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Common features of fecal-oral route
Portal of entry: mouth
Portal of exit: feces
Human as the principle host, if not the only host (no animal reservoir)
Transmitted from human to human, directly or indirectly
Low infectious inoculum of the etiological agents
Thus highly contagious
Transmission of fecal oral route
Direct contact: caretakers, nursing homes, food handlers, family members
Contaminated water
Contaminated food
Human-Digestive System Parts
Mouth
Stomach
Small Intestine
Large Intestine
Normal Microflora

Defense of the Human Digestive System
High pH
IgA
Phagocytic cells and tissues rich in lymphocytes underneath the mucosal membrane
Microbiome
Hepatitis A: Virology
Family: Picornaviridae
(+), ss RNA virus. One serotype (vaccine effective)
Genome is 7,478 nucleotides, codes for 4 proteins
Infectious inoculum: 10-100 viral particles
Hepatitis A: Epidemiology
Worldwide
After vaccine developed, incidence has been reduced
Hepatitis A: Clinical Features
15-45 day incubation
Symptoms
Fever, Headache, Diarrhea, Nausea, Vomiting, Jaundice. Occasional death
Hepatitis
Self-limiting (2 weeks to several months)
Diagnosis
IgM to HAV
Life long immunity
Noroviruses: Virology
Genus: Norovirus
Family: Caliciviridae
Group of related ss RNA, non-enveloped viruses. 7,654 bases.
Genetically and antigenically diverse
Five geno-groups (I, II, IV infect human) and over 20 genetic clusters
Highly contagious
Noroviruses: Epidemiology
Very common; highly contagious
Major cause for stomach flu (viral gastroenteritis)
Believed to cause >50% of food borne outbreaks of gastroenteritis
Noroviruses: Clinical Features
**No serious long-term sequela
Incubation: 12 – 48 hours
Acute gastroenteritis. Symptoms last 24-60 hours.
Complications: dehydration
Primary Symptoms: Vomiting, watery, non-bloody diarrhea, abdominal cramps, nausea
Secondary Symptoms: Fever, Headache, Chills, Muscle aches, Tiredness
Norovirus: Treatment
Supportive only
Recovery complete, no long term consequences
Follows iceberg phenomenon; asymptomatic infections high
Norovirus: Transmission
Fecal-oral route
Viral shedding
Highly contagious
Environmental / fomite contamination
Aerosolized vomitus
Poliomyelitis Other Name
polio or infantile paralysis
Poliomyelitis: Virology
Family Picornaviridae
Ss (+) RNA genome about 7,500 nucleotides
Non-enveloped with only RNA and a non-enveloped icosahedra protein coat
Three serotypes, PV1, PV2 and PV3
Poliomyelitis: Clinical Manifestations
Follows iceberg (95% asymptomatic, 5% fever/headache, & <1% paralytic poliomyelitis)
paralytic poliomyelitis
post-polio syndrome
paralytic poliomyelitis
Muscle paralysis, skeletal deformity, and movement disability
post-polio syndrome
25% of in paralytic poliomyelitis survivors develop post-polio syndrome decades later
including muscle weakness, extreme fatigue, or paralysis
Poliomyelitis: Transmission
Fecal-oral route
Viral shedding
Highly contagious
Poliomyelitis: Vaccines
IPV: Inactivated Vaccine, developed by Jonas Salk,
Protects against paralysis, but not transmission of PV
OPV: attenuated vaccine, developed by Albert Sabine
Able to replicate in the gastrointestinal tract but not the central nervous system.
IPV vs. OPV
OPV: Attenuated, Able to replicate in the GI tract but not the CNS
Used for global campaigns because of its (1) immunity in GI tract (2) ease of administration.
IPV: Inactivated, Protects against paralysis, but not transmission
*** OPV was discontinued in the US in 2000 to avoid vaccine-associated poliomyelitis. IPV is used exclusively.
SARS-CoV-2: Virology
Genome: 29,903 bases, 27 open reading frames
Classification: (+) RNA virus, coronaviridae
Receptor: ACE2
SARS-CoV-2 and COVID-19: Symptoms
GI symptoms
occur in 20 to 30% of patients
usually mild
Viral RNA detected in fecal samples
not been shown to transmit through fecal-oral route
Parasitic GI Diseases-Common Features
Infections by parasites including protozoans and parasitic helminths
Life cycle: taking different forms to complete a life cycle (eggs or cysts, trophozoites, larva, adult forms, etc).
Some need additional hosts before transmitting to humans
Incubation period: 1-3 weeks
Can be treated
No permanent damage in most cases
Giardiasis Protozoa
Giardia intestinalis
Giardiasis: Life cycle
Cyst form survive, but not trophozoites (due to harsh environment)
Cyst -> trophozoites -> cyst
Cyst: infective stage
Trophozoites: diagnostic stage

Giardiasis: Clinical features
**Leading intestinal parasite
Symptoms: diarrhea, bloating, cramps, fatigue
Incubation period: 1 – 3 weeks
Treatment: chemotherapy (metronidazole)
Amebiasis Protozoan
Entamoeba histolytica
Amebiasis: Life Cycle
Excystation: trophozoites - can either multiply into more or turn into cysts
Passed in feces

Amebiasis: Clinical Features
Common in tropical areas with poor sanitary conditions
Symptoms: often mild and can include loose stools, stomach pain, and stomach cramping
Amebic dysentery is a severe form.
Incubation period: 2-4 weeks
Complications: liver abscess and intestinal blockage
Amebiasis: Treatment
Treatment: chemotherapy (metronidazole, paromomycin)
Protozoan GI Diseases and their protozoa
Giardiasis: Giardia intestinalis
Amebiasis: Entamoeba histolytica
Balantidiasis: Balantidium coli
Cryptosporidiosis: Cryptosporidium
Cyclosporiasis: Cyclospora cayentanensis
Gastrointestinal Nematodes
Trichinosis
Trichinella spiralis
Hookworms
Ascariasis
Ascaris lumbricoides
Trichuriasis
Whipworm
Trichuris trichiura
Strongyloidiasis
Strongyloides stercoralis
Pinworms
Roundworm
Enterbius vermicularis
Ascaris lumbricoides: Life Cycle
Fertilized egg
Unfertilized egg will not undergo biological development

Ascaris lumbricoides: Clinical Manifestations
Largest intestinal round worm. Worldwide spread.
Symptoms: abdominal pain, vomiting
Incubation period: weeks
Complications: no permanent damage
Ascaris lumbricoides: Treatment
Treatment: chemotherapy (mebendazole, albendazole, or pyrantel pamoate)
Gastrointestinal Helminths
Flukes
Tapeworms
Guinea Worm (Dracunculus medenisis): Life cycle
Water fleas ingest worm larvae.
People drink water contaminated with water fleas, and the larvae resist digestion and migrate to the small intestine and penetrate the intestinal wall into the body cavity where they grow up and mate.
Then they move through connective tissue through various areas of the body (usually lower limbs)
Worm forms a painful blister near skin surface and blister burst exposing worm

Guinea Worm Name
Dracunculus medenisis
Helicobacter pylori: Microbiology
Gram (-), spiral shape, highly mobile
Genome size: ~1.6 Mb, highly AT rich
Displays high interstrain diversity
major species causing human diseases
**Produces large amount of urease to neutralize stomach acid (so bact can survive in stomach)
Helicobacter pylori: Clinical Features
Follows iceberg
Stomach or duodenal ulcers (10-20%)
Cancers (1-2%)
Helicobacter pylori: Transmission
currently unknown
Helicobacter pylori: Diagnosis + Treatment
Diagnosis (none is fool-proof; many methods to confirm)
blood test for antibodies
urea breath test
biopsy combined with urease test and histological exam
Treatment: triple therapy
antibiotics amoxicillin and clarithromycin
proton pump inhibitor such as omeprazole
Ulcers
Ulcers were believed to be caused by stress, spice and excessive acid in the stomach
Barry Marshall and Robin Warren (nobel prize 2025)
observed small curved bacteria in lower stomach of biopsies of ulcer patients
No one believed them so barry marshall drank culture of Helicobacter and treated himself with antibiotics to prove