pbhtlh section 3

fecal-oral route transmission mechanisms

direct contact

contaminated water

contaminated food

defenses of the human digestive system

high stomach acidity

IgA: secretive antibody on muscosal surface (1st line)

phagocytic cells and tissues rich in lymphocytes underneath the mucosal membrane

endogenous organisms in intestines (microbiome)

why is the microbiome important?

regulate intestinal environment

control proliferation of pathogens

affect metabolism

regulate development of immune system

protect against tissue damage in intestines

hepatitis A virology

picornaviridae

+ss RNA, one serotype

clinical features of hepatitis A

15-45 day incubation

fever, headache, diarrhea, nausea, vomiting, jaundice

self limiting: 2 weeks - months

treatment of hepatitis A

HAVRIX vaccine

inactivated virus

norovirus virology

norovirus, calciviridae

ss RNA, non-enveloped

genetically and antigenically diverse

5 geno-groups (3 infect humans)

norovirus epidemiology

very common

major etiological agent for stomach flu (viral gastroneteritis)

occurs in children, elderly, immunocompromised

many asymptomatic cases

norovirus clinical features

incubation 12-48 hours

primary symptoms: watery diarrhea, cramps, nausea

secondary symptoms: fever, headache, chills, muscle aches

supportive treatment, no long term consequences

transmission of noroviruses

highly contagious

fecal oral route

viral shedding

environmental/fomite contamination

poliomyelitis virology

picornaviridae

+ ss RNA virius, non enveloped

3 serotypes: PV1-3

poliomyelitis clinical features

95% infectious asymptomatic

5% fever, headache, and sore throat

paralytic poliomyelitis: muscle paralysis, skeletal deformity, and movement disability

post polio syndrome: 25% of paralytic poliomyelitis - muscle weakness, extreme fatigue, paralysis

transmission poliomyelitis

fecal oral route

viral shedding

highly contagious

poliomyelitis vaccines

inactivated vaccine (IPV): protects against paralysis but not transmission

attenuated vaccine (OPV): able ro replicate in GI tract but not CNS

• used for global campaigns because immunity for GI tract and ease of administration

common features of parasitic GI diseases

protozoans, parasitic helminths

life cycle: take different forms to complete, some need additional hosts before transmitting to humans

incubation period: 1-3 weeks

can be treated

giardiasis

protozoan GI disease

giardia intestinalis

clinical features of giardiasis

leading intestinal parasite

symptoms: diarrhea, bloating, cramps, fatigue

incubation period: 1-3 weeks

treatment: chemotherapy

amebiasis

protozoan GI disease

entamoeba histolytica

clinical features amebiasis

common in tropucal areas with poor sanitary conditions

symptoms: often mild, can include loose stools, stomach pain and cramps

amebic dystenery: severe form

incubation period: 2-4 weeks

treatment: chemotherapy

complications: liver abscess and intestinal blockage

protozoan GI diseases

giardiasis: giardia intestinalis

ambiasis: entamoeba histolytica

balantidiasis: balantidium coli

cryptosporidiosis: cryptosporidium

cyclosporiasis: cyclospora cayentanensis

GI nematodes

trichinosis

hook worm

ascariasis

trichuriasis

strongyloidiasis

pin worms

clincal manifestations of GI nematodes

large intestinal round worm

abdominal pain, vomiting

incubation period: weeks

treatment: chemotherapy

Helicobacter pylori

gram -, spiral shaped

displayes high interstain diversity

major species causing human diseases

produces large amount of urease to neutralize stomach acid

Helicobacter pylori clinical features

most infections asymptomatic

stomach ulcers: pain, bloating, nausea, vomiting

cancers: stomach, gastric lymphoma

Helicobacter pylori transmission, diagnosis, and treatment

transmission unknown

diagnosis:

• blood test for antibodies

• urea breath test

• biopsy combined with urease test and histolgical exam

treatment: triple therapy

what determines if infectious disease eradication is possible?

pathogen characteristics

• no/limited non-human reservoirs

• easily identifiable/clear diagnostics

• emerging resistance to intervention

• minimal susceptible population needed for pathogen to survive

• mode of transmission

• vector control

intervention effectiveness

• efficient and practical interventions: vaccines

• reduce and susceptible population significantly

technical and operational factors

• practical diagnostics

• effective surveillance systems

socionomic and poltical factors:

• strong societal and political commitment

• funding/cost effectiveness

if eradication is not possible, what should we aim for?

disease elimination in a specific area/population

disease control: reduce incidence, prevalence, morbidity, or mortality

targeted interventions: areas of highest disease burden and tailored approaches based on local conditions

addressing social and economic factors/strengthening health systems

where do emerging infectious diseases come from

viruses: mostly zoonotic infections

bacteria: mostly emergence of antibiotic resistance

emerging infectious diseases: viral pathogens

covid 19

crimean congo hemorrhagic fever

ebola virus and marburg disease

lassa fever

MERS-CoV

Zika

Rift valley fever

what should we do for emerging diseases?

building vaccine, clinical testing, and pre-clinical capacity

enhance global surveillance to detect human or animal outbreaks

establish communication structures

improved building design and operation to limit disease transmission

technology/workforce development/collaboration

vaccine development

antibiotic development

pathogen surveillance

epidemic modeling

education

pathogen surveillance

environmental and wastewater sequencing can provide real time information

easier and more accurate than relying on mass testing/self-reporting

impact of food borne diseases in developed countries

medical expenses

loss of productivity

loss of lives

major killers of children worldwide

pneumonia

diarrhea

measles

malaria

* malnutrition contributes to half of childhood deaths

types of food borne diseases

infection

intoxication

metabolic food disorders

allergy

food borne infection symptoms

GI issues in healthy individuals: diarrhea, nausea, vomiting

other symptoms in very young, old, or immunocompromised: systemic infection

onset delayed by 8 hours-days/weeks

types of toxins for food borne intoxication

toxins generated by microorganisms

toxins of plant origins

toxins of industrial origins

symptoms of food borne intoxication

diverse, depending on type of toxin

occurs minutes-hours after ingestion

can be acute or chronic

• ex: aflatoxin —> liver cancer

infection vs intoxication

	infection	intoxication
sources	microorganisms	variable-microorganisms, naturally occurring substances or industrial sources
incubation period	almost always	variable, some are immediate, others develop over time
inactivation	always (except prions)	variable, some toxins can, some cannot heat stable toxins from microorganisms persist after inactivated
transmission	always	rarely

salmonella

gram - bacteria

reservoir: poultry, cattle (food animals), pests & wild animals

food vehicles: chicken, egg, almonds, chocolate, lettuce, tomato

salmonella typhi

only infects humans

typhoid fever: more sever disease

campylobacer

gram - bacterium

grows under microaerophillic condition (3-5%) oxygen

• does not grow in aerobic conditions, so does not replicate in a lot of food

• fragile, easily killed, does not survive freezing

reservoir: mostly poultry, water, unpasteurized milk

relatively high infectious inoculum

severe complications

• C. jejuni: guillain barre syndrome (autoimmune disease attacking the nerves, causing muscle weakness)

carried asymptomatically in animals (ubiquitous)

Escherichia coli

gram - bacterium

enteropathogenic

entero toxic

enteroinvasive

enteroaggregative

enterohemorrhagic**

hemorrhagic colitis

bloody diarrhea caused by enterohemorrhagic e coli (EHEC), shiga toxin producing e coli (STEC)

shiga toxins inhibit protein synthesis by inactivating ribosomes

leads to kidney problems (esp in immunocompromised)

treatment: supportive care

travelers diarrhea

entertoxic e coli (ETEC)

symptoms:

• abrupt onset of multiple loose stools a day

• urgent need to defecate

• abdominal cramps

• nausea, vomiting

• fever

• self-limited in healthy individuals

• complications in susceptible populations: severe dehydration, fever, bloody diarrhea

prevention

• drink clean water

• eat cooked food

• eat fruits that can be peeled

listeria monocytogenes

gram + bacterium

grows at cold temperatures

blood brain berrier —> encephalitis

fetoplacental barrier —> miscarriages, and stillbirth

vehicles: soft cheese, deli meat

shigella

gram - bacterium

food vehicle: fecal oral: only infects humans

vibrio

gram - bacterium

faculative anaerobe

food vehicles: filter feeders such as clams

cholera toxin

• diarrhea

• dehydration (stage 2)

staphylococcus

gram + bacteria

food vehicle can be anything

ubiquitous

avoid human contact of the food

food processing/cooking: toxin is heat stable

clostridium botylinum

gram + bacterium

sporeforming, anaerobic

causes botulism

food vehicle: canned food

rotavirus

most common cause of severe diarrhea in children

fecal-oral: food vehicle

symptoms: diarrhea, dehydration, 1-3 days

• shortens microvilli in SI

vaccine: rotarix (live attenuated), Rota Teq (live oral)

norwalk viruses/noroviruses

comprised of many genogroups

food vehicle: fecal oral

symptoms: diarrhea, vomiting, cramps, headache 12-48 hours post digestion

low infectious dose

long survival on surface: resistance to cleaning

hepatitis A virus

food vehicle: clams, green onions (fecal-oral)

symptoms: fever, malaise, nausea, anorexia, and followed by jaundice

treatment: supportive

complications: mild, self limited

life long immunity

prions

proteinaceous infectious particles that lack nucleic acids

abnormal protein, infectious due to ability to convert normal protein into abnormal form

cause bovine spongiform encephalopathy (BSE) in cattle and variant Creutzfeldt-jacobs disease in human

only pathogen free of nucleic acids

conditions that can not inactivate prions

boiling, dry heat

chemicals: formalin, alcohols

urea and SDS w or w/o heating

UV irradiation at 254 nm

proteases

acids (between pH3-7)

conditions that inactivate prions

1N NaOH

guanidine hydrochloride

2% bleach

autoclaving for 4.5 hours

toxins produced by and secreted from bacteria: exotoxins

staphylococcus aureus

E coli (EHEC, ETEC)

shigella

vibrio cholerae

clostridium botulinum and pefringens

bacillus cereus

toxins produced by fungi

aspergillus flavus and parasiticus: alfatoxin

treatment of diarrhea

rehydration: keep fluid and electrolyte balance

oral rehydration therapy

what can industry do to prevent food borne diseases

reduce pathogen load

follow hygiene guidelines

store and handle food properly

what can consumers do to prevent food borne illness>

store food at cold temperature

cooking eliminates all pathogens except prions

Dermatophytosis

caused by fungi:

Tricophyton

Microsporum

Epidermophyton

 

Reservoir: human, animal, or soil

 

Transmission: direct contact of skin with reservoir or fomites

 

Common: ring-shaped lesion (ringworm), athletes foot

Pathogenesis of dermatophytes

Cells of the immune system cannot reach the layer where dermatophytes grow and destroy it

 

Keratin is a nutrient for the fungi

 

Blood products diffuse into these layers

 

Dermatophyte growth inhibited by cell mediated immunity and serum substances operating in this area

Diagnosis of dermatophytosis

Wood’s light (UV)

 

Fluorescing dermatophyte: scalp lesion

 

Microscopic diagnosis of a fermatophyte from a skin scraping

 

Dermatophyte test medium: basic pH when dermatophyte grows

Treatment of dermatophytosis

Topical ointment: clotrimazole

 

Iodine

 

Severe cases: oral griseofulvin

Prevention of dermatophytosis

Keep vunerable areas dry

 

Wear loose underclothing made of cotton

 

Antifungal body powder

 

Avoid humans/animals with inflamed bald spots

Yeast infection of skin and mouth

Caused by candida albicans

 

Reservoir: human

Pathogenesis of candida albicans

Grows on moist areas of skin

 

Growth inhibited by endogenous bacteria and cell mediated immunity

 

Common in immunosuppressed or people undergoing heavy antibiotic treatments

Clinical manifestations of candida abicans infections

Diaper rash

Thrush: candidiasis of the mouth

Skin under breasts

Diagnosis of c. albicans

Direct smear

Treatment of c. albicans

Topical anti fungal ointment for skin

 

Wiping of togue and anti-fungal mouthrinse

Prevention of c.albicans

Avoid letting skin areas get moist: apply talcum or antifungal powder

 

Minimize systemic antibiotic treatment

 

Correction of underlying immunosuppressive disease

Bacterial skin diseases: staphylococcus pyogenes

Scarlet fever

 

erysipelas

Pyodermas/impetigo

trachoma

Chlamydia trachomatis

Infection and destruction of cornea and conjunctiva

cause of preventable blindness

Keratitis

Bacteria, viruses, and fungi

Ulceration of the cornea occurs mainly in immunodeficient and debilitated patients

Common eye infections: causative organism and disease

Most caused by bacteria (staph. aureus)

Most occur on conjunctiva (inner eyelid)

Warts

Human papilloma virus (HPV)

Reservoir: humans

Transmission: dermal, genital

- Direct skin-skin contact or via fomites

- Autologous transmission: spreading to different parts of ones own body

Pathogenesis of warts

HPV multiplies in lower layers of epidermis without killing the cells

Alters growth properties, causing an excess of cells to accumulate

Treatment of warts

Destruction of wart tissue

- Freezing

- Burning with cauterizing needle

- Laser beam

- Acid treatment

Prevention of warts

avoid using towels and manicure instruments of others

Wear properly fitting shoes

Herpesviridae skin diseases

Roseola

Chickenpox/shingles

Varicella zoster visues (VSV)

Alpha-herpes virus

Varicella: chicken pox (primary infection)

Latency in ganglia

Zoster: shingles (reactivation)

Hemorrhagic varicella

Classes cases of chickenpox of newborn

Severe skin infections on face and neck

VZV disease model

1. Enter mucosal surface

2. Infect T cells

3. Transmitted by infected T cells (1st viremia)

4. Amplified in the internal organs

5. 2nd viremia

6. Infect skin causing chickenpox

7. Infect sensory ganlia and establish latent infection

8. Infect skin causing shingles’post-herpetic neuralgia (PHN) / reactivation

Zoster (shingles)

Reactivation from dorsal root ganglia: viruses transport to skin

Occurs only in persons who have previously had chicken pox

Symptoms: rash that develops into clear blisters

Nerve damage results in post-herpetic neuralgia (PHN)

Types of herpesvirus

Alpha herpes viruses: latency in sensory ganglia

- Herpes simplex virus 1, 2

- Varicella zoster virus (VZV)

Beta-herpesvirus: latency in monoctyes or T cells

- CMV

- HHV-6

- HHV-6

Gamma herpes virus: latency in B cells

- Epstein barr virus (EBC)

- Kaposi’s sarcoma associated herpesvirus (KSHV/HHV-8)

Cold sores

Caused by human herpes virus 1 (HHV1)

Reservoir: humans

Transmission: during early childhood

- Direct contact via kissing

- Fomites: towels and drinking glasses of family members