Week 10 Diseases and vocab

causative agent -flu

influenza virus

causative agent- hepatitis a

hepatitis a virus

causative agent -hepatitis b

hepatitis b virus

classification- flu

8 segment ssRNA (-) gnome, enveloped virion 80-00nm, four types (A-D), hemagglutinin (HA) spikes, neuraminidase (NA) spikes, H1N1, H7N7.

classification- hepatitis a

Single-stranded ssRNA (+) genome of 7.48 kb, 3 different genotypes I, II, and III, spherican viron 27-30 nm, non-enveloped.

classification- hepatitis b

Single and double-stranded circular DNA, enveloped, spherical virion 42 nm, 4 protein coding genes

reservoir- flu

humans and other vertebrates

poe- flu

respiratory tract

mot- flu

direct, airborne/ droplet, contaminated surface contact

reservoir- hep a

humans

poe- hep a

digestive tract

mot- hep a

fecal-oral route, contaminated food or water, virus may be viable and infectious in environments for months

reservoir- hep b

humans and chimps

poe- hep b

compromised skin or mucosa

mot- hep b

direct via contaminated body fluids including blood and semen, vertical, sharing items with contaminated blood, viability or virus outside host is 7 days

incubation- flu

1-2 days

incubation- hep a

2-7 weeks

incubation- hep b

8-21 weeks

pathogenesis- flu

Hemagglutinin (HA) spikes facilitate attatchment and entry into ciliated epithelial cells. Viruses replicate and spread to other cells of lower respiratory tract including alveolar cells. Damage to mucociliary escalator results in secondary bacterial infections.

pathogenesis- hep a

Ingested virus infects liver. Virus replicates in liver cells and is eventually released into bile and eliminated in feces. Cellular damage and acute inflammations interfere with normal liver function.

pathogenesis- hep b

Virus enters the blood stream and travels to liver. Attaches to and enters liver cells via HBsAg. Immune cells attack infected liver cells causing cirrhosis. Integration of viral DNA into the host genome can lead to cancer.

symptoms- flu

Fever, cough, sore throat, runny/ stuffy nose, body aches, headache, chills, fatigue, somestimes diarrhea and vomiting, ussualy resolved in about week. More serious stymptoms include difficulty breathing, shortness of breath, pain or pressure in chest, dizziness, confusion, severe vomiting.

symptoms- hep a

Lasting 2-3 weeks: dark urine (bilirubinemia), jaundice (7% <5 yrs, 37% 5-9yrs, 70% adolescents and adults), clay colored feces, enlarged liver, mild flulike symptoms.

symptoms- hep b

Can persist for as long as 6 months, latency stage (months -years) asymptomatic, acute, fever, fatigue, loss of appetite, nausea, vomiting, abdominal pain, dark urine, clay-colored stools, joint pain, jaundice.

complications- flu

Upper respiratory tract infections, ear infections, worsening of asthma or other chronic conditons, pneumonia, inflammation of other organs including heart, brain and kidneys, sepsis, death.

complications- hep a

Relapsing hepatitis, autoimmune hepatitis, loss of bile production (cholestatic hepatitis), rarely sever liver damage or failure (fulminant hepatitis).

complications- hep b

Chronic infection 10% (90% 0-1, 25-50% 1-5, 6-10% 10+) may be symptoms free or suffer from malaise, loss of appetite, general fatigue, liver cirrhosis, liver cancer, liver failure, mortality 15-25% of chronically infected.

treatment- flu

rest, fluids, supportive care, antiviral drugs, m2 inhibitors, neuraminidase inhibitors (Tamiflu)

treatment- hep a

rest, fluids, adequate nutrition

treatment- hep b

acute: rest fluids, adequate nutrition

chronic: antivirals, interferon

prevention- flu

Vaccination (egg-based cell or recombinant, mRNA (mFlusia), regular prevention of germ spread.

prevention- hep a

Vaccination, good hygiene practices, safe food handling procedures, effective sanitation.

prevention- hep b

Vaccination, practice universal precautions, avoid exposure to contaminated fluids,

causative organism- c jakob disease

Miss folded Prion Protein (PRP^SC)

classification- c jakob

Prion protein coded by PRNP gene, predisposing sequence mutations (Valine-12 + Glutamic acid-200 > lysine)

reservoir- c jakob

humans, mammals, environment

poe- c jakob

digestive tract or open wounds

mot- c jakob

ingestion of infected meat, contact with infected tisssue or environmentsal prion (<1% of cases) Non-contagoius acquisition: sporadic (85-94%) hereditary (10%), mean age onset 50-60 years.

incubation- c jakob

weeks to years

pathogenesis- c jakob

Miss folded prion proteins resist digestion and induce miss folding of normals (PRP) protiens. PRP^SC forms water insouluble aggregates that damage nerve cells and impair brain function.

symptoms- c jakob

Dementia, memory loss, hallucinations, paranoia, OCD, sleep disturbance, problem with muscle control.

complications- c jakob

Severe brain damage, secondary infections, mortality 85% within 2 years of symptom onset, median life expectancy about 4 months.

treatment- c jakob

no cure, palliative care

prevention- c jakob

Don't eat contaminated met, avoid blood or tissue transfusions from possible infected individuals, follow strict safety precautions, incinerate contaminated material.

gene

segment of dna that encodes a functional product, usually a protein

genome

all of the genetic material in a cell (or population)

genotype

dna sequence variant usually associated with a phenotype

phenotype

observable trait associated with expression of genes

nucleotide polymers

adenine, thymine, cytosine, guanine

backbone

sugar (deoxyribose)- phosphate

strands

held together by hydrogen bonds between AT and CG

polymerase

enzyme which replicates dna

gyrase- type II topoisomerase

uncoils dna and removes/prevents super coils

helicase

pulls dna apart

primase

adds rna primer

Okazaki fragments

pieces of new dna which are added to the lagging strand

ligase

seals the gap between the 3’ and 5’ ends of Okazaki fragments

quinolones and novobiocin

dna replication inhibitors