-
Epidemiology
The study of the spread, control and prevention of disease in populations
-
Communicable Diseases
Diseases that can be transmitted from one host to another
-
Typhoid Fever
- Caused by Salmonella enterica strain Typhi
- Transmission: fecal-oral
-
Typhoid Fever Symptoms
Diarrhea, abdominal pain, nausea, vomiting and fever
-
Attack Rate
# of cases in a population exposed to an infectious agent
-
Morbidity Rate
#cases/population at risk
-
Mortality Rate
# deaths/population at risk
-
Prevalence
# of total cases in a population at risk
-
Incidence
# of NEW cases in a specific time period in a population at risk
-
Endemic
- Constantly present
- Cold and seasonal flu
-
-
Outbreak
- Cluster of cases
- Ebola in Uganda, January 2001
-
-
Determinants of Infections Diseases
- Communicable Diseases:
- Reservoir
- Mode of transmission
- Portal of entry
- Portal of exit
-
Human Reservoir
- Symptomatic
- Carriers-asymptomatic
-
Animal Reservoir
- Fleas, mosquitoes & ticks
- Mammals (rabies)
- Birds (flu, Salmonella)
- Lower vertebrates (Salmonella & turtles)
-
Transmission
- Horizontal
- Vertical
- Direct contact
- Indirect contact
- Food and Water
- Vector
- Droplet
- Air
-
Vertical Transmission
Mother to fetus
-
Direct Contact Transmission
- Nosocomial infections
- Fecal-oral
-
Indirect Contact Transmission
Fomites
-
Food and Water Transmission
- Cross contamination
- Fecal-oral
-
Vector Transmission
- Mechanical
- Biological
- •Biting
- •Defecating
- •Regurgitating
-
Air Transmission
Droplet nuclei
-
Dose
- < 10 cells for bacillary dysentery (Shigella spp.)
- 1000 cells for gonorrhea
- 1,000,000 cells for cholera
-
Incubation Period
Cold vs. AIDS
-
Population Characteristics
- Immunity – genetic or predisposed
- Age
- Religious or cultural practices
- Health
- Genetic background
-
Nosocomial Infections
- Hospital acquired
- 5-6% rate in US
- Half of all infectious diseases treated
- One-third preventable
-
Usual Suspects of Nosocomial Infections
- Enterobacteriaceae
- -Intestinal flora
- Escherichia coli
- -Intestinal flora
- Pseudomonas sp.
- -Moist, nutrient poor areas
- Staphylococcus aureus
- -Nose flora
- Klebsiella pneumoniae
-
Reservoirs of Nosocomial Infections
- Patient’s flora
- Health care worker
- Other patients
-
Transmission of Nosocomial Infections
- Medical devices
- Airborn
- Lack of proper handwashing
-
Prevention of Nosocomial Infections
- Handwashing
- Gloves
- Mask, eye protection, gown, face shield
- Patient care equipment
- Environmental controls
- Linens
- Needles
- Patient placement
-
Infection
- Colonization of microbe causing illness
- Primary
- Secondary
-
Infectious Disease
Impaired body function due to infection
-
Pathogen
Microbe capable of causing disease (can also be opportunistic)
-
Virulence
Degree to which pathogen can cause disease
-
5 Characteristics of Infectious Diseases
- 1. Incubation period
- 2. Incubation and illness
- 3. Convalescence and carrier- recovery
- 4. Duration
- 5. Distribution
-
Incubation Period of Infectious Diseases
- Infectious dose
- 10 cells for Shigella
- 1,000,000 cells for cholera
- Health of host
-
Incubation and Illness of Infectious Diseases
- Days (cold virus); weeks (Hep A)
- Months (rabies); years (leprosy)
- Symptomatic or asymptomatic
-
Convalescence and Carrier-Recovery of Infectious Diseases
Carrier- someone who is helping but shows no sign of illness
-
Duration of Infectious Diseases
- Acute- short (a week or 2)
- Chronic (forever)
- Latent (goes away and comes back)
-
Distribution of Infectious Diseases
- Localized- stays in one area
- Systemic- body wide
- HIV
- Bacteremia- a few cells in bloodstream
- Septicemia- massive infection in bloodstream
-
Mechanisms of Pathogenesis
- Production of toxins that are ingested
- Colonization of host mucous membranes, then toxin production
- Invasion of host tissues
- Invasion followed with toxin production
-
Production of Toxins that are Ingested
- Clostridium botulinum
- Canned foods
- Can eat bacteria, toxin causes disease
-
Colonization of Host Mucous Membranes, then Toxin Production
Vibrio cholerae; Escherichia coli O157:H7
-
Invasion of Host Tissues
Yersinia pestis
-
Invasion Followed with Toxin Production
Streptococcus pyogenes
-
Establishments of Infection
- Adhesins or penetration
- -Attach or enter body
- Colonization
- -Avoid IgA’s
- Uptake by host cell
- -Effector molecules
- Avoiding host defenses
- -Hiding
- -Avoiding killing
- Damage to host
-
Establishment of Infection: Adhesion
- Pili, capsule or cell wall proteins
- Highly specific
- •Can have more than one type to broaden range
-
Establishment of Infection: Colonization
- IgA proteases- degrades IgAs: avoiding antibodies
- •Complement system, enhance phagocytosis
- Antigenic variation- constantly change out proteins: avoid recognition (antibodies)
- Siderophores – iron binding molecules
- •Lactoferron is produced by bacteria
-
E. coli and the Body
- Normal E. coli in gut attach to large intestine
- Ingestion of E. coli by cow causes infection attaches to small intestine
- E. coli causes urinary tract infection attaches to bladder
- Each has specific adhesions to attach to specific cells
-
Establishment of Infection: Uptake by Host Cell
- Utilize sampling cells of intestine (M cells)
- •Shigella sp. causing shigellosis
- •Avoids getting degraded
-
Establishment of Infection: Effector Molecules
- Yersinia pestis causing plague
- Salmonella
- Induce endocytosis
- Gram negative
- -Type III secretion system
- -Ruffling
-
Shigella Uptake
- Hops from one cell to the next while damaging each cell he passes through
- Oral transmission
-
Determinants of Infectious Diseases: Avoiding Host Defenses
- Hiding in host cell – Shigella sp.
- Avoiding complement
- Avoid phagocytes by having C5a peptidase, toxins; Streptococcus pyogenes will destroy bacteria around
- Avoid recognition
-
Avoiding Complement
- Gram + not affected by MAC
- Thick layer of peptidoglycan on outside
- Neisseria gonorrhoeae- has proteins on surface to inactivate c3b
- Ex. Neisseria gonorrhoeae
- Cell wall contains a protein that binds and inactivates C3b
-
Avoid Recognition
- Capsules avoid complement proteins
- Fc receptors – Staphylococcus aureus
- Binds antibodies backwards
- Interfere with MCH I (found on all cells)
- Avoiding cytotoxic t cells
-
C5a
Inflammation cells release this (chemokine)
-
C5a Peptidase
Avoiding inflammation
-
Streptococcus pyogenes
- Strep throat, necrotizing fasciitis
- Destroys C5a with a peptidase
- Toxin streptolysin O damages host cell membranes
-
Interfering with MHCI
- Herpesviruses – ds DNA ex. Epstein Barr (mononucleosis)
- •Block processing and movement of MHC I to host cell surface
- Cytomegalovirus
- •Encodes for a “counterfeit” MHC class I molecule
-
Determinants of Infectious Diseases: Damage to Host
Exotoxin and endotoxins
-
Exotoxins
- Protein
- Neurotoxin (nervouse system), cytotoxin (cell death) and enterotoxin (intestine)
- A-B toxins
- Membrane damaging toxins
-
Endotoxins
- Lipopolysaccharides
- Dissemination of bacterial cell components result in inflammation throughout body - shock
- Part of bacterial cell wall breaks off lowering blood pressure not allowing blood to flow to organs, so body goes into shock
- Gram negatives
-
A-B Exotoxins
- Diphtheria toxin – Corynebacterium diptheriae
- Single molecule sufficient to kill cell
- B portion binds receptor
- A portion has catalytic activity
- Stops protein synthesis
- Causes heart failure
- Main targets are heart and respiratory tract
-
Lipopolysaccharides
- Lipid A- antigenic
- Immense innate response- inflammatory process that goes through whole body
- Septic shock
- Heat-stable- can add as much heat as wanted, has no effect
-
Bubonic Plague
- Yersinia pestis
- Found in Africa, South America, Middle East, Russia, and SW United States
- The bacteria multiply in the gut of the fleas
- Fleas regurgitate infectious material into bite wound
- Fleas transmit the disease to amplifying reservoir (rats, rabbits, etc.)
- Massive die-offs result in humans becoming next target
-
Vector Transmission
From flea to human
-
How Bubonic Plague Spreads
- Bacteria multiply at site of flea bite
- Enter lymph nodes; localized swelling & necrosis = bubo
- Accompanied by fever, headache, chills, nausea, weakness, & pain
- Swells because B and T cells are in the lymph nodes
-
Yersinia's Mechanisms
3 plasmids: small, medium, large
-
Yersinia's Small Plasmid
Protease Pla destroys C3b and C5a- avoids inflammation, opsonization
-
Yersina's Medium Plasmid
- Yops (Yersinia outermembrane proteins) injected by Type III secretion
- Yop H – disables phagocytes-avoids
- Yop M – blocks cytokine release- avoids signaling other immune responses
-
Yersina's Large Plasmid
- F1 capsule protein
- Resists phagocytosis
- Avoid complement proteins
-
Bubonic Plague
- Bacteria spread to blood in large numbers (septicemic plague)
- Intravascular coagulation & hemorrhage causes darkening of skin (“Black Death”)
- 50-80% mortality rate if untreated
- May spread to lungs (pneumonic plague)
-
History of HIV in US
- 1981 report showing unusual infections (P. carinii) in young homosexual men
- 1982 CDC had evidence cases were caused by infectious agent
- 1983 Pasteur Institute and NIH co-discovered retrovirus
- Both researchers created blood tests and applied for patents
- 1987 Pres. Reagan settled dispute
-
Central Africa in 1950's
- Simian Immunodeficiency Virus similar to HIV, hence HIV may have originated in African primates
- Spread from Africa to the Caribbean, and then to the US
-
Transmission of HIV
- Indiscriminate unprotected sexual contact, multiple partners
- Blood contact
- Transfusions
- Needle sharing
- Mother to fetus
- 1 in 10 miscarry
- 15-40% infants develop AIDS
-
Progression of HIV Disease
- Acute HIV syndrome initially
- Clinically latent stage
- Clinical AIDS
-
Acute HIV Syndrome Initially
- 1-6 weeks after exposure; virus replicates and is abundant in blood
- Acute retroviral syndrome (ARS): fever, sore throat, pharyngitis, rashes, moodiness
-
Clinically Latent Stage
- May last 10 years or longer
- Majority of transmission period
-
Clinical AIDs
- Lymphadenopathy syndrome (LAS)
- AIDS-Related Complex (ARC)
- Includes weight loss & diarrhea
- AIDS-defining conditions occur
-
AIDs Defining Conditions
- Cancer of uterine cervix, invasive
- Candidiasis of esophagus, trachea
- Mycobacterial disease
- Pneumonias occurring repeatedly
- Salmonella infection of bloodstream
-
HIV Type 1
- 10 subgroups of major group
- Single stranded RNA – 2 copies
- Surface proteins on envelope for entry
- Gp41
- Gp120
-
3 Proteins of HIV
- Reverse transcriptase
- Protease
- Integrase
-
Attachment of HIV
- Gp120 binds CD4 molecule an co-receptor on lymphocyte, macrophage, or dendritic cells
- Gp 120 brings virus to membrane
-
HIV Pathogenesis
- Internalization and uncoating
- Reverse transcriptase makes DNA copy of genome
- Viral DNA inserts into host cell genome
- Transcription of viral genome proceeds
- TH cells lyse while macrophages release virus
-
HIV Pathogenesis
- Results in depletion of CD4+ lymphocytes particularly TH
- Lysis
- Attack by CD8 T cells
- Antibody-dependent cellular cytotoxicity and natural killer cells
- Generalized dysfunction of uninfected cells also evident
- Steady drop of CD4+ cells over time
- High variability when vial genome is copied:
- Error rate in reverse transcriptase
- Ex. variable regions in gp120
-
Treatment of HIV
- No vaccine approved
- Medications to prolong asymptomatic stage:
- HAART (highly active antiretroviral therapy)
- Protease inhibitors
- R. t. inhibitors: analogs (AZT) or direct inhibitors
-
Side Effects of HIV
Anemia, vomiting, fatigue, liver and muscle damage, rashes, ulcers, etc.
-
Meninges
Three membranes that cover the brain and spinal cord
-
Meningitis
Inflammation or infection of meninges
-
Encephalitis
Generalized inflammation or infection of brain
-
Pathways to Central Nervous System
- Bloodstream – although it is difficult to cross the blood brain barrier
- Nerves
- Extensions from bone
-
Bacterial (Septic) Meningitis Symptom
- Bacteria enter by respiratory tract, spread to blood and taken to meninges
- Neutrophils and other inflammatory responses attempt to destroy
-
Viral (Aseptic) Meningitis
- Viremia occurs after infection of throat, intestine and lymphoid tissue
- Upon entering meninges, fewer neutrophils react
-
Viral Meningitis Infectious Agent
- Enteroviruses
- (ex. Echovirus and mumps virus)
-
Viral Meningitis Transmission
- Respiratory route
- (shaking hands, wiping nose)
- Fecal –oral route
-
Viral Meningitis Treatment
Only for symptoms
-
Viral Meningitis Symptoms
Stiff neck, severe headache, confusion, nausea – last 7-10 days; recovery is complete
-
Bacterial Meningitis Infectious Agent
- Haemophilus influenzae
- Streptococcus pneumoniae
- Neisseria meningitidis
-
Bacterial Meningitis Transmission
- Respiratory route
- (coughing, kissing, sneezing)
-
Bacterial Meningitis Treatment
- Antibiotics for specific agent:
- Penicillin
- (preventative measure with rifampin)
-
Bacterial Meningitis Symptoms
- High fever, stiff neck, severe headache, nausea several hours or 1-2 days
- Death or disability if not treated promptly – due to bacterial cell wall components leading to toxic shock
-
Conjugate Vaccine for Meningitis
- H. influenza type b polysaccharide bound to a bacterial protein like the diptheria toxoid
- Administered since 1980s
-
Leprosy
- Also known as Hansen’s Disease
- Once common in Europe and Americas
- Now concentrated in India, Nepal, Myanmar, Madagascar, Mozambique and Brazil
- WHO goal of eradication by 2005
- Caused by infection by Mycobacterium leprae
- Aerobic, acid-fast, rod
-
Leprosy Symptoms
- Onset of increased or decreased sensation on patches of skin
- Areas enlarge, thicken and loose hair
- Loose all sensation
- Arms and legs become painful
- Eventual numbness in limbs with loss of fingers or toes
- Nose and ears also affected
-
Leprosy Pathogenesis
- Spread by contact with nasal secretions or skin abrasions
- M. leprae invades the small nerves of the skin, preferably in cooler areas
- Immune response can slow growth causing tuberculoid leprosy
- Bacterium can grow in macrophages and eventually grow uninterrupted, lepromatous leprosy
-
Leprosy Treatment
- Tuberculoid leprosy
- Rifampin and dapsone combination
- Lepromatous leprosy
- Multiple drug therapy used to avoid drug resistance
-
Staphylococcal Wound Infection Symptoms
- Swelling, redness, pain at site
- Fever and toxic shock
-
Pathogenesis of S. aureus
- 30-100% patients are carriers
- Coagulase to clot blood
- Clumping factor for colonization
- Protein A binds Fc of IgG
- Alpha toxin and other superantigens
- Can grow aerobically and anaerobically
- Gram positive cocci
-
Pathogenesis of S. epidermidis
- Adhere to medical devices then makes a glycocalyx
- Causes small abscesses in healthy
- If carried to bloodstream can cause subacute bacterial endocarditis
- Can grow aerobically and anaerobically
- Gram positive cocci
-
Staphylococcal Wound Infection Treatment
- Clean wounds or prompt closure
- Antistaphylococcal medication immediately before surgery
- Cephlasporins
- Lipopeptide – Cubicin
- Linezolid – Zyvox
-
Cat Scratch Disease Symptoms
- Enlargement of lymph nodes in 1-7 weeks after bite or scratch
- 22,000 annual cases mostly under age 18
-
Cat Scratch Disease Pathogenesis
- Bartonella henselae- gram negative bacillus
- Zoonosis of cats and occasionally fleas
- Bacillary angiomatosis:Skin lesions develop in AIDs patients
-
Cat Scratch Disease Treatment
- Clean wound
- Ampicillin for severe infections
- Disappears within 2-4 months
-
Tetanus
- Frequently fatal but rare in US
- Clostidium tetani
- Anaerobic, spore forming, Gram +
- Found in soil and sometimes gut of humans
- Know mode of action for diseases
- Not transmitted from person to person
-
Tetanus Symptoms
- Restlessness, irritability and difficulty swallowing
- Sustained, painful and uncontrolled muscle spasms
- Death by pneumonia or regurgitation into lungs
-
Pathogenesis of Tetanus
- Endospore introduced into tissue by deep wound
- Vegatative cells produce tetanospasmin (AB toxin) into blood
- Enters neurons in brain
- Prevents release of neurotransmitters by inhibitory neurons
- Results in spastic contraction of muscles
- Neonatal tetanus
- Cutting of umbilical cord by unsterile instrument
-
Treatment of Tetanus
- Prevention- vaccine with tetanus toxoid
- Booster required at school age and every 10 years
- Can cross the placenta
- Tetanus immune globulin (TIG)
- Wound cleaned of dead tissue
- Antibacterial - metronidazole
-
Bacterial Cystitis Symptoms
- Frequent and painful urination
- -Because of inflammation
- Cloudy and/or red urine
- -Cloudy-white blood cells/pus killing off cells that are infected or bacteria
- -Red-capillaries are broken during the process of infection
- Complication: pyelonephritis
-
Bacterial Cystitis Pathogenesis
- Multiple species; commonly E. coli
- Travel up urethra to cause inflammation
-
Bacterial Cystitis Treatment
Antibiotics for species; usually β lactam
-
People most Susceptible to Bacterial Cystitis
- Sexually active women
- Men over 50
-
During intercourse, fecal matter gets pushed back into the anus and near the urinary tract
Why would E. coli be the common infectious agent for bacterial cytosis?
-
Leptospirosis Symptoms
- Many asymptomatic
- Headache, fever, chills, muscle pain
- Severe: momentary relief then bleeding; heart, brain, kidney damage
- Generally last 1-2 weeks, but small percentage still has infection although symptoms are gone (body starts shutting down)
-
Leptospirosis Pathogenesis
- Leptospira interrogans
- Enters mucous membranes then multiplies in bloodstream
- Ig’s and complement destroy most of pathogen
- Larger immune response injures host causing blood clotting
- Uses hook to attach to mucus membrane
- Once attached to mucus membrane past epithelial cells wants to replicate in bloodstream not mouth/nose
- Massive inflammatory response in vital organs ie damage to organs
-
Leptospirosis Epidemiology
- Exposure to urine of infected animals
- Can hang out and be infectious for 2 or 3 days, in mud can last 2-3 weeks
-
Leptospirosis Treatment
- Tetracycline
- Vaccines for domesticated animals
-
What is the mode of action for tetracycline?
- Blocks tRNAs from entering ribosome
- Bacteriostatic: Keeps it from growing
- Broad spectrum: Have a variety of organisms it can be effective against
- Inhibiting translation
-
Non Venereal: Bacterial Vaginosis Symptoms
- Thin, grayish white discharge
- Strong odor
-
Non Venereal: Bacterial Vaginosis Pathogenesis
- Increase in Gardnerella vaginalis and anaerobic bacteria
- Decrease in normal vaginal flora
- Increase in clue cells
- Not a sexually transmitted disease, but only women who are sexually active show the symptoms
- Deals with air, but is not aerobic
-
Most Susceptible to Non Venereal: Bacterial Vaginosis
- Women during childbearing years
- Preterm birth in pregnant women, can cause miscarriage
-
Non Venereal: Bacterial Vaginosis Treatment
Metronidazole
-
Clue Cells
Epithelial cells covered in bacterial vaginosis
-
Metronidazole
- Antiprotoxoal and antibacterial agent
- Disrupts DNA’s helical structure
- Affects replication and transcription
-
Venereal: Trichomoniasis Symptoms
- Itching in genital area
- Frothy, yellow-green vaginal discharge
- Men usually asymptomatic
-
Venereal: Trichomoniasis Pathogenesis
- Unknown method by Trichomonas vaginalis
- Froth produced by hydrogen gas
-
Venereal: Trichomoniasis Treatment
Metronidazole- anti-protazoic and anti-bacterial
-
Venereal: Trichomoniasis Epidemiology
- 5 million Americans acquire each year
- Sexual transmission
- Humans only reservoir
-
Sexually Transmitted Diseases
15 million Americans (3 million teenagers) annually
-
Types of Sexually Transmitted Diseases
-
-
-
Prevention of STDs
- Abstinence
- Monogamous relationship
- Condom (decreases chance of transmission)
-
Chlamydia Symptoms
- Frequent and painful urination
- Thin gray-white discharge
- Possible abdominal pain
-
Chlamydia Pathogenesis
- Chlamydia trachomitis
- Travel up urethra or vagina; can attach to sperm
- Induces endocytosis by epithelial cells
- Inflammation by cytokines, sends off MHC I
- Inflammation of fallopian tubes – pelvic inflammatory disease
- Inflammation of epidimymis – sterility
-
Chlamydia Treatment
- If sexually active, have yearly tests
- Azithromycin, tetracycline and erythromycin
- Inhibit translation
-
Most Susceptible to Chlamydia
One study: 14% high school and college women were carriers
-
Inflammation of Fallopian Tubes
Causes scars, blocking eggs to transport
-
Inflammation of Epidimymis
Sperm can’t move and travel outside of penis, long term effect
-
Ectopic Pregnancy
Egg is fertilized outside of uterus
-
Chlamydia
- Attaches to epithelial cells as an elementary body and induces endocytosis
- Attaches using pili specific for epithelial cells
- Obligate intracellular bacteria inside host cell is called reticulate body
- Repeatedly divides to allow release of elementary bodies from host
- Divides so fast, before immune system catches up, infection is released to other cells
-
T-cells, t-cytotoxic
- Much of the tissue damage results from the cell-mediated immune response”
- Who is actually damaging tissue?
-
Chlamydia and the Population
- Females show more symptoms
- Males are more likely to be carriers
-
Chancroid Symptoms
- Painful ulcers in genital region – soft chancres
- Swelling of lymph nodes
-
Chancroid Pathogenesis
- Uncertain of method by Haemophilus ducreyi
- Small pimple occurs then ulcer
- Pus filled lymph nodes may rupture
-
Chancroid Epidemiology
- Largely unreported or undiagnosed
- May contribute to HIV transmission
- Men more likely to show symptoms
-
Chancroid Treatment
Erythromycin
-
The epithelial cell walls have been broken down
An ulcer is an open wound
As with any STD that produces ulcers, HIV transmission can be enhanced during unprotected sex. Why is this the case?
-
Genital Warts Symptoms
- Small warts at site of infection – papillomas
- Lesions of cervix
- Asymptomatic
-
Genital Warts Pathogenesis
- Human papillomavirus; non-enveloped, ds DNA
- -Replication is easy because of ds DNA, can rely on host
- 30 types by sexual transmission
- 15 types linked to cervical cancer
- Infect deeper epithelial cells by small abrasions
- Latent infection
- Waits on host to die to exit body (naked or non enveloped)
-
Genital Warts Transmission
- Single sexual exposure – 60% chance of infection
- Can infect mouth as well as genitalia
- Even if you wear a condom, infection can affect outside of vagina instead of inside
-
Genital Warts Treatment
- Freezing or laser
- Imiquimod
- Yearly Pap smear
-
Imiquimod
Anti-viral agent to inhibit replication of virus
-
Genital Warts
- 20 million in US currently infected
- Half are ages 15 through 24 years
- 12,000 women are diagnosed with cervical cancer yearly; 4,000 women die
-
Genital Warts Prevention
- HPV vaccine
- Non-infectious HPV-like particles
- HPV 16 and 18, which cause 70% of cervical cancers, and HPV 6 and 11, which cause 90% of genital warts
- Recommended for 11 and 12 year-old girls
- Inactivated vaccine
- Sub-unit vaccine
-
Meningococcal Meningitis Symptoms
- Mild cold, throbbing headache, fever, stiffness of neck and back, nausea and vomiting
- Purplish spots – petchiae on skin
-
Meningococcal Meningitis Infectious Agent
- Neisseria meningitidis
- Gram negative, aerobic
- Polysaccharide capsule
-
Endotoxin of Meningitis
- N. meninigitidis releases endotoxin into bloodstream during binary fission or autolysis
- Resulting in shock
-
How does endotoxin cause shock?
- Shock is the state where not enough blood pressure is circulate blood properly
- Circulating endotoxin causes inflammatory response body-wide
-
Tuberculoid Leprosy
- 6 months
- Rifampin and dapsone combination
- Dapsone acts as a metabolite inhibitor
-
Lepromatous Leprosy
- 2 years
- Multiple drug therapy used to avoid drug resistance
- Third drug of clofazimine which binds mycobacterial DNA
-
Superanitgen
- Overrides the specificity of T-cells and causing massive release of cytokines by a large number of TH cells
- Stimulates hundreds more T cells by binding to MHC II and T cell
- Results in fever, nausea, vomiting and shock
- Toxic shock
-
Staphylococcus
- Transmitted by wound or surgical site
- Results in
- Delayed healing
- Formation of abscesses
- Spread of bacteria or their products into other tissue or blood
- 20% of healthy adults are carriers
- Transfer usually by hands
-
You’re trying to get rid of the toxin and the source so you give both
Would you administer both the immune globulin AND the antibiotic? If not, which one and why?
-
Yes, you just have to be exposed to the toxin
Could someone have tetanus without finding bacteria in the wound?
-
Streptococcal Pharyngitis Symptoms
- Painful swallowing, fever
- Red throat with white patches
- Enlarged neck lymph nodes
- Activate B and T cells
-
Streptococcal Pharyngitis Epidemiology and Pathogenesis
- Streptococcus pyogenes by inhalation of respiratory droplets
- Gram positive coccus
- Peak incidence among school children in winter and spring months
-
Streptococcal Infections
- Group A streptococci: Streptococcus pyogenes
- Virulence factors
- Hemolysins : streptolysin O and S- beta hemolysis- likes red blood cells, wants to take up as much iron as it can
- Protein G- Fc receptor
- Protein F for attachment
- Capsules of hyaluronic acid- coats itself in the capsule by avoiding the immune system response
- C5a peptidase
- M protein: Inactivates C3b- Compliment
-
What is the advantage of inhibiting C5a and C3b?
- C5a- cytokine for chemotoxins
- The “bread crumb trail” neutrophils follow to infection
- C3b part of complement system- binds to surface of bacterial cells
- Opsinization
- Memory attack complex
- Inflammation
- Strep cuts off trail for neutrophils to find infection phagocytosis does not occur
- Fc binds antibodies tail side in (opposite)
-
Strep Throat Pathogenesis
- Streptococcal pyrogenic exotoxins - superantigens
- Complications due to lack of treatment
- Scarlet fever – during infection, roughening of skin and red rash caused by erythrogenic toxin
- Acute rheumatic fever – inflammation of joints, heart, skin and brain 3 weeks after recovery
- Results in permanent heart valve damage
-
Strep Throat Treatment
Penicillin or erythromycin
-
Strep Throat Pathogenesis
- T helper cells are activated huge immune response
- Super antigens cause a body wide rash during strep throat infection
- Heart valve damage- bacteria can start colonizing in the area- clot of bacteria leaves area of infection and can go to brain causing a stroke
-
Whooping Cough (Pertussis) Symptoms
- Runny nose then violent uncontrollable coughing
- -Infective during this period
- Paroxysmal coughing
- Infants most at risk for mortality
- Pneumonia can inset and kill you
- -Caused by bordetella pertussis or another infection
-
Whooping Cough (Pertussis) Causing Agent
- Bordetella pertussis
- Aerobic gram negative rod
-
Whooping Cough (Pertussis) Pathogenesis
- Inhalation of droplet and attachment of respiratory epithelium
- Grow in dense masses on surface
- Pertussis toxin and filamentous hemagglutinin
- Increased mucus production and sloughing of ciliated cells
- Pneumonia or secondary bacterial infection causes death
-
Pertussis Toxin
- A-B toxin
- B portion binds to host surface
- A portion penetrates cytoplasmic membrane
- Causes overproduction of cAMP thus increasing mucus production
-
Pertussis Treatment
- Acellular vaccine given with diphtheria and tetanus toxoids –DTaP
- 5 doses before 18 months and one more at age 4
- Erythromycin for infection
- A-cellular vaccine- injecting parts of the cells or a protein off of the cell
- DTaP- inactivated vaccine
-
Respiratory Syncytial Virus (RSV) Symptoms
- Cough wheezing and difficulty breathing
- Causes of croup, cold with loud high-pitched cough in older infants
- 90,000 hospitalizations yearly with 4,500 deaths
-
Respiratory Syncytial Virus (RSV) Causative Agent
Respiratory syncytial virus, enveloped with SS RNA genome
-
Respiratory Syncytial Virus (RSV) Pathogenesis
- Enters by inhalation and infects respiratory tract epithelium
- Bronchiolitis with partial plugging by dead sloughed cells and mucus
- Obstructed airway by dead cells
-
Respiratory Syncytial Virus (RSV) Prevention
Palivizumab, no vaccine
-
Highly contagious during runny nose period
Causes mucus productions and schlepping off ciliated cells
Baby doesn’t have enough antibodies
Why does the incidence of whooping cough rise promptly when pertussis immunizations are stopped?
-
Cytotoxins
How would you classify the pertussis toxin?
-
Passive active immunity
Palivizumab for RSV is a monoclonal antibody. What kind of immunity is acquired from it?
-
Rotaviral Gastroenteritis Symptoms
- Vomiting, slight fever, profuse watery diarrhea
- Almost every child in the US is infected at some time before age of 5
-
Rotaviral Gastroenteritis Causative Agents
- Rotaviruses
- Double walled capsid- two layers of protein
- Double stranded, 11 segment RNA genome
-
Rotaviral Gastroenteritis Pathology and Epidemiology
- Infects epithelial cells of small intestine, causing death
- Fecal–oral; fomites
- Responsible for 25% of traveler’s diarrhea
-
Uses his own RNA polymerase that recognizes RNA to replicate not DNA
How does rotavirus replicate its genome in small intestine epithelial cells? What does it require to replicate?
-
Yes
- Would it be possible for reassortment to occur if there was a coinfection of rotaviruses?
- Reassortment- two different viruses affect the same cell- share their genetic information
-
Cell lysis because of virus replication using all of the body’s nutrients
How does cell death occur since it is a naked virus?
-
Norovirus Gastroenteritis Symptoms
- Nausea, vomiting and diarrhea that lasts 12-60 hours
- Infects from age 5 to adult
-
Norovirus Gastroenteritis Causative Agent
- Norovirus
- Nonenveloped, single stranded RNA genome
-
Norovirus Gastroenteritis Pathology and Epidemiology
- Fecal–oral, highly contagious
- Typically infect children and adults
- Infect upper small intestinal epthelium
-
Norovirus Gastroenteritis Prevention
Hand washing
-
Hand scanners in dorms, dining halls, and gym
What would be a likely scenario to how the students obtained the virus?
-
Hepatitis A
- “Infectious hepatitis”
- No animal reservoir
- Hepatitis A virus (HAV)
- Single stranded, +RNA, icosahedral, naked
- Humans are the only ones who carry hepatitis A
-
Hepatitis A Symptoms
- Fatigue, fever, nausea, diarrhea, chills, jaundice, clay colored feces
- Children – asymptomatic- how a lot of transmission occurs
- Adults – 20% require hospitalization
- Recovery within a month
-
Hepatitis A Epidemiology and Pathogenesis
- Fecal-oral
- Fecal contaminated water was being used to wash green onions
- Ingested virus replicated in intestinal epithelium
- Once in blood, targets liver to replicate
- Liver tissue damaged with inflammation
- New viruses released into feces by bile secreted to small intestine
- T-cytotoxic cells come in to kill
- When red blood cells die, hemoglobin is being used replacing it with billyreuben cells
- Liver can’t clear out billyreuben causing feces to be clay like color
- In 2007- 1 in 100,000 people will get Hepatitis A
- Termed infection hepatitis
-
High Risk Groups for Hepatitis A
- Crowded and poor sanitation areas
- Day care centers, nursing homes
-
Hepatitis A Prevention and Treatment
- Detected by anti-hepatitis A antibody
- Hepatitis A vaccine - inactivated virus (1990s)
- Routine immunization schedule for infants
-
Vaccines
What would account for the drop in overall incidence of Hepatitis A?
-
CDC put out an announcement to health centers to promote Hepatitis A vaccine
There is a typical pattern of peak incidence in the US every 10-15 years. Why would there be a second drop in incidence particularly in the West right before 2000?
-
Hepatitis B
- "Serum hepatitis”
- 40% viral hepatitis cases in US
- 4.5 million cases for Hepatitis B and C infection
- Can become chronic
- Hepatitis B (HBV)
- Double-stranded circular DNA, enveloped
- Antigen: HBsAg (surface antigen); core antigen (HBcAg); e antigen (HBeAg)
- Normally acute, but can turn chronic
- Different virus that Hepatitis A
-
Hepatitis B Symptoms
- May be asymptomatic
- Similar to HAV but more severe
- Death from liver failure in up to 10% of hospital cases
-
Hepatitis B Epidemiology
- Exposure by blood, semen, sweat, saliva, urine, feces
- Can be passed by injection, rubbed into minor wounds or by mouth
- Most likely passed among homosexual men
-
Hepatitis B Pathology
- Carried to liver by bloodstream
- Causes liver injury by inflammation
- HBsAg appears in blood days or weeks after infection
- Found as small, large spherical or tubular particles
- 1-6% become chronically infected
- 40% die of cirrhosis or liver cancer
- Generally don’t see jaundice
-
Hepatitis B Virus
When budding, virus can have envelope particles with no nucleus in it
-
HBV Replication
- Upon entry, DS DNA is transcribed in host nucleus
- RNA copy of genome packaged in capsid
- Reverse transcriptase makes copy of single DNA then double strand
- Does not have a complete dsDNA
- -Host polymerase completes dsDNA
-
Hepatits B Prevention
- Genetically engineered HBsAg vaccine
- Recommended for adults with multiple partners and homosexual men
- Known exposure: hepatitis B immune globulin (HBIG)- given artificial passive immunity
-
Hepatitis B Treatment
- Injections of genetically engineered interferon
- Antiviral medication – reverse transcriptase inhibitor
- Inactivated subunit vaccine
- -Injecting just a piece of genetically engineered HBV
- Interferon's is the cell signal to alert other cells to come attack HBV infection
-
Hepatitis C
- Most common chronic blood-born infection in US
- Hepatitis C virus (HCV)
- Single-stranded, +RNA, enveloped
- Considerable genetic variation among infected individuals
- You see subtypes- hard to find a vaccine
-
Hepatitis C Symptoms
None or very mild symptoms similar to HAV, HBV
-
Hepatitis C Epidemiology
- Blood exposure, fecal-oral, sexual, organ transplantation
- Toothbrush, razors, towels, tattoos, needles
-
Hepatitis C Pathogenesis
- 80% of those infected become chronic
- Inflammation and immune response causes scarring of liver
- Cirrhosis and liver cancer develops in 10-20%
-
Hepatitis C Treatment
- No vaccine
- Interferon treatment along with an antiviral nucleoside derivative helps relieve symptoms for 30 50% of those infected
-
Yes, because they are three totally different viruses
You will receive a booster for A and B if you have C
If you had chronic hepatitis B, could you still be infected by hepatitis A and C?
|
|