• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/92

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

92 Cards in this Set

  • Front
  • Back
Results of microbe-human interactions
a. Microbes acquired on exposed area of body
Infection = entry, establishment and multiplication of pathogenic organism in a host
Disease—several outcomes
Normal flora
resident flora, micro flora—are commensal organisms= benefit w/o harming host, sometimes host benefits as well
Normal Flora Continued
1. On body surfaces exposed to environment
2. Places to find normal flora= skin, mucous membrane, parts of digestive system, urinary tract, upper respiratory tract, reproductive tract
3. Colonization of normal flora—starts just before being born throughout life
Colonization of Normal Flora (ct)
a. Inutero—germfree
b. Birth canal—lactobacillus (part of normal vaginal canal, becomes part of child’s intestinal floral
c. 8-12 hours after birth: E.coli → large intestine and skin also staph bacteria that will colonize skin. Beneficial effects= produce vitamin K + B, aid in develop of immune system and GI sys
Some other human interactions
ii. Some transients—on body for a short period of time
1. Cleaning
2. Immune system
iii. Some→ allergy or hypersensitivities
iv. Some with greater infectious potential evade host defense→ infection
Disease--Pathology
the study of disease
Pathogenesis
creation/formation or how the disease develops
Virulence
the ability of a microbe to invade and damage host tissues
True pathogen
produce virulence factors that allow it to evade host defense cause damage
Opportunistic pathogen
not highly virulent (not normal/ not beneficial/ not normally harmful, but with the right opportunity of immune suppressed patients)
Virulence factors
Antipagocyte chemicals, enzymes, toxinsand endotoxins
Antipagocytic chemicals
Capsule
Leikocidins—kills WBC/poison
Enzymes
Exoenzymes (digest host tissue→invasion)
Toxins
other chemicals that can cause damage to host
may affect local distain targets
Toxigenicity
ability of a microbe to produce toxins at the cite where it grows/ is multiplying
Toxemia
toxins in the blood + spread
Exotoxin
protein secreted by bacteria w/powerful effects on a specific organ
EX. Clostridium botulinum→ causes Botulism
1. In soil—anaeroboic
2. Toxin= boulinum toxin
a. Usually causes death
b. Acts on CNS
c. Blocks nerve conduction
d. W/o nerve conduction= paralysis
e. Includes all muscles (resp.)
f. Block release of Ach from motor end plate
g. Protein→ so denatured by heat
Endotoxin
part of the lipopolysaccharide of G- outer membrane
1.Causes more generalized and weaker toxicity
2. Can cause pyrogenic response (fever)
3. Also—shock, inflammation, hemorrhage, diarrhea
Example of endotoxin
E. coli, Salmonella
Infection = entry, establishment and multiplication of pathogenic organism in a host
1. Immune system can arrest infection before injury to tissue/organs
• 2. Infectious agent—not arrested
o entrenched into tissue
o pathologic effects cause damage
Disease—several outcomes
• 1. Eventually—immune system arrest microbes and stop disease progression
• 2. Damaged tissues can lead to tissue/muscle/organ disfunction—morbidity
• 3. Damage can be severe→ death (mortality)
• 4. Microbe can be harbored inconspicuously (carrier state)
Mechanisms of Action of infection process
entry, adherence, invasion, multiplication, disrupting of target tissues
Entry- portal of entry
= route by which microbe enters tissues

• Skin
• GI tract
• Respiratory tract
• Urogenital tract
• Placenta
Entry- Origin of Pathogens
• Exogenous (outside of the body/from the environment)
• Endogenous (nf gone bad/ immunocompromised/ originate from normal flora)
Mechanism--what is also important
size of infectious dose!
Adherence
o Microbes attach to host cell via:
• Fimbriae
• Flagella
• Capsule
• Receptors
Classification of Infectious diseases
A. Based on transmission
o 1. Contagious—easily spread from one host to another (cold/flu)
o 2. Route of transmission
• a. Contact transmission
 direct—coughing, sneezing host→ host (w/o anything in between)
 indirect—intermediary (nonliving) is present; example= cup/ phone/ water cup, germs passed
• b. Vehicle transmission
 water borne
 food borne
 air borne
 vectors (insects)
Based on the frequency
o Epidemic= large # of people in restricted geographic area—get infected in short period of time
o Pandemic= like epidemic but world=wide
o Endemic= not like big outburst, if you go to this country, it is always there; disease that is always present in a particular population
Disease based
o Acute= rapid onset, relatively short duration
o Chronic = develops slowly, long onset, long duration
Stages of Infectious Disease Incubation Period
period of initial contact with microbe→ appear of 1st symptoms
Prodromium
=period of initial, vague symptoms
Period of Invasion
variable period in which microbes multiply in high #’s, time of most severe symptoms
Convalescent period
period of recovery, decline of symptoms
Botulism • 3 forms=
o food borne botulism
o infant botulism
o wound botulism
C. Botulism
o G+ rod
o Anerobic
o Soil
o Makes 7 toxins A-G
Botulism In United States
o ~145 cases/year
o 15% food
o 65% infant
o ~20% wound
Symptoms
o Blurred vision
o Droopy eyelids
o Slurred speech
o Difficulty swallowing
o Muscle Weakness→ paralysis

onset (18-36 hours)
6 hours- 10 days (food)
Syphilis
Treponema pallidum
o Human host
o Sensitive pathogen
• Can’t live outside host
• Sensitive to: heat, drying, disinfectants, soap increased O2 levels, pH change
o People in history who had disease
• Bram Stoker
• Henry VIII
• Vincent Van Gogh
Pathogenesis
• transported through: mucous membrane/abraded skin (STD)
• Spirochete w/hook
 Uses hook to bind to epithelial cells
 @ binding site→ multiply
 penetrate through the capillaries by dissolving junctions between the endothelial cells→ move into circulation and can get into blood vessels
 Once in blood vessels→ multiply more (body becomes incubator)
 Any tissue can be a potential target
• Slow doubling/generation time→ slow, but progressive disease
Stages of infection (syphillis) Primary Lesion
• microbe hooks cells
• inflmatory cells come to site—block circulation
• treatment w/penicillin= EFFECTIVE
• if untreated→ chancre site of inoculation (appears 9 days- 3months after coming into contact with 57 mic)
 small red bump that then breaks down and creates shallow crater @ base—swarming w/ microbes
 can have enlarged lymph nodes in affected region
 no head ache or fever
• chancre heals 3-6 weakes when bacteria→ go to circulation (slowly b/c they double so slowly
Secondary Syphilis
• between 3 weeks- 6 months
• depends on infectious dose
• systemic→ many body systems invaded
• HA/ fever/ soar throat/ lymph nodes swollen/ red & brown rash over all skin surface
• Major complications→ bones, hair follicles, joints, liver, eyes, hair, kidneys
• Symptoms usually disappear→ in few weeks can linger for months-years
Latent Syphilis
• organism is still there, but no symptoms
Tertiary Syphilis
a. cardiovascular syphilis
 die due to heart failure ~85%
 damage to small aortic in aortic wall
 heart valves damaged
 heart failure
Summas
 painful, swollen syphilitic tumor
 benign (NOT CANCER)
 center—necrotic tissue
 found in: skin/ bone/ liver/ cartilage
Neurosyphilis ~10%
 any part of the nervous system can be involved
 usually blood vessels in brain: cranial nerves, & dorsal roots of spinal cord
 symptoms: HA/ convulsion/ atrophy of optic nerve (blindness)/ mental deterioration/ muscle wasting and loss of activity and coordination
The Tuskegge Syphilis experiment
400 w and 200 w/o, injected told they were being treated, weren't CDC let it happen, able to pass it on to their families, 1932-1972
**Cholera**
• Caused by a bacteria—vibrio cholera
• Comma-shaped
• Found commonly in soil and water –free living
• Ingested in cont. food & water
• Encounters acidic stomach→ penetrate tract mucous barriers, using flagella→ adheres to surface of epithelium of LI→ multiply (doesn’t penetrate further)
Virulence of Cholera microbe- virbrio cholera
enterotoxin= cholera toxin (targets mucous membrane of intestinal cells)
o Toxin binds receptors on the intestinal cells → activates a signaling cascade→ cells send electrolytes into LI (not in cells or passed into tissues→ they are shed through the LI, water will follow) → diarrhea/ vomiting → dehydrated
o Loss of blood volume K+ depletion→ bicarbonate loss→ acidosis/ coma/ shock = death
Treatment
o *****Water***** and electrolyte replacement (Bananas)
o Tetracycline
Defenses of the Nervous System
• Structural—boney structures
• CFS
• Blood-brain barrier
Normal Flora of NS
Any microbes in the peripheral or central indicate infection—NOT NORMAL TO BE THERE
Meningitis
• Inflammation of the meninges (covering around the brain)
• Can be caused by bacteria/virus
• Diagnose: symptoms, spinal tap/CP, and Gram stain
Meningitis (s & s)
o Head Ache
o Painful/stiff neck!
o Light sensitivity!
o Fever
o Increase in # of WBV in CSF
Neisseria meningitis-Characteristics
o Bacteria that can cause meningitis
• G-
• Diplococcus
• Memingococcus
• Most often associated with outbreaks/epidemics of men.
• Causes most serious form of meningitis
Transmission
• doesn’t survive long in the environment
• respiratory droplets/ close contact or secretions
Virulence factors and infections
• in the nasopharynx→ spread to the roof of nasal cavity→ boarders highly vascular area @ base of the brain (usually asymptomatic) → use polo to attach to mucosa (carriage state)—can last few days, several months (3-30% of adult population have this) –spreads when in close proximity—cause infection to non-immune individuals → enter blood stream → CSF→ penetrates meninges (fever, soar throat, HA, stiffness, convulsions, vomiting) → can lead to meningococcemia (in blood) → bacteria release an endotoxin into general circulation→ stimuli WBC → release cytokines (too much) → BV damage/hemorrhage/ intravascular clotting→ cardiac failure/ damage to adrenal glands (on kidneys—epinephrine)→ death
• also has IgA protease and capsule
Treatment
• natural immunity via exposure early in life
• penicillin G (high dose, usually IV)
• vaccine—trying to make one
• if treated—15% mortality rate
• Prophylaxis for anyone in close contact: tetracycline/ rifampin
Viral Form of meningitis
o Similar symptoms
o No antibiotic cure unless infection caused by herpes
• Supportive
o More common than bacteria meningitis
o Virus more readily cross blood-brain barrier
o Spread: resp., drops, feces
Encephalitis
• Inflammation of the brain
• Extremely sensitive to damage caused by the inflammatory process
Encephalitis Characteristics
o Can be acute or sub-acute
o Almost always caused by virus→ especially acute
o Viral infection→ insect borne
o Can be caused by bacteria
Encephalitis Symptoms
o Behavior changes (moody—severe)
o Confusion
o Seizures
o Similar symptoms of meningitis can be present
Arboviruses
o Are all arthropod borne/ spread by insects
o Ticks/ mosquitos
Arboviruses types
A. Western equine encephalitis (WEE)
 In western US/ Canada
 ssRNA virus
 enveloped
 mortality 5%
 normal host: wild birds
 also found in horses—able to infect humans-jump
West Nile Encephalitis (WNE)
 ssRNA
 enveloped
 found on eastern coast of US/Canada/ Africa/ Uganda
 host: wild birds
Eastern equine encephalitis (EEE)
 Eastern Coast and Canada
 ssRNA
 enveloped
 wild birds = host to horses to humans
 50% mortality
Pathogenesis of EEE
• Host= bird
• Mosquito acquires virus from bird
• Mosquito bites a human (in saliva of mi)
• Virus enters blood stream via mosquito’s saliva
• Replicates in monocytes (WBC in circulation and nearby lymphatic tissue)
o Enters endothelial cells (capillary) → prolonged viremia→ enters CNS (either direct or with viremia)→ damages perikaryon (cell body of nerve cells) & dendrites → brain→ with immune response (inflammation of the brain)→ damage (brain/nerve/meninges)
o Crosses placental barrier and can infect fetus
Virulence Factors of Arboviruses
• Not well understood
• Enveloped—pieces of this facilitate attachment in body to specific cells
• Proteins in the env. that promote fusion w/host cell membrane
Symptoms/ Arboviruses
• when virus is in lymphatic tissue
 fevers/ chills/ weakness/ swollen lymph nodes/ HA
• 4-10 days after bite
 severe memory deficits
 tremors
 loss of coordination
 personality changes, can be severe w/o reas.
 Convulsions
 Speech changes
 Coma/death
Treatment
• supportive
• may try antiviral drugs
• vaccine—lab workers/ vets/ ranchers/ horse handlers
• live attenuated
Clostridium tetani
• Tetanus—stiff neck, spasms, sweating
• Affects axon of the neuron and the spinal cord & brain (muscle spasms)
• Treatment: clean wounds, bed rest, non-stimulating environment, tetanus immunoglobulin is also used.
Mycobacterium Tuberculosis
• Tuberculosis
• Bacteria—alveoli of lungs, if stays there =pulmonary TB, if not exterior TB (obligate aerobe)
• Treatment: Streptomycin—along with: isoniazid & ethambutol
• Vaccine: Bacille Calmette- Guerin (BCG vaccine)
HIV—Human immunodeficiency Virus
• Retrovirus—attacks and destroys the immune system (t-lymphocytes)
• Causes AIDS
• No vaccine/ no cure only medications to slow process
Yersinia pestis
• Bacteria –member of enterbacteriaceae family
• Causes: Black Death/ Plague (from rodent); fever, chills, red rash (ring around the rosy) 75 % mortality rate
• Treatment: streptomycin/tetracycline, also gentamicin and chloramphenicol, for septicemic plague: isolation/antibiotics (doxycycline, supportive care)
• Prophylactic treatment for suspected exposure, 7-10 day antibiotics
Hepatitis B
causes Hep. B
• Virus-Hepadnavirus family
• Affects liver cells
• Fatigue, nausea, jaundice, liver cancer/ blood tests
• Preventions: avoid used syringes, vaccination, safe sex
• No treatment usually needed, but for chronic: interferon alfa-2b, and lamivudine
Variola Virus
• Virus
• Causes smallpox
• Transmitted through: inhalation of droplets or dried crusts, body fluids
• Blood and lymph (spreads through the entire body)
• No Treatment! Treat symptoms→ prevention!
• Vaccine! Very contagious and very fatal!
Lassa Fever Virus
• Virus
• Lassa Fever
• Transmission: food contaminated through feces of rat/ air with rat feces/ bodily fluid
• Works specifically on the blood vessels—capillary lesions
• Rifampin
Streptococcus Pyogenes
• Colonizes on the throat or skin, also heart valves and tissues
• Causes impetigo, strep throat, scarlet fever, pneumonia, necrotizing fasciitis, streptococcal toxic shock syndrome
• Bacteria
• Treatment: penicillin/ amoxicillin/erythromycin/ beta lactams
• Oral cephalosporin
Varcella- Zoster Virus (human herpes virus 3)
• Virus
• Chicken Pox/Shingles
• Transmitted through: droplets/ lesion contact
• Nerve cells
• Treatment: applying lotions, not touching/scratching, antiviral meds.
• 2 vaccines: varivax/ Zostavax
Clostridium botulinum
• Botulism
• Bacteria
• Not harmful to the host by itself
• Endospores are the cause
• Affect the nerve cells (neuromuscular junction bloakcage of AcH)
• Treatment: supportive care, botulism immunoglobulin, mechanical ventilation, tube feeding, antibiotics are not used, because massive death of these cells, which would creates toxin
Haemophilus influenza
• Bacteria
• Respiratory (alveoli) / organs/ inflammation of the meninges
• Meningitis, pneumonia, bacteremia
• Vaccines and boosters (1-year)
• Treatment: combination of antibiotics
Aroboviruses (3 different families)—West Nile Virus (transmitted via arthropods)
• Falviviruses
• West Nile Encephalitis
• transmitted through birds by mosquito bite
• cerebral capillary endothelial cells into CNS (dendrites, perikaryon, myelin sheaths)
• Treatment: symptomatic treatment. No vaccines
Hantavirus
• Virus
• Can only get it through rodent; through inhalation of feces, saliva
• Hantavirus pulmonary syndrome—vessels and capillaries of lungs
• Hemorrhagic Fever with Renal Syndrome—vascular endothelium
• Treatment: manage fluid and electrolytes, Ribavirin
Human Papillova Virus
HPV
Virus
Epithelial cells
Treatment: removal/surgery, medication
Poliovirus
• Poloi Virus
• Motor neuron cells
• Treatment: no cure, but to control symptoms (orthopedic braces) and iron lung (artificial respirator), 2 vaccines!
Nuclear polyhedrovirus
• Virus
• Wilting/ Melting disease
• Gastrointestinal cells
• Treatment→ not finding treatment (used for insecticides)
Toxoplasam Gondi
• Parasite
• Toxoplasmosis (in fetus and immunodifficient people)
• Oocysts/ neurological
• S/S—mental status changes, fever, muscle pain
• Wash hands. Litter box clean, avoid raw food, wash all fruits
Neisseria Gonorrhoeae
• Gonorrhea
• Bacteria
• Epithelial tissue
• Painful urination/ 50% of women asymptomatic (destroy fallopian tubes)
• Treatment: inject mercury into the tip of the penis→ penicillin→ flouroquinilones→ sephlosporines
Staphylococcus aureus
• MRSA
• Epithelial cells
• Treatment with: lotion/topical, antibiotics (vancomycin)
• Prevention: wash hands
Borrelia Burgdorferi
• Lyme Disease
• Bacteria
• Lymph
• Treatments: antibiotics (doxycycline, amoxicillin, cefuroxime; ceftriaxone, penicillin)
• Repellant and wash clothing
Bacillus anthracia
• Anthrax
• Bacteria
• Neutrophils/ Lungs
• Treatment: vaccine, antibiotivs—ciproflaxicin and doxycycline
Rabies Virus
• Nerve cells, all animal cells
• Treatment: seek medical care, vaccine, tetanus shot