Diseases of the Alimentary Tract Flashcards
Hepatitis
[Viral disease of the lower alimentary system]
Hepatitis A virus- naked RNA virus, one serotype (no mutation)
Fecally/orally spread
Very long incubation period promotes spread (3-5 weeks)
Mild self-limiting infection
Vaccine
Hepatitis B virus- enveloped DNA virus, reverse transcriptase
1-6% become chronic carriers- chronic carriers are at risk for cirrhosis of liver and liver cancer
Transmission is primary by blood/sexual contact as well as some body fluids
Pathogenesis is most likely from immune system attacking infected cells
Recombinant vaccine available (Hep.B surface antigen). Treatment by injections of interferon
Hepatitis C- enveloped RNA virus that mutates rapidly
Causes milder symptoms than B during acute infection. Leads to progressive liver damage and cancer
Majority of those infected become chronic carriers
Spread by IV drug use/blood/sexual contact
No vaccine because it is an RNA virus that mutates
Norovirus
[Viral disease of the lower alimentary system]
Single stranded RNA virus
Symptoms: vomiting, abdominal cramps, slight fever, diarrhea; symptoms last 1-2 days
Transmission is through fecal/oral route
Infects primarily adults
Treatment is handwashing, no vaccine
Rotavirus
[Viral disease of the lower alimentary system]
Naked RNA virus that is very stable in the environment
Primary cause of viral gastroenteritis in infants and children
Symptoms: vomiting, abdominal cramps, slight fever, diarrhea
Symptoms last 5-8 days, cause dehydration and death in the very young if not treated
Fluid replacement necessary
Cause of traveler’s diarrhea in secondary infections
Transmission: fecal/oral route
Childhood epidemics occur, some immunity by age 4
Attenuated vaccine available
Staphylococcus aureus food poisoning
[Bacterial disease of lower alimentary tract]
Grows well in high osmotic pressure (salinity/sugar)
Produces superantigens that activate vomiting and diarrhea responses from T helper cytokine storm
S. aureus is not good at out competing other organisms, but in environments where others are inhibited (creamy or salty food), it will proliferate
Bacteria reproduce and produce exotoxin when other organisms are inhibited by presence of salt/sugar/high osmolarity
Toxin produced is heat stable and its cause of action is not well understood. Toxin can survive high temperature for 30 min
Food is eaten, but bacteria cannot survive the acidity of the stomach, however the toxin does. After ingestion, toxin acts quickly (within 1-6 hours)
Clostridium difficile
[Bacterial disease of lower alimentary tract]
Clostridium difficile- gram positive, endospore forming
Colonization occurs through disruption of normal flora by antibiotic therapy
Causes intense inflammation and lesions in the colon
Can cause pseudomembranous colitis composed of connective tissue tissue and pus from bacteria and white blood cells- Toxin A causes inflammation and diarrhea. Toxin B causes formation of pseudomembrane.
Innate immune responses aid in ridding body of organism- diarrhea enhances elimination of toxin and bacteria. reestablishing normal flora is key (probiotics and fecal transplants)
Campylobacter gastroenteritis
[Bacterial disease of lower alimentary tract]
Campylobacter jejuni- gram negative spirals
Symptoms: fever, cramping, abdominal pain, and diarrhea (Traveler’s diarrhea). Self-limiting
A leading cause of foodborne illness, especially from poultry (most retail chicken contaminated)
Salmonellosis gastroenteritis
[Bacterial disease of lower alimentary tract]
Salmonella enterica- gram negative rod, facultative anaerobe
Infection, incubation time is 12-36 hours (short), reproduces in intestinal epithelia cells
Symptoms: low grade fever, nausea, diarrhea, cramps
Salmonella Enterica is a normal intestinal flora of many animals- 90% of reptiles are carriers, contamination of poultry occurs during processing and in eggs
Fecal/oral transmission
Treatment: oral rehydration
Typhoid fever
[Bacterial disease of lower alimentary tract]
Salmonella Typhi
Limited to fecal contamination by human carriers, human only reservoir
Symptoms: initial headache with high fever, diarrhea between week 2 and 3
Reproduces in phagocytic cells (macrophages)
Disseminates into body and can be isolated in blood, urine and feces
1-3% of infected individuals become chronic carriers, from chronically infected gallbladder
Treatment: proper sanitation vital. antibiotic therapy necessary
Enterotoxigenic E. coli (Enterobacteria)
[Bacterial disease of lower alimentary tract]
E.coli: gram negative rod, facultative anaerobe, normal gut flora
Primary cause of traveler’s diarrhea
Must have infection to have disease
Fecal/oral transmission
Symptoms: fever, vomiting, profuse watery diarrhea
Different strains have differing virulence factors: fimbriae, toxins, plasmids transmitted through conjugation
Treatment: oral rehydration primarily, with some antibiotic therapy in very severe cases
Enterohemorrhagic E. coli (Enterobacteria)
[Bacterial disease of lower alimentary tract]
O157:H7 - serovar found mainly in cattle where no disease occurs
Contamination occurs during processing of meat and on alfalfa sprouts
Has Shiga-like toxins that produce inflammation of the colon with bleeding, hemmorhagic colitis
Complication of blood in urine, which leads to kidney failure (meolytic uremic syndrome)
Children are most at risk
ID50 as low at 10
Shigellosis (Enterobacteria)
[Bacterial disease of lower alimentary tract]
All Shigella species are gram negative rods, facultative anaerobes
Can replicate in macrophages, humans only reservoir (but can be found in filter feeders such as oysters)
Very low ID50 because Shigella can survive acidity of stomach
M cell bring in organisms, macrophages phagocytose, bacteria escape, replicate in cytoplasm, then die from bacterial replication
Create actin tail to become motile and move from epithelial cell to cell
Shigella sonnei: cause of Traveller’s Diarrhea- mild diarrhea, fever, self-limiting
Bacillary Dysentery- Shigella dysenteriae
Fecal/oral transmission
Shigella dysenteriae produces an A-B exotoxin- Shiga toxin which destroys intestinal epithelia cells, forms mucosal abscess
Severe diarrhea with blood and mucous, abdominal cramps, fever. Can cause hemolytic uremic syndrome
Antibiotic therapy necessary necessary, with oral rehydration. Severe problem with growing antibiotic resistance
Cholera
[Bacterial disease of lower alimentary tract]
Vibrio cholerae- comma shaped, gram negative rod
Has pili and produces an A-B enterotoxin- cholera toxin, which causes the secretion of water and electrolytes
Requires high ID50 to survive stomach acidity to induce disease
Use pili to bind to walls of small intestine
Causes a disease called “rice water stools” due to presence of water, intestinal mucus, epithelial cells and bacteria
Seriousness of disease depends on serovar and severity of fluid loss/dehydration lack of electrolytes- in severe cases, loss of fluids causes shock and death as blood becomes so viscous that vital organs cannot function
Treatment: fluid and electrolyte replacement (vital that replacement fluids are not also contaminated)
Vaccine
Mumps
Mumps virus- enveloped RNA virus, does not mutate (one antigenic strain)
Symptoms: inflammation and swelling of the parotid glands, fever, sometimes meningitis
Symptoms in individuals past puberty are more severe due to change in target organs (glands) as individuals mature
Orchitis- swelling of the testicles
Inflammation of the ovaries
Transmission: most contagious 48 hours before clinical symptoms appear, spread by respiratory droplets
Treatment: humans only reservoir, vaccination part of MMR vaccine
Gastritis/Stomach ulcers
Causative agent: Helicobacter pylori- short spiral gram negative with polar flagella, urease, covered flagella, CagA
Destruction of stomach epithelium due to inflammatory response to infection
Injects CagA proteins into cells which lead to change in shape and surface characteristics
Localized abdominal pain can lead to bleeding with ulcers and cancer
Fecal/oral transmission
