Microbiology

presence of microorganism

can be from microorganism

microorganism cause of disease

capacity of microorganism

mechanism of pathogen

measure of pathogen

toxin capsule receptors pili flagella

mouth eye nose genitals wounds

specific to host cells part of how pathogen cause disease

inter-cellular spaces
bodily fluids
intracellular
ways for pathogen to cause disease

cells die induce host immune response
ways for pathogen to cause disease

maintain a ______________ in nature

no apparent symptoms carrier

can transmit disease to others

zoonosis, inadvertent

caused by normal flora or transient bacteria
host immune system is compromised

obvious infection or disease

infection subsequent to primary infection

two or more microbes infecting the same tissue

rapid onset brief duration

last for long duration

affecting many organ systems

pus forming

microbes ascend in a duct or tube against the flow of secretions

occur suddenly and intensely

fingers
body fluids
fomites
food
flies
feces

hygiene
*personal hygiene
*water treatment
*sewage
*antimicrobial
Vaccination
*live-dead-toxoid-recombinant

antibiotics antivirals
supportive
*treat symptoms

*symptoms
blisters
itchy
virus becomes latent in spinal ganglia
Reyes syndrome in children

varicella zoster virus
herpes virus family

respiratory
skin to skin contact

cell mediated immunity (t cells)

clinical presentation

avoid exposure to virus
vaccination

zoster
reactivation of latent virus
virus travels down nerves and produces blisters
appear in band
can be life threatening in immunocompromised

*symptoms
– Raised overlapping rash over the entire body
– Pustules arise deep in the skin
– Pustules form a crust and scab over
– Scabs fall off

Variola major
• Severe form• Very high fever
• 30% fatality rate– Blindness–
Variola minor
• Less rash
• Lower fever
• 1% fatality rate

Transmission
– Direct contact (inhalation
– Bodily fluids
– Fomites

Host Defense:
– Interferon
– Humoral and cellular immunity

Diagnosis:
– Clinical presentation
– Isolation of virus

Prevention & Treatment
– Vaccine (Jenner)

Current interest:
– Last US case 1949, Last case in the world, Somalia 1977
– Cultures at CDC and Russia– Fear of bio-terrorism

• 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

Cause
– virus
– Enveloped, RNA virus
– Only human host

Transmission
– Inhalation
– Highly contagious

Host Defense
– Cell mediated immunity

Diagnosis
– Presence of giant cells (formed by virus fusing together human cells and RBC)
– Koplik spots

Prevention & Treatment
– Live attenuated vaccine

German measles/ three day measles

Symptoms
– Rash
- Fever
– Enlarged lymph nodes
- stiff joints

Cause– Rubella virus

Transmission
– Respiratory droplet
– Virus multiplies in respiratory tract and spread throughout the body
– Mother to fetus: teratogen

Host Defense
– Life long immunity
– Cellular and humoral

Diagnosis
– Symptoms
– Serology

Prevention & Treatment
– Live attenuated virus vaccine
– Antiserum for pregnant women exposed to virus

HSV-1

Symptoms
– Cold sores/ fever blister
– Sub-clinical

Transmission
– Oral
– Respiratory
– Contact

Latency
– Latent in trigeminal nerve ganglion

Occurrence
– 90% of people infected

Treatment
– None

Impetigo:• Superficial, skin wound• Oozes a clear fluid• Forms a crust• Most common in children• Glomerulonephritis

Erysipelas:• Infection of the dermis• Spreads rapidly through lymph• Enter blood stream, could be fatal

Streptococcal gangrene• Deep tissue infection• Intense inflammation destroys blood vessels & tissue• Bacteria enter blood, could be fatal

Transmission– Contact with wound secretions

Host Defense– Antibodies to surface proteins & toxins

Diagnosis– Isolation of bacteria

Prevention & Treatment– Antibiotics

Impetigo• Superficial skin layers

Folliculitis & Cellulitis• Pus filled lesions within hair follicles• Diffuse skin infection

Scalded skin syndrome• Exfoliating toxin• Skin peels off

Transmission– Contact with wound or fomites

Host Defense– Antibodies

Diagnosis– Isolate bacteria from the wound

Prevention & Treatment– Clean all wounds– Good hygiene– Antibiotics

Causative agent Strains of Staphylococcus aureus

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)

Risk factors– Barrier contraceptives– Tampons– Surgery– Open wounds– S. aureus infection

• Toxin– Toxic shock syndrome toxin (TSST
)– Toxic shock-like syndrome toxin by Streptococcus spp.

Treatment– Antibiotics– Supportive– Eliminate predisposing factors

Symptoms– Infects deep wounds– Produces alpha-toxin and gas– Skin turns black, renal failure & death

Cause– Clostridium perfringens– Gram positive anaerobic rod– Grows in soil

Transmission– Contamination of wounds with soil

Host Defense:– Antibodies
Diagnosis:– Gas under the skin– Isolation of bacteria

Prevention & Treatment– Antibiotics– Antitoxin– Hyperbaric chamber– Remove dead tissue (amputation

Mostly in men, rarely women
• Symptoms– Infection of the skin– Skin is locally red, may oozefluid– Tinea pedis, capitis, cruris,unguinum, corporis

Cause– Trichophyton– Microsporum– Epidermophyton

Transmission– Soil
Clothes
Fomites

*Host Defense– Cell mediated immunity– Local inflammation
• Diagnosis– Symptoms
• Prevention & Treatment– Topical antifungals: miconazole– Oral: griseofulvin

• Symptoms
– Thrush: white plaques on mucous membranes
– Diaper rash: red raised rash
– Vaginitis: Women susceptible following antibiotics,contraceptives, hormonal changes
– Systemic: immunocompromised, fatal

Cause
–Candida albicans
– Opportunistic pathogen

• Prevention & Treatment
– Antifungals: miconazole or nystatin
– Keep skin dry

• Symptoms
– Mite lives in the epidermis
– Severe itch
• Cause
– Sarcoptes scabiei
-mite

• Transmission
– Close contact
– Fomites
– Found worldwide, epidemicsevery 15 years and last 15 years

*Host Defense:– none
• Diagnosis– Identifying mites and eggs undermicroscope
• Prevention & Treatment– Medication kills mites– Itching stops only after the infectedskin layer is shed

Allows very few compounds to pass throughinto the brain

cerebrospinal fluid

Organisms (Bacterial meningitis)
– Neisseria meningitidis• meningococcal
– Haemophilus influenzae
– Streptococcus pneumoniae• pneumococcal
– E. coli (oppirtunistic)

spinal tap

Pathogenesis
– inflammation of the meninges membrane
• brain and spinal cord
– sudden fever, severe headache, neck rigidity

Occurs mostly in children (6 months to 4years)
• Gram-negative aerobic bacteria,• normal throat microbiota
• Capsule antigen type b
• Prevented by Hib vaccine

• 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.

• 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

– viral origin
– Most common type of meningitis
– No treatment

– Cryptococcus neoformans
– occurs with underlying condition (surgery,immunocompromised

*Treatment
– Antibiotics for bacterial infections
• Prevention
– Vaccine against meningococcal meningitis, Hib

• Organism– Clostridium tetani– Spore former– Anaerobic growth• deep wounds• decaying tissue

• Pathogenesis– tetanospasmin• neurotoxin• ink dot enough for 30 deaths– contraction of muscles• spastic paralysis• lockjaw• respiratory distress

• 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

• 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%

• Different types of toxin– produced by different strains of C. botulinum
– Type A
• most potent
• west of Mississippi River

• Age associated
– infant botulism
• differences in normal biota
– adult botulism
• food poisoning
• heat-labile toxin

Symptoms
– Skin rash Chronic infection
– Peripheral nerve damage
– Loss of sensation

• 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

• Cause– Mycobacterium leprae– Hansen’s disease (Gerhard Hansen)– Bacteria grow slowly– Grows in peripheral nerves and skin cells
• Transmission– Direct contact– Nasal secretions

• 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

• Cause– virus
– Bullet-shaped
• Epidemiology– reservoir: all mammals– humans: end of infectious cycle

• Symptoms– Flu-like initially– Excitation phase:
• Neurological symptoms, loss of muscle control, speechimpaired, hydrophobia– Paralytic phase• muscles weaken, loss of consciousness and death

• Prevention– reduce exposure of virus in animals• wild mammals--uncontrollable reservoir• bats--dormant for long periods• domestic—vaccine

• Diagnosis– Clinical symptoms– Identifying virus in nerve tissue– brain tissue (negri body)• Treatment– Vaccine– Immune globulin immediately following infection

• Cause– virus– Picornavirus

• 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

• Prevention &treatment– two vaccines• oral (OPV)--attenuated--Sabin
• injected (IPV)--inactivated—Salk
– WHO eradicationeffort

• Encephalitis– Inflammation of the brain
• Symptoms– Fever - headache - stiff neck– Confusion - paralysis - convulsions– Sleepiness - Coma

• Eastern Equine Encephalitis (EEE)– severe
• Western Equine Encephalitis (WEE)
• California Encephalitis (CE)
• St. Louis Encephalitis (SLE)
• Japanese B encephalitis– endemic areas of Asia

• Diagnosis– Based on symptoms & case history– Easier during epidemics
• Transmission– Mosquitoes (Culex, Aedes)– Birds are the carriers– Small mammals, birds and horses are reservoirs

• Treatment & Prevention– Supportive care– Japanese encephalitis has a vaccine– Control mosquito population

• Diseases– Bovine spongiform encephalitis– Sheep scrapie– Creutzfeldt-Jakob disease– Kuru
• Cause– Prions– Aberrant proteins

Transmission– Consumption of infected animal products– Transfusion of infected blood

• Prevention– Screen blood– Screen animal products
• Treatment– None– Chronic, fatal

bacteria in blood

bacteria persist in blood and is fatal

• 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

• Cause– Yellow fever virus– Small RNA virus
• Transmission– Mosquito, Aedes aegypti– Non-human primates-mosquitoes-humans
• Host Defense– Immune after infection

• Diagnosis– Symptoms
• Prevention & Treatment– Restrict mosquito population– Treat standing water– Live attenuated vaccine for people in regions with disease andtravelers (strain 17D)

• Disease– Ebola hemorrhagic fever– Extensive bleeding– Destruction of internal organs– >90% fatality rate (25-90%)

• 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

• Cause– Ebola virus– Enveloped RNA virus

• Transmission– Maintained in animals– Index case: contact with infectedanimal– Person to person: Direct contact withinfected blood or bodily fluids– Fomites

• Prevention & Treatment– Supportive care– Isolation of patients and properdisposal of infected items to preventspread

• Disease– Infectious mononucleosis– Fever, fatigue, sore throat, swollenlymph nodes– Enlarged atypical lymphocytes– Enlarged spleen (could rupture)

• Cause– Epstein Barr Virus (EBV)– Enveloped DNA virus– Latent in B lymphocytes

• 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

• Lower respiratory tract infection
• Symptoms– Fever– Muscle aches– Respiratory distress, fluid in airspaces– Death by catastrophic lung failure

• Cause– virus: Sin nombre– Known to cause kidney disease as well– Known to Native Americans before the 1993 incidence
• Transmission– Mouse droppings aerosolized

• Occurrence– In small clusters, rural– Places with known large rodentpopulations– Four corners region
• Host defense– None

• Prevention & Treatment– Avoid contact with rodents– Keep areas free of rodents– Treatment is supportive care

• 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

• 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

• Occurrence– Endemic in the Caribbean and tropics– United States sees mostly imported cases– Vector is present along the Gulf coast
• Host defense– Interferon– Antibodies

• Diagnosis– Serology– Virus isolation and culture– Epidemiology
• Treatment & Prevention– Mosquito control– Prevent mosquito bites-no vaccine

– 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

– Lungs infected by inhaling bacterial cells– Symptoms within 2 days– >99 mortality within 24 hours

• 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

• Diagnosis– Culturing bacteria from bubo or sputum
• Prevention & Treatment– Antibiotics– Eliminate rodents from homes– Vaccine for scientists

• 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

• Transmission– Carried in small mammals & ticks– Humans infected accidentally through open wounds– Through infected tick bite
• Diagnosis– Based on patient history
• Prevention & Treatment– antibiotics

• 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)

• Cause
– Brucella abortus & B. canis (mild)
– B. suis & B. melitensis (severe to fatal)
– Gram negative coccobacilli

• Transmission
– Direct contact with infected animals & secretions
– Inhalation, broken skin, conjunctiva
– Infected milk (unpasteurized)/ cheese
• Diagnosis– Culturing bacteria– Rising antibody titer

• Prevention & Treatment– Antibiotics– Avoid unpasteurized diary product

– Bacteria enter through wound– Blister at site of infection, black crater ulcer– Septicemia possible– Treated with antibiotics

– Caused by inhaled spores– Respiratory distress– Septicemia and death

– Caused by eating contaminated meat

• 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)

*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

• Cause– Borrelia burgdorferi– Spirochete

*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

• 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

• Transmission– Transovarian from tick to tick– Tick to human
• Diagnosis– Clinical and epidemiological information
• Prevention & Treatment– Tetracycline & chloramphenicol

• Disease– Cyclical chills-fever-sweating
• Cause– Plasmodium vivax, P. falciparum, P. malariae, P. ovale
• Transmission– Female anopheles mosquito

• Diagnosis– Presence of plasmodium in blood smears
• Prevention & Treatment– Mosquito nets (insecticides)– Control mosquito population

• 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

• Cause– Wuchereria bancrofti– Brugia malayi

• Transmission– Mosquitoes: Anopheles, Aedes, Culex
• Diagnosis– Presence of microfilariae in blood– Symptoms: Elephantiasis
• Prevention & Treatment– Control mosquito population– Treat with antihelminths before elephantiasis stage

• 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)

• Transmission– Contaminated water– Infected snails
• Diagnosis– Eggs in the stool or urine

• Disease– Often asymptomatic– Fever, muscle ache, headache and swollen lymphnodes– Congenitally infected children: impaired vision, mentalretardation– Immunocompromised: encephalitis

• Cause– Toxoplasma gondii– Protozoan– Cats are carriers and definitive hosts
• Transmission– Contact with cat feces– Eating undercooked meat containing cysts

• 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

• Disease & symptoms– Parasite replicates in red blood cells– Prolonged Fever, chills, night sweats– Often mistaken for malaria– Serious/ fatal in immunocompromised– Hemolytic anemia

• Cause– Babesia microti– Protozoan– Known in animals before it was recognized inhumans

• 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

• Treatment and prevention– Combination antimicrobials– Supportive care (blood transfusion, fevercontrol)– Tick and rodent control– Check for ticks– Screen blood supply