25 - Digestive Infections

can break while chewing

Causative Agent – Streptococcus mutans, colonize teeth,
thrive in acidic conditions, produces glucans, dietary sugars

Pathogenesis – Adherence of bacteria to receptors on teeth,
sugar production causes drop in pH

Epidemiology – Heredity, young more susceptible than old

Prevention – Cut down dietary glucose

Treatment – Removal of plaque, drilling out and filling of
cavity

gums, loose discolored teeth

Causative Agent – Dental Plaque

Pathogenesis – Plaque/Tartar forms at gum line, gets into
gingival crevice, causes inflammation

Epidemiology – 90% of those over 65, people with underlying immunodeficiency

Prevention – Brushing, cleaning flossing

Treatment – Cleaning out inflamed gingival crevice and
removing plaque

Causative Agent – Treponema genus, spirochete

Pathogenesis – Bacterial invasion causes necrosis and
ulceration

Epidemiology – Stress, malnutrition, immunodeficiency

Prevention – Brushing and flossing

Treatment – antibacterial

tenderness

Causative Agent – Heliobacter pylori, short, spiral, gram
negative microaerophile with multiple flagella

Pathogenesis – Able to neutralize acidity of stomach, uses
flagella to corkscrew through stomach lining

Epidemiology – fecal-oral route, clusters in families, poor
people most susceptible

Prevention – No prevention

Treatment – Antibiotics

Causative Agent – Herpes simplex virus, medium sized, double
stranded enveloped, type 1 or 2

Pathogenesis – Blisters contain large numbers of virons,
stress can precipitate recurrances

Epidemiology – Wide spread, transmitted by close physical
contact

Prevention – close physical contact

Treatment – Antivirals

spasms, usually disappears within a week, symptoms more severe in people past
puberty, can effect ovaries, testes, pregnancies often miscarry

Causative Agent – Mumps virus, paramyxovirus family,
enveloped, single stranded DNA

Pathogenesis – respiratory droplets, incubation 15 – 20 days,

Epidemiology – Humans only natural host, lifetime immunity,
contagious 1 week before and 2 weeks after symptoms

Prevention – Immunization

Treatment – None

Causative agent – Vibrio cholerae, gram negative, curved bacillus

Pathogenesis – Large numbers must be present, B fragment no toxicity, A fragment toxic

Epidemiology – Fecal contamination of water

Prevention – Clean water

Treatment – rapid replacement of water

convulsions, joint pain

Causative Agents - S. flexnuri , S. boydii , S. sonnei , S.
dysenterriae

Pathogenesis – Begins in large intestine, cells multiply at
high rate, nonmotile, dead cell slough off, lots of blood and pus

Epidemiology – fecal oral, low infecting dose, day cares and
gay men

Prevention – Sanitation

Treatment – Fluid and electrolyte replacement,
antimicrobials

stool, usually lasts 10 days

Causative Agent – E. coli, 4 types

Pathogenesis – enterotoxin, adheres to cells in small
intestine

Epidemiology – Person to person, contaminated food and water

Prevention – hand washing, proper preparation of food and
drinks

Treatment – replace fluids and electrolytes, antibiotics for
infants, Pepto

Causative Agent – Salmonella, motile, gram negative,
enterobacteria

Pathogenesis – large number required for infection, adhere
to receptors on small intestine

Epidemiology – Most cases have animal source, bacteria can
survive a long time in environment, children most often infected

Prevention – Adequate cooking, tracing outbreak of
infections

Treatment – vaccine, surgical removal of gall bladder

Causative agents – campylobacteria jejuni, motile, gram
negative, curved bacillus

Pathogenesis – small infecting dose, causes inflammation,
guillen barre syndrome

Epidemiology – food and waterborn outbreaks, usually live in
animal intestines,

Prevention – proper treatment of water and food

Treatment –subside on its own, severe cases, erythromycin

generally gone within a week

Causative agents – Rotovirus, double walled capsid, double
walled dna

Pathogenesis – infects cells of upper small intestine,
decreased production of enzymes

Epidemiology – fecal oral route, childhood epidemics occur
in winter

Prevention – handwashing, disinfectant, attenuated vaccine

Treatment – none

60 hours

Causative agents – Norovirus, small, nonenveloped, single
stranded RNA

Pathogenesis – infects upper small intestine

Epidemiology – fecal/oral route, incubation 12 to 48 hours

Prevention – handwashing/disinfectants

Treatment – none

side abdominal pain, dark urine, clay feces, jaundice, children less than 6
years asymptomatic

Causative agent – Hepatitis A virus, small, single stranded
RNA

Pathogenesis – contaminated food or water, reaches liver,
released into bile

Epidemiology – fecal oral, restaurants, shell fish, daycare,
nursing homes, homos

Prevention – vaccine

Treatment – Gamma globulin within 2 weeks of exposure

abdominal pain, dark urine, jaundice, formerly known as serum hepatitis

Causative agent – hepatitis B virus, enveloped, double
stranded DNA

Pathogenesis -
carried in liver, replicates via reverse transcriptase

Epidemiology – Needles, toothbrushes, sex

Prevention – Vaccine, passive immunization

Treatment – none

Causative agent – hepatitis C virus, enveloped, single
stranded RNA, flavivirus family

Pathogenesis – infected blood, 6 week incubation

Epidemiology – needles, syringes, tattooing,

Prevention – no vaccine

Treatment – avoid alcohol, no treatment

disappear within 4 weeks

Causative Agent – Giardia Lambdia, flagellated, pear shaped,
2 sided nuclei, can exist in 2 forms

Pathogenesis – cyst responsible for infection, attach to
epithelium of small intestine and move to large intestine

Epidemiology – single stool can carry 300 million cysts,
cysts can live in cold water up to 2 months, chlorination often ineffective,
fecal oral route, oral/anal sex

Prevention – Filtration of water

Treatment - Flagyl