digestive system infections MICRO

normal microbiota in digestive system

• synthesize a number of vitamins, including niacin, thiamine, riboflavin, pyridoxine, vitamin B12, folic acid, pantothenic acid, biotin, and vitamin K

• degrade dietary fiber to produce short chain fatty acids, which serve as energy sources for colonocytes

• maintain mucosal barrier between the intestinal lumen and underlying tissues

• essential for normal development of mucosal immunity

• prevent pathogens from colonizing intestines

pathogen of cholera

Vibrio cholerae

cause of cholera

• vibrio cholerae: curved, gram negative rod

• several serotypes grouped by O antigen 

• halotolerant, can grow in alkaline conditions 

mode of transmission for cholera 

spreads by fecal-oral transmission, most commonly through contaminated water but also through foods such as contaminated crabs, oysters, and vegetables. 

prevention and transmission for cholera

• replacement of fluids and electrolytes decreases mortality from over 30% to below 1%

• sanitation and safe water supplies

• two vaccines available

symptoms of Hep A

• acute illness

• older children and adults develop jaundice, fever, fatigue, clay colored feces, and vomiting ~1 month after incubation

• most young children and many older children are asymptomatic

cause of Hep A 

hepatitis A virus, naked single-stranded RNA virus of picornavirus family 

pathogenesis of Hep A

following ingestion, reaches liver via unknown route. replicated, is released into bile, eliminated in feces.

mode of transmission for Hep A

spreads via fecal-oral route, principally by contaminated hands, food, or water

treatment and prevention for Hep A

• no antiviral treatment available 

• immune globulin can be given via injection, gives short term protection if administered within 2 weeks 

• HAV vaccine 

symptoms of Hep B

range from asymptomatic to severe. acute disease rarely fatal. can become chronic.

cause of Hep B

hepatitis B virus: enveloped, mostly double stranded DNA genome; a portion is single stranded. remarkably resistant; visions can be infectious after a week outside the body. member of hepadnavirus family.

useful markers for Hep B 

• hepatitis B surface antigen (HBsAg) 

• hepatitis B core antigen (HBcAg) 

• hepatitis B e antigen (HBeAg) 

pathogenesis of Hep B

bloodstream carries to liver; HBsAg allows virus to attach. liver damage likely from cell-mediated immune response

mode of transmission for Hep B

transmitted in body fluids, so activities that mix fluids are risk factors.

• sharing needles, toothbrushes, razors, towels, unsterile tattooing

• about half of new cases from unprotected sex

treatment and prevention of Hep B 

• no curative antiviral treatment 

• reverse transcriptase inhibitors plus interferon injections yield improvements 

• vaccine 

symptoms of Hep C

similar to A and B except generally milder. 65% have no symptoms and only 25% have jaundice. more than 80% develop chronic infection

cause of Hep C

hepatitis C virus: eveloped, single stranded RNA virus of flavivirus family. considerable genetic variability.

pathogenesis of Hep C

few details known; infection generally from infected blood. incubation averages 6 weeks, ranges 2 weeks to 6 months 

mode of transmission for Hep C

transmitted in blood, although, the mechanism of exposure is not always obvious. items that can become contaminated with blood are possible sources of infection.

treatment and prevention of Hep C

• no cure but interferon injection plus ribavirin may help

• prolonged interferon treatment may prevent chronic form

• No vaccine, but vaccination against Hep A and B often recommended to help prevent dual infection that might severely damage the liver.