-
presence of microorganism
infection
-
can be from microorganism
disease
-
microorganism cause of disease
pathogen
-
capacity of microorganism
pathogenicity
-
mechanism of pathogen
pathogenesis
-
measure of pathogen
virulence
-
toxin capsule receptors pili flagella
virulence factors
-
mouth eye nose genitals wounds
how pathogens enter host
-
specific to host cells part of how pathogen cause disease
adhere to host cell
-
inter-cellular spaces
bodily fluids
intracellular
ways for pathogen to cause disease
invade or colonize
-
cells die induce host immune response
ways for pathogen to cause disease
inflict damage
-
maintain a ______________ in nature
reservoir
-
no apparent symptoms carrier
in-apparent sub-clinical
-
can transmit disease to others
dormant latent
-
zoonosis, inadvertent
accidental
-
caused by normal flora or transient bacteria
host immune system is compromised
opportunistic
-
obvious infection or disease
primary
-
infection subsequent to primary infection
secondary
-
two or more microbes infecting the same tissue
mixes
-
rapid onset brief duration
acute
-
last for long duration
chronic
-
affecting many organ systems
generalized
-
-
microbes ascend in a duct or tube against the flow of secretions
retrograde
-
occur suddenly and intensely
fulminant
-
fingers
body fluids
fomites
food
flies
feces
six ways to spread pathogens
-
hygiene
*personal hygiene
*water treatment
*sewage
*antimicrobial
Vaccination
*live-dead-toxoid-recombinant
prevention of disease
-
antibiotics antivirals
supportive
*treat symptoms
treatment
-
*symptoms
blisters
itchy
virus becomes latent in spinal ganglia
Reyes syndrome in children
chicken poxs
-
varicella zoster virus
herpes virus family
chicken pox
-
respiratory
skin to skin contact
chicken pox
-
cell mediated immunity (t cells)
host defense chicken pox
-
clinical presentation
chicken pox diagnosis
-
avoid exposure to virus
vaccination
chicken pox prevention and treatment
-
zoster
reactivation of latent virus
virus travels down nerves and produces blisters
appear in band
can be life threatening in immunocompromised
shingles
-
*symptoms
– Raised overlapping rash over the entire body
– Pustules arise deep in the skin
– Pustules form a crust and scab over
– Scabs fall off
smallpox
-
Variola major
• Severe form• Very high fever
• 30% fatality rate– Blindness–
Variola minor
• Less rash
• Lower fever
• 1% fatality rate
smallpox
-
Transmission
– Direct contact (inhalation
– Bodily fluids
– Fomites
smallpox
-
Host Defense:
– Interferon
– Humoral and cellular immunity
smallpox
-
Diagnosis:
– Clinical presentation
– Isolation of virus
smallpox
-
Prevention & Treatment
– Vaccine (Jenner)
smallpox
-
Current interest:
– Last US case 1949, Last case in the world, Somalia 1977
– Cultures at CDC and Russia– Fear of bio-terrorism
smallpox
-
• Symptoms
– Fever, cough, runny nose
– Koplik spots
– Rash begins on face and spreads through out the body
– Complications:
• Brain damage from encephalitis
• Could have secondary bacterial infection
– Death from bacterial pneumonia
measles
-
Cause
– virus
– Enveloped, RNA virus
– Only human host
measles
-
Transmission
– Inhalation
– Highly contagious
measles
-
Host Defense
– Cell mediated immunity
measles
-
Diagnosis
– Presence of giant cells (formed by virus fusing together human cells and RBC)
– Koplik spots
measles
-
Prevention & Treatment
– Live attenuated vaccine
measles
-
German measles/ three day measles
rubella
-
Symptoms
– Rash
- Fever
– Enlarged lymph nodes
- stiff joints
rubella
-
Cause– Rubella virus
rubella
-
Transmission
– Respiratory droplet
– Virus multiplies in respiratory tract and spread throughout the body
– Mother to fetus: teratogen
rubella
-
Host Defense
– Life long immunity
– Cellular and humoral
rubella
-
Diagnosis
– Symptoms
– Serology
rubella
-
Prevention & Treatment
– Live attenuated virus vaccine
– Antiserum for pregnant women exposed to virus
rubella
-
HSV-1
Herpes Simplex Virus
-
Symptoms
– Cold sores/ fever blister
– Sub-clinical
hsv
-
Transmission
– Oral
– Respiratory
– Contact
hsv
-
Latency
– Latent in trigeminal nerve ganglion
hsv
-
Occurrence
– 90% of people infected
hsv
-
-
Impetigo:• Superficial, skin wound• Oozes a clear fluid• Forms a crust• Most common in children• Glomerulonephritis
Streptococcus pyogenes
-
Erysipelas:• Infection of the dermis• Spreads rapidly through lymph• Enter blood stream, could be fatal
Streptococcus pyogene
-
Streptococcal gangrene• Deep tissue infection• Intense inflammation destroys blood vessels & tissue• Bacteria enter blood, could be fatal
Streptococcus pyogenes
-
Transmission– Contact with wound secretions
Streptococcus pyogenes
-
Host Defense– Antibodies to surface proteins & toxins
Streptococcus pyogenes
-
Diagnosis– Isolation of bacteria
Streptococcus pyogenes
-
Prevention & Treatment– Antibiotics
Streptococcus pyogenes
-
Impetigo• Superficial skin layers
Staphylococcus aureus
-
Folliculitis & Cellulitis• Pus filled lesions within hair follicles• Diffuse skin infection
Staphylococcus aureus
-
Scalded skin syndrome• Exfoliating toxin• Skin peels off
Staphylococcus aureus
-
Transmission– Contact with wound or fomites
Staphylococcus aureus
-
Host Defense– Antibodies
Staphylococcus aureus
-
Diagnosis– Isolate bacteria from the wound
Staphylococcus aureus
-
Prevention & Treatment– Clean all wounds– Good hygiene– Antibiotics
Staphylococcus aureus
-
Causative agent Strains of Staphylococcus aureus
toxic shock syndrome
-
Symptoms– High fever with chills– Nausea Vomiting– Diarrhea Headache– Red rash followed by peeling of the skin(especially palms & soles of feet)– Confusion Seizures– Hypotension– Organ failure (kidneys and liver)
Toxic Shock Syndrome
-
Risk factors– Barrier contraceptives– Tampons– Surgery– Open wounds– S. aureus infection
Toxic Shock Syndrome
-
• Toxin– Toxic shock syndrome toxin (TSST
)– Toxic shock-like syndrome toxin by Streptococcus spp.
Toxic Shock Syndrome
-
Treatment– Antibiotics– Supportive– Eliminate predisposing factors
Toxic Shock Syndrome
-
Symptoms– Infects deep wounds– Produces alpha-toxin and gas– Skin turns black, renal failure & death
Clostridium perfringens
-
Cause– Clostridium perfringens– Gram positive anaerobic rod– Grows in soil
Clostridium perfringens
-
Transmission– Contamination of wounds with soil
Clostridium perfringens
-
Host Defense:– Antibodies
Diagnosis:– Gas under the skin– Isolation of bacteria
Clostridium perfringens
-
Prevention & Treatment– Antibiotics– Antitoxin– Hyperbaric chamber– Remove dead tissue (amputation
Clostridium perfringens
-
Mostly in men, rarely women
• Symptoms– Infection of the skin– Skin is locally red, may oozefluid– Tinea pedis, capitis, cruris,unguinum, corporis
ringworm
-
Cause– Trichophyton– Microsporum– Epidermophyton
Ringworm
-
Transmission– Soil
Clothes
Fomites
ringworm
-
*Host Defense– Cell mediated immunity– Local inflammation
• Diagnosis– Symptoms
• Prevention & Treatment– Topical antifungals: miconazole– Oral: griseofulvin
ringworm
-
• Symptoms
– Thrush: white plaques on mucous membranes
– Diaper rash: red raised rash
– Vaginitis: Women susceptible following antibiotics,contraceptives, hormonal changes
– Systemic: immunocompromised, fatal
candidiasis
-
Cause
–Candida albicans
– Opportunistic pathogen
candidiasis
-
• Prevention & Treatment
– Antifungals: miconazole or nystatin
– Keep skin dry
candidiasis
-
• Symptoms
– Mite lives in the epidermis
– Severe itch
• Cause
– Sarcoptes scabiei
-mite
scabies
-
• Transmission
– Close contact
– Fomites
– Found worldwide, epidemicsevery 15 years and last 15 years
scabies
-
*Host Defense:– none
• Diagnosis– Identifying mites and eggs undermicroscope
• Prevention & Treatment– Medication kills mites– Itching stops only after the infectedskin layer is shed
scabies
-
Allows very few compounds to pass throughinto the brain
blood brain barrier
-
cerebrospinal fluid
fluid contained within spinal column
-
Organisms (Bacterial meningitis)
– Neisseria meningitidis• meningococcal
– Haemophilus influenzae
– Streptococcus pneumoniae• pneumococcal
– E. coli (oppirtunistic)
meningitis
-
spinal tap
diagnosis of meningitis
-
Pathogenesis
– inflammation of the meninges membrane
• brain and spinal cord
– sudden fever, severe headache, neck rigidity
meningitis
-
Occurs mostly in children (6 months to 4years)
• Gram-negative aerobic bacteria,• normal throat microbiota
• Capsule antigen type b
• Prevented by Hib vaccine
Haemophilus influenzae Meningitis
-
• N. meningitidis
• Gram-negative aerobic cocci, capsule
• 10% of people are healthynasopharyngeal carriers
• Begins as throat infection, rash• Serotype B is most common in the UnitedStates
• Vaccination recommended for collegestudents.
Neisseria Meningitis,Meningococcal Meningitis
-
• Gram-positive diplococci
• 70% of people are healthynasopharyngeal carriers• Most common in children (1 month to 4years)
• Mortality: 30% in children, 80% in elderly
• Prevented by vaccination
Streptococcus pneumoniae Meningitis,Pneumococcal Meningitis
-
– viral origin
– Most common type of meningitis
– No treatment
Aseptic meningitis
-
– Cryptococcus neoformans
– occurs with underlying condition (surgery,immunocompromised
Cryptococcal meningitis (fungal)
-
*Treatment
– Antibiotics for bacterial infections
• Prevention
– Vaccine against meningococcal meningitis, Hib
meningitis
-
• Organism– Clostridium tetani– Spore former– Anaerobic growth• deep wounds• decaying tissue
tetnaus
-
• Pathogenesis– tetanospasmin• neurotoxin• ink dot enough for 30 deaths– contraction of muscles• spastic paralysis• lockjaw• respiratory distress
tetnaus
-
• Treatment– before clinical symptoms• antitoxin• blocks toxin– after clinical symptoms• no treatment
• Prevention:– vaccine every 5-10 years– toxoid• develop antibodies against toxin, not organism
tetanus
-
• Organism– Clostridium botulinum• spores• growth inhibited by low pH
• Pathogenesis– blocks release of acetylcholine– interferes with nerve impulse– Flaccid paralysis– paralysis of respiratory muscles– mortality 35%
botulism
-
• Different types of toxin– produced by different strains of C. botulinum
– Type A
• most potent
• west of Mississippi River
botulism
-
• Age associated
– infant botulism
• differences in normal biota
– adult botulism
• food poisoning
• heat-labile toxin
botulism
-
Symptoms
– Skin rash Chronic infection
– Peripheral nerve damage
– Loss of sensation
leprosy
-
• Indeterminate: skin lesions, early stage• Tuberculoid– Cell mediated response– Infection is contained– Positive skin test– Loss of sensation in discrete spots
• Lepromatous– Poor immune response– Skin damage– Negative skin test (no T-cell response)– Loss of fingers, toes, nose
leprosy
-
• Cause– Mycobacterium leprae– Hansen’s disease (Gerhard Hansen)– Bacteria grow slowly– Grows in peripheral nerves and skin cells
• Transmission– Direct contact– Nasal secretions
leprosy
-
• Host Defense– Effective cell mediated response– Antibodies are present but not protective
• Diagnosis– Positive skin test– Bacteria in nasal secretions
• Prevention & Treatment– Multidrug therapy– Killed M. leprae vaccine
leprosy
-
• Cause– virus
– Bullet-shaped
• Epidemiology– reservoir: all mammals– humans: end of infectious cycle
rabies
-
• Symptoms– Flu-like initially– Excitation phase:
• Neurological symptoms, loss of muscle control, speechimpaired, hydrophobia– Paralytic phase• muscles weaken, loss of consciousness and death
rabies
-
• Prevention– reduce exposure of virus in animals• wild mammals--uncontrollable reservoir• bats--dormant for long periods• domestic—vaccine
rabies
-
• Diagnosis– Clinical symptoms– Identifying virus in nerve tissue– brain tissue (negri body)• Treatment– Vaccine– Immune globulin immediately following infection
rabies
-
• Cause– virus– Picornavirus
polio
-
• Pathogenesis– alimentary phase--primarymultiplication– lymphatic phase--tonsils,lymph nodes– viremic phase--spread inblood– neurological phase--CNS,extraneural tissue
• requires persistent viremia
• low levels of antibodiesprevent spread
• >l% of infections lead to severe paralytic infection
poliomyelitis
-
• Prevention &treatment– two vaccines• oral (OPV)--attenuated--Sabin
• injected (IPV)--inactivated—Salk
– WHO eradicationeffort
polio
-
• Encephalitis– Inflammation of the brain
• Symptoms– Fever - headache - stiff neck– Confusion - paralysis - convulsions– Sleepiness - Coma
Arbovirus Encephalitis
-
• Eastern Equine Encephalitis (EEE)– severe
• Western Equine Encephalitis (WEE)
• California Encephalitis (CE)
• St. Louis Encephalitis (SLE)
• Japanese B encephalitis– endemic areas of Asia
- • Arthropod borne viruses
- arbovirus encephalitis
-
• Diagnosis– Based on symptoms & case history– Easier during epidemics
• Transmission– Mosquitoes (Culex, Aedes)– Birds are the carriers– Small mammals, birds and horses are reservoirs
arbovirus encephalitis
-
• Treatment & Prevention– Supportive care– Japanese encephalitis has a vaccine– Control mosquito population
arbovirus encephalitis
-
• Diseases– Bovine spongiform encephalitis– Sheep scrapie– Creutzfeldt-Jakob disease– Kuru
• Cause– Prions– Aberrant proteins
Spongiform encephalitis
-
Transmission– Consumption of infected animal products– Transfusion of infected blood
spongiform encephalitis
-
• Prevention– Screen blood– Screen animal products
• Treatment– None– Chronic, fatal
prion diseases
-
bacteria in blood
bateremia
-
bacteria persist in blood and is fatal
septicemia
-
• Dr. Carlos Juan Finlay & Dr. Walter Reed
• Disease– Mosquito bite introduces virus into host– Virus travels to lymph node and blood– Multiplies in the liver– Fever, headache, weakness– Severe fever, chills, headache, jaundice, uncontrolledbleeding– 15 - >50% mortality in severe cases
yellow fever
-
• Cause– Yellow fever virus– Small RNA virus
• Transmission– Mosquito, Aedes aegypti– Non-human primates-mosquitoes-humans
• Host Defense– Immune after infection
yellow fever
-
• Diagnosis– Symptoms
• Prevention & Treatment– Restrict mosquito population– Treat standing water– Live attenuated vaccine for people in regions with disease andtravelers (strain 17D)
yellow fever
-
• Disease– Ebola hemorrhagic fever– Extensive bleeding– Destruction of internal organs– >90% fatality rate (25-90%)
ebola
-
• Symptoms– Fever, headache, joint & muscleache, sore throat, weakness– Diarrhea, vomiting, stomachpain– Rash, red eyes, internal & external bleeding– Death in those who do notdevelop an immune response
ebola
-
• Cause– Ebola virus– Enveloped RNA virus
ebola
-
• Transmission– Maintained in animals– Index case: contact with infectedanimal– Person to person: Direct contact withinfected blood or bodily fluids– Fomites
ebola
-
• Prevention & Treatment– Supportive care– Isolation of patients and properdisposal of infected items to preventspread
ebola
-
• Disease– Infectious mononucleosis– Fever, fatigue, sore throat, swollenlymph nodes– Enlarged atypical lymphocytes– Enlarged spleen (could rupture)
epstein barr virus
-
• Cause– Epstein Barr Virus (EBV)– Enveloped DNA virus– Latent in B lymphocytes
EBV
-
• Transmission– EBV is secreted into the saliva– Saliva containing fomites
• Diagnosis– Clinical diagnosis– Serological: increased number of lymphocytes/WBC– Presence of enlarged suppressor T cells (which stopproliferation of infected B cells)
• Prevention & Treatment– Present in >90% of adults– Reactivates periodically and is present in saliva
EBV
-
• Lower respiratory tract infection
• Symptoms– Fever– Muscle aches– Respiratory distress, fluid in airspaces– Death by catastrophic lung failure
hantavirus
-
• Cause– virus: Sin nombre– Known to cause kidney disease as well– Known to Native Americans before the 1993 incidence
• Transmission– Mouse droppings aerosolized
hantavirus
-
• Occurrence– In small clusters, rural– Places with known large rodentpopulations– Four corners region
• Host defense– None
hantavirus
-
• Prevention & Treatment– Avoid contact with rodents– Keep areas free of rodents– Treatment is supportive care
hantavirus
-
• Disease Symptoms– Fever; Severe muscle and joint pain ‘Breakbone fever’; Rash– Severe form: dengue hemorrhagic fever (DHF)
• Occurs during subsequent infections
• Antibodies from a previous infection combine with the virus.
• Rash on face and extremities from skin hemorrhages
• Drop in blood pressure, shock, death.
• >90% in children with multiple infections
dengue virus
-
• Causative agent– virus (grows in white blood cells)– RNA virus
• Transmission– Aedes aegypti– Aedes albopictus
• Transovarian in the mosquito
• Person to person via mosquito– No known animal reservoir
dengue virus
-
• Occurrence– Endemic in the Caribbean and tropics– United States sees mostly imported cases– Vector is present along the Gulf coast
• Host defense– Interferon– Antibodies
dengue fever
-
• Diagnosis– Serology– Virus isolation and culture– Epidemiology
• Treatment & Prevention– Mosquito control– Prevent mosquito bites-no vaccine
dengue fever
-
– Fleas bite humans and transfer thebacteria– Bacteria enter lymph and concentrate inlymph node– High fever– Swollen lymph node (bubo)– Bacteria grow within phagocytes– Bacteria spread to the blood– Black spots from destroyed blood vessels death
bubonic plague
-
– Lungs infected by inhaling bacterial cells– Symptoms within 2 days– >99 mortality within 24 hours
penumonic plague
-
• Cause– Yersinia pestis– Gram negative coccobacillus• Transmission– Infected fleas
• Bacteria clogs the fleas digestive tract, flea regurgitates bacteriainto host during blood meal• Bites more often because it can not feed completely– Carried by many mammals
plauge
-
• Diagnosis– Culturing bacteria from bubo or sputum
• Prevention & Treatment– Antibiotics– Eliminate rodents from homes– Vaccine for scientists
plague
-
• Disease– Small sore at site of infection– Swollen lymph node– Bacteria multiply in phagocytes & enter blood– Persistent fever, chills, headache
• Cause– Francisella tularensis– Gram negative coccobacillus
tularemia
-
• Transmission– Carried in small mammals & ticks– Humans infected accidentally through open wounds– Through infected tick bite
• Diagnosis– Based on patient history
• Prevention & Treatment– antibiotics
tularemia
-
• Disease– Bacteria survive within phagocytes, pass intolymph & blood.– Acute stage: headache, chills, fever, malaise– Undulant fever (rises and falls): spikes everyevening (104°F, 40°C)
brucellosis
-
• Cause
– Brucella abortus & B. canis (mild)
– B. suis & B. melitensis (severe to fatal)
– Gram negative coccobacilli
burcellosis
-
• Transmission
– Direct contact with infected animals & secretions
– Inhalation, broken skin, conjunctiva
– Infected milk (unpasteurized)/ cheese
• Diagnosis– Culturing bacteria– Rising antibody titer
burcellosis
-
• Prevention & Treatment– Antibiotics– Avoid unpasteurized diary product
brucellosis
-
– Bacteria enter through wound– Blister at site of infection, black crater ulcer– Septicemia possible– Treated with antibiotics
cutaneous anthrax
-
– Caused by inhaled spores– Respiratory distress– Septicemia and death
respiratory anthrax
-
– Caused by eating contaminated meat
gastrointestinal anthrax
-
• Cause– Bacillus anthracis– Gram positive, spore forming, rod
• Host Defense– Antibodies to toxin
• Diagnosis– PCR using specific primers
• Prevention & Treatment– Antibiotics immediately following infection(Ciprofloxacin)
anthrax
-
*First stage• Red bulls eye rash at site of tick bite– *Second stage• Headache, stiff neck, muscle aches, fatigue
*Third stage• Bacteria spread to lymph, blood & majororgans• Meningitis or myocardial damage– *Fourth stage• Chronic arthritis• Swelling of joints
lyme disease
-
• Cause– Borrelia burgdorferi– Spirochete
lyme disease
-
*Transmission– Deer tick Ixodes scapularis, Ixodes damini– Tick must have a blood meal from a large mammal(deer or humans)
• Diagnosis– Rash, history
• Prevention & Treatment– Antibiotics– Avoid tick bites
lyme disease
-
• Symptoms– Fever– Spotted rash– Abnormal blood clotting, death
• Cause– Rickettsia rickettsii– Small gram negative rod, obligate intracellularpathogen– Bacteria multiply in the inner lining of bloodvessels causing them to burst and forming thered rash
rocky moutian spotted fever
-
• Transmission– Transovarian from tick to tick– Tick to human
• Diagnosis– Clinical and epidemiological information
• Prevention & Treatment– Tetracycline & chloramphenicol
rocky mountian spotted fever
-
• Disease– Cyclical chills-fever-sweating
• Cause– Plasmodium vivax, P. falciparum, P. malariae, P. ovale
• Transmission– Female anopheles mosquito
malaria
-
• Diagnosis– Presence of plasmodium in blood smears
• Prevention & Treatment– Mosquito nets (insecticides)– Control mosquito population
malaria
-
• Disease– Infection of blood and lymph– Mosquitoes introduce the worm larvaeinto humans during blood meal– Larvae travel to lymph nodes in groin orextremities– Mature into adults, mate and producemicrofilariae that enter the circulation– Worms block circulation of lymph,lymph accumulates causing elephantiasis
filariasis
-
• Cause– Wuchereria bancrofti– Brugia malayi
filariasis
-
• Transmission– Mosquitoes: Anopheles, Aedes, Culex
• Diagnosis– Presence of microfilariae in blood– Symptoms: Elephantiasis
• Prevention & Treatment– Control mosquito population– Treat with antihelminths before elephantiasis stage
filaraisis
-
• Symptoms– Fever, fatigue– Pain in infected organ– Hypersensitivity reaction to masked worms– Blood in urine
• Cause– Flatworm– Schistosoma mansoni (colon), S. japonicum (small intestine), S.haematobium (bladder)
schistosomiasis
-
• Transmission– Contaminated water– Infected snails
• Diagnosis– Eggs in the stool or urine
Schistosomiasis
-
• Disease– Often asymptomatic– Fever, muscle ache, headache and swollen lymphnodes– Congenitally infected children: impaired vision, mentalretardation– Immunocompromised: encephalitis
toxoplasmosis
-
• Cause– Toxoplasma gondii– Protozoan– Cats are carriers and definitive hosts
• Transmission– Contact with cat feces– Eating undercooked meat containing cysts
toxoplasmosis
-
• Host defense– Cell mediated immune response– Protects from reinfection
• Diagnosis– Serology– Examination of tissue
• Treatment and prevention– Cooking meat– Management of cats– Antimicrobials for acute cases
toxoplasmosis
-
• Disease & symptoms– Parasite replicates in red blood cells– Prolonged Fever, chills, night sweats– Often mistaken for malaria– Serious/ fatal in immunocompromised– Hemolytic anemia
babesiosis
-
• Cause– Babesia microti– Protozoan– Known in animals before it was recognized inhumans
babesiosis
-
• Transmission– Rodents are wild reservoir– Ixodes spp– Northeast and Midwest US have high incidence
• Diagnosis– Known in animals for a long time– Blood smear to look for B. microti in RBCs
babesiosis
-
• Treatment and prevention– Combination antimicrobials– Supportive care (blood transfusion, fevercontrol)– Tick and rodent control– Check for ticks– Screen blood supply
babesiosis
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