Esophagus and stomach are relatively bacteria free

Mouth> Different Streptococci in

different micro environments> Teeth colonized by bacteria

forming biofilm—plaque 1012 bacteria per gram!

Small Intestine—few microbes> Aerobic and facultative

anaerobes> Gram-negative rods,

streptococci, lactobacillus, yeast

Large Intestine (1/3 fecal mass):› Bacteroides--anaerobic› Enterobacteria—facultative

anaerobes

Actions› Synthesis of Vitamins:

Niacin, thiamine, riboflavin, pyridoxine, folic acid, pantothenic acid, biotin, and vitamin K

› Digestion of fiber—gas production!› Opportunistic pathogens of urogenital tract› Prevent colonization by pathogens

Antibiotic treatament that disrupts normal flora can result in diarrhea Antibiotic-associated colitis due to colonization by clostridium difficile

Tooth decay › Dental caries› Streptococcus mutans

Produce lactic acid and thrive in acid environment Produce extracellular glucans, base for biofilm

› Prevention: decrease refined sugar, mechanical removal of plaque, fluoride

Periodontal disease› Caused by plaque formation and tartar in gingival

crevice› Gingivitis

› “Trench mouth” Acute necrotizing ulcerative gingivitis: poor dental hygiene and stress› Treponema sp., anaerobic spirochete

Helicobacter pylori› Generally asymptomatic

unless accompanied by ulcers or cancer Survive in stomach acid

due to urease which converts urea to ammonia

› Flagella allow penetrataion of mucosal layer and attachment to mucosal epithelium

Cold Sores and Fever Blisters› HSV-1

Ds-DNA Enveloped virus

› Latent infection of sensory nerve endings Life-long infection, treatment of symptoms does not remove latent virus

› Transmitted in saliva either directly or by fomits (2-3 hours)

› Large portions of the population are infected with the virus

Acute viral infection of parotid gland› Paramyxovirus

Ss-RNA virus

› Infects parotid, pancreas, ovary, testicles› Immune response produces symtomatic

swelling and accompanying pain› Complications can include: meningitis,

orchitis, miscarriage, encehpalitis.› Vaccination aims at eradication of mumps

Causitive agents> Microbial toxins (food intoxication)> Bacterial infection> Viral infection> Protozoa infection

Symptoms› Diarrhea

Dysentery: blood and pus in feces

› Loss of appetite› Nausea and vomiting› fever

Fecal-oral transmission (contaminated water supply)

Dehydration as result of diarrhea Generalities in pathogenic mechanisms:

> Attachment: pili or adhesin (proteins)> Toxin production • Increase secretions• cytotoxin

> Alteration of host cells• Type III secretion

> Cell invasion

Vibrio cholerae› Curved, gram-negative rod› Salt tolerant› Acid sensitive

Produce exotoxin: cholera toxin › A-B toxin stimulates adenyl cyclase and locking cAMP

cycle in “on” position› Stimulates Cl- secretion resulting in loss of water and

electrolytes from the cells Treatment focuses on oral rehydration therapy Prevention: avoidance and vaccination

Causitive agent:› S. flexneri, S. boydii, S. sonneri, and S.

dysenteriae› Gram-negative enterobacteria with plasmid› Acid tolerent› Increasingly antibiotic resistent

Invasion of intestinal epithelial cells Dysentery Shiga toxin

› A-B cytoxin: inhibits ribosome› Hemolytic uremic syndrome (HUS)

RBC lysis, anemia, kidney failure

Normal flora› Pathogenic forms identified as cause of

Epidemic gastroenteritis, 1945 traveler’s diarrhea, 1970s Dysentery and HUC

Pathogenicity:› Enterotoxigenic (plasmid mediated)› Enteroinvasive› Enteroaggregative (plasmid mediated)› Enterohemorrhagic (Shiga toxin production)

Salmonella enterica and S. bongori› Gram-negative, lactose-negative, Acid

sensitive› Over 2400 serotypes indicated with non-

italicized name› Zoonotic

Source of increased antibiotic resistance

› Human reservoir—typhoid fever Enteric fever: S. typhii

Gastroenterisis› Adhesion and Type III secretion

C. jejuni isolated in 1972: leading cause of diarrhea in US› Mobile, gram-negative rod› Microaerophile

Pathogenisis› Invasion of intestinal epithelium causing

inflammatory response› Guillain-Barre syndrome complication in 0.1%

of cases Progressive paralysis 5% fatality, 95% recovery with treatment

Viroid› Double walled capsid› Ds, segmented RNA

Gastroenteritis› Abrupt onset vomiting and

diarrhea› Fluid replacement therapy

Viroid› Small non-enveloped, ss-

RNA› Survive well in enviroment› Incubation 12-48 hurs

Considered a type B bioterrorism agent› Not cultivated in

laboratory

Infectious Hepatitis› HAV

Small ss-RNA picornavirus

› Liver is only infected organ› Spread through fecal contamintion of food

and water Symptoms

› Fatigue, fever, abdominal pain, jaundice Vaccine available since 1995

Serum hepatitis› Infects 5% of world population and 9th leading

cause of death› HBV virus—hepadanvirus

Ds-DNA, Lipid envelope, reverse transcriptase HBsAg: surface antigen responsible for adhesion and

infection

› Long term infections result in cirrhosis of the liver and liver cancer

› Spread in blood, blood products, semen, and vertically to newborns

Prevention by vaccination and avoidance

Most common blood-borne infection in the US Symptoms similar to Hepatitis A or B or

asymptomatic. Viroid

› Enveloped ss-RNA flavivirus No vaccine Pathogenesis

› Inflammation of liver› Chronic infection leading to 10-20% cirrhosis or

liver cancer.

Giardia lamblia› 6-20 day incubation› 1-4 week symptoms› Traveller’s diarrhea and

local outbreaks› Present in water systems

and spring water Cysts are resistant to

water purification chemicals, removed by filtration

Cryptodporidium parvum › Gastroenteritis symptoms› Parasite of the intestinal epithelium› More resistant to chemical treatment and

filtration than Giardia› Infects both human and animal populations› Person to person spread is possible

Cyclospora cyetanensis› Spore forming protozoan› Gastroenteritis symptoms begin at about 1

week and last 3-4 days, relapse common up to 4 weeks.

› No person to person spread, no animal sources identified

Entamoeba histolytica› Sarcodina species with

cyst form that survives stomach acid

› Some strains produce cytotoxin that allows entry into deeper tissue or blood

Symptoms are generally mild but can be chronic › Amebic dysentery