megacolon, ameboma.



Diagnosis Finding trophozoite or cysts in stool.  Direct mount smear from the endoscope, if stool examination is negative.  Differential diagnosis.  Imaging tech for liver abscess.  Serology, Abs or Ags.  Aspiration of liver abscess, treatment, and diagnostic. 






Treatment     

Problems with therapy. Asymptomatic cases do we treat. Ag and Ab detection can differentiate between E. dispar from E. hisolytica. Stool analysis follow up is important to follow treatment. Diloxanide furoate, paromomycin, tetracycline, Metronidazole, Tinidazole. Dehydroemetine. Abscess drainage. Surgery ?


prevention Food and water fecal contamination.  Vegetables (lettuce), water and chlorine.  Strong detergent soap, soak with acid.  Only boiling of water is effective.  Proper waste disposal and water purification.  Sexual practices. 



Giardia lamblia Flagellated enteric protozoan.  Endemic and epidemic diarrhea.  Zoomastigophora class, trophozoite, cyst.  G. lamblia, intestinalis, duodenalis.  Antigenic variation.  Culture in presence of biliary lipids, mucus 







Cryptosporidium Morphology  Epidemiology.  Life cycle.  Pathogenesis.  Diagnosis.  Treatment.  Prevention. 



















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