Exam 3* Flashcards
vibrio cholerae: background
cholera: found in water
polar flagellum: gram-negative
*thiosulfate-citrate-bile-sucrose (TCBS) agar: medium used to grow
high pH: grows in pH of 9
*Cholera red test: medium test; after organism is isolated & grown in TCBS agar, sulfuric acid is added & tube turns red if cholera is present
vibrio cholerae: antigenic structure
O antigen: LPS; H antigen: flagella
vibrio cholerae: enterotoxin
biochemistry: protein of the toxin
*ganglioside: where the toxin binds
*adenylate cyclase: enzyme that speeds up toxin & causes patient to produce 20L of fluid daily
*cholera cots: plastic cot (bed) with hole so that the patient can have a bowel movement without getting up
*LT E. coli toxin: hemolysins, neuraminidase, and RBC digestive enzymes
vibrio cholerae: pathogenesis
inoculum dose: 10^8-10^10 dose
host: not rare in nature
*small intestine: only in small intestine; not invasive
*enterotoxin: toxin causes the disease
*dehydration: part that kills people; causes too much fluid loss
vibrio cholerae: clinical findings
incubation period: 1-4 days
symptoms: NVD, abdominal cramps
*rice water stools: no solid matter in stools
vibrio cholerae: diagnostic tests
*mucus flecks: taken from stool; clumps from intestine wall
vibrio cholerae: immunity
*gastric acid: in gastrointestinal tract; kills bacteria
serum antibodies: do not last long (gone after 6 months)
vibrio cholerae: treatment
*mortality rate: 50% of people without treatment
dehydration and salt depletion: causes death; important to replenish water and electrolytes.
antibiotic of choice: tetracycline
vibrio cholerae: epidemiology
*pandemic: epidemics covers wide area of globe
*endemic areas: India, SE Asia, Texas, Louisiana, Chesapeak Bay
transmission: dirty water & food; touching stool
*out-houses: dangerous for spreading disease
exposed people: 1 of 5 people who get exposed obtain disease
carrier state: 3-4 weeks of carrier spreading disease
control: improved sanitation, isolate patients, give treatment, & vaccine
campylobacter jejuni: background
gram-negative rod; motile; comma-shaped
campylobacter jejuni: culture
atmosphere: low O2 more CO2 needed to grow
temperature: 42 degrees centigrade
campylobacter jejuni: selective media
media needed to grow
*skirrows medium: vancomycin, polymyxin B, and trimethoprim
*campy BAP medium: cephalothin
separate campylobacter from feces
campylobacter jejuni: colony variation
not all the same; vary from watery & spread to round & convex
campylobacter jejuni: biochemistry
does not like carbs
campylobacter jejuni: toxins
LPS & enterotoxin; small toxin; help cause disease
campylobacter jejuni: pathogenesis
transmission: food and beverage; contact with animals; sexual activity
inoculum dose: 10^4 cells
small intestine and epithelium: where campylobacter likes to attack
*RBC & WBC: elevated in stool
*diarrhea: extremely bloody
*enteric fever: symptom of organism in blood
campylobacter jejuni: clinical findings
abdominal pain, headache, malaise, *severely blood diarrhea
campylobacter jejuni: cases
2 million reported cases per year
campylobacter jejuni: diagnostic test
stool sample, gram stain, grows in lab
campylobacter jejuni: treatment
*self-limiting: goes away in 5-8 days in healthy patient
erythromycin: antibiotic treatment; makes disease get bad then good
campylobacter jejuni: control
stop contamination & stop sexual activity in gay people
helicobacter pylori: background
gram-negative rod
*microaerophillic: does not like O2
*gastritis: H. pylori causes disease of stomach
*stomach and duodenal ulcers: symptom
*gastric adenocarcinoma: what disease develops into in severe cases
helicobacter pylori: pathogenesis
*urease: enzyme; neutralizes gastric acid
*acid inhibitory protein: blood secretion of acid
*LPS:
*catalase and superoxide dismutase: protects bacteria from WBC
*mucinase: breaks down mucus
helicobacter pylori: epidemiology
all people with gastritis
helicobacter pylori: transmission
person to person & sexual activity
helicobacter pylori: diagnostic tests
*biopsy:
*urease test:
*microaerophilic atmosphere: high CO2 atmosphere
serology: AB used to test for AG presence
helicobacter pylori: treatment
omeprazole, clarithromycin, amoxicillin, and metronidazole
legionella pneumophila: background
recognized in 1970s; aerobic
american legion convention: where disease was vastly spread
*fastidious: disease is difficult
basic fuschin: dye used; stains the bacteria
legionella pneumophila: culture
*buffered charcoal-yeast extract agar (BYCE): medium used to grow
air: humidity; 90%; takes 3 days
variation: speckles, shapes, sizes, & colors
legionella pneumophila: antigens
*gas-liquid chromatography: testing technique; differentiates stains
*fatty acids: proteases, phosphatases, lipase, DNASE, RNASE, hemolysis, and cytotoxin
legionella pneumophila: pathogenesis
environment: warm & moist (AC units, showerheads, respirators, machinery dealing with water)
host: lungs –> leads to pneumonia
*grows intracellularly: bacteria grows in lung
legionella pneumophila: individuals at risk
elderly, debilitated, immunosuppressed, diabetics, & smokers
legionella pneumophila: clinical findings
*symptoms: delirium & flu-like
mortality rate: 10% of those untreated
legionella pneumophila: diagnostic tests
bronchial washings, pleural fluid, lung biopsy, & blood
patient urine: AG will show (created by Dr Weeks)
legionella pneumophila: treatment
erythromycin
legionella pneumophila: epidemiology
not passed from person to person; inhalation/ingestion
legionella pneumophila: control
cleaning shower heads & machinery
yersinia, francisella, & pasteurella: background
not motile; gram-negative
facultative anaerobes: grows with or without presence of O2
bipolar staining: ends of rods stain better
yersinia pestis: background
*plague, black death: common name
rodents: rats; how bacteria causes disease
fleas: flea bites
*pandemic: bacteria causes pandemic
yersinia pestis: antigens and toxins
endotoxin: LPS
exotoxin: cardiotoxin
*V-W antigens: virulent (does something bad)
plasmid: gene is on plasmid
*coagulase: made in flea 28 C
yersinia pestis: pathogenesis
flea bites: flea jumps off rat onto people
hungry fleas: coagulate in intestinal tract
lymph nodes: swell
lesions, meningitis, and pneumonia: diseases that arise
*pneumonic plague: plague that comes from coughing w/ pneumonia
yersinia pestis: clinical findings
incubation: 2-7 days
symptoms: *buboes (swelling of armpit and groin)
*bubonic plague: caused by buboes
*lymphadenopathy: sore-like lymph nodes
yersinia pestis: diagnostic tests
specimen: sputum, CSF, blood
giemsa’s stain and immunofluorescent stains: dyes used
blood agar and macconkey: medium used
yersinia pestis: treatment
streptomycin or tetracycline
mortality: 50%
yersinia pestis: epidemiology
common in animals; south america, western US, mexico, india, asia, africa
yersinia pestis: control
surveys: of infected animals
formalin-killed vaccine: treats bubonic plague; recommended for forest rangers & lumberjacks
francisella tularensis: background
rabbit fever
*tularemia: medical name
francisella tularensis: culture
aerobic: likes O2
glucose cysteine blood agar & glucose blood agar: medium used; needs blood
francisella tularensis: two strain categories
jellison A: lethal to rabits; severe to people
jellison B: not lethal to rabbits; mild to people
francisella tularensis: immunology
antigens: take 2 weeks to grow
agglutinins: AB causes RBC to clump
skin test: like TB
delayed hypersensitivity: if there is reaction patient is positive
francisella tularensis: pathogenesis
inoculum dose: 50 cells; used as warfare method
entry: skin break or inhalation
papule: pimple –> sore –> ulcer –> necrotic
inhalation: pneumonia
eye infection: rubbing eyes
francisella tularensis: clinical findings
fever, malaise, headache, flu-like symptoms
francisella tularensis: diagnostic tests
smears & culture
serology: most common test; looks for high titers
skin tests
francisella tularensis: prevention and control
rabbits or muskrats: don’t deal with them
ticks or deerflies: other way to get disease
immunization: only if you work with infections
pasturella: background
found in animals
pasturella: various species
p. multocida: gut of animals –> septicemia –> cause of foul cholera
p. hemolytica: found in the respiratroy tract –> pneumonia –> does not infect people
p. pneumotropica: respiratory tract and gastrointestinal tract of rodents –> septicemia and pneumonia
p. ureae: human lung disease with mixture of other bacteria
pasturella: clinical findings
animal bite: bite or scratch (cat scratch fever)
lymphadenopathy: swelling of lymph nodes
haemophilus influenzae: background
coccobacilli: short rod
upper respiratory tract: where bacteria lives
haemophilus influenzae: culture
brain-heart infusion (BHI) agar: medium used to grow
*chocolate agar: heated/cooked blood agar
*x factor: hemen
*v factor: NAD
cooked agar has both nutritional factors
*satellite phenomenon:
haemophilus influenzae: transformation
ability to take DNA from one cell and use the genes, which are used for drug resistance
haemophilus influenzae: variation
some have capsule and some do not; the bacteria with the capsule harms the person
haemophilus influenzae: antigenic structure
capsule, LPS, protein
haemophilus influenzae: pathogenesis
entry: inhalation
respiratory tract infection, otitis, and meningitis: diseases caused
*secondary infection: flu virus
*septic arthritis: people may get arthritis
antibodies: 3/4 of population has Aby
*asymptomatic infection: infection can go unnoticed, especially in children
haemophilus influenzae: diagnostic tests
specimen: pus sample, blood, CSF when meningitis is suspected.
*nasopharyngeal swab: key diagnostic test
identification: immunofluorescent, lab made Aby against bacteria
haemophilus influenzae: treatment
mortaility: 90% of untreated cases
ampicillin, chloramphenicol or cephalosporin: treatment for RTI
haemophilus influenzae: epidemiology
person to person; vaccine given to mothers to be
haemophilus aegyptius: background
*contagious conjunctivitis: medical name
*pink eye: common name
caused by gram-negative rod
haemophilus aphrophilus: background
respiratory tract infection
pneumonia and endocarditis: diseases caused by bacteria
haemophilus ducreyi: background
vinerial disease
soft chancre: common name
erythromycin: treatment
swollen lymph nodes and ulcers
haemophilus parainfluenzae: background
respiratory tract infection: not pathogen
bordetella pertussis: background
*whooping cough: common name
*metachromatic granules: pear-like; crystals in oval shape; have capsule
*bordet-gengou medium: medium to grow; potatoes, blood, & glycerol
mercury drop or pearl drop colonies: take a few days to grow
variation: differences between colonies
bordetella pertussis: antigenic structure
*LPS:
*pertussis toxin: causes coughing
*two hemagglutinins: chemical on germs, sticks to blood cells
bordetella pertussis: pathogenesis
transmission: air
trachea and bronchi: where bacteria grows
cilia: when infected, cilia do not work
blood:
*secondary invaders:
bordetella pertussis: clinical findings
incubation period: 2 weeks
*paroxysmal stage: coughing & sneezing get worse
*whoop: cough noise
bordetella pertussis: diagnostic tests
nasopharyngeal swab or cough plate: specimen is collected then a fluorescent AB test is done
smear:
bordetella pertussis: treatment
erythromycin
bordetella pertussis: immunity
bordetella pertussis: prevention
DTP, given again later in life
bordetella pertussis: epidemiology
children < 5; death occurs within 1st year of life
bordetella pertussis: control
bordetella parapertussis: background
similar to whooping cough, weaker colonies
bordetella bronchiseptica
kennel cough and pneumoitis: whooping cough in dogs
brucella: background
*brucellosis, undulant fever, and malta fever: names for bacterial disease
*b. melitensis, b. suis, b. abortus, and b. canis: species
brucella: morphology and identification
aerobic; not motile; has capsule
coccobacillus: shape
intracellular: live inside of cells
trypticase-soy broth, thinine-tryptose agar: medium used to grow
*candle jar: like CO2/CO2 incubator; takes a few days to grow
H2S, nitrates, thionine, and basic fuschin: variations/characteristics
brucella: variation
virulent organism:
avirulent organism:
brucella: antigenic structure
brucella: pathogenesis
host: from animals
infection routes: eating, mucous membranes of the skin
lymphatics to lymph nodes to thoracic duct to blood stream to organs: disease process
abscesses: form in various organs
*placentas: will cause abortions from infection; animals have abortion on farms and cats & dogs may be interested and get infected
brucella: clinical findings
incubation period: 6 weeks to show symptoms
onset symptoms: malaise, fever, weakness, aches and pains, sweats
chronic stage: there may be a relapse of the disease
brucella: diagnostic tests
agglutination test; looks for high titers
brucella: immunity
a person who has had the disease may have resistance but still get it
brucella: treatment
tetracycline; can only fight outside of cell
brucella: epidemiology
infection contact: animals/waste products
control: 4% of cattle are infected
government gets involved, kill sick animals, and vaccinate
neisseria: background
*morphology and identification: cocci, gram-negative; paits
kidney shaped cells: shape
location: upper respiratory tract and genital tract
mueller-hinton, thayer-martin, chocolate and GCB agar: medium used to grow
aerobic: O2 used to grow
candle jar: gives organism CO2
*oxidase +: enzyme; made by neisseria; people are infected by this enzymes presence
fermentation:
autolytic: explode themselves; part of sex process; the explosion causes DNA to explode everywhere and this allows other cells to adopt the diseases genes
neisseria gonorrhoeae: antigentic structure
*pili: help attact to tissue and keep WBC away
DNA rearrangement:
proteins: protease digests Aby
LPS: part of structure
variation: likes to change antigen
neisseria gonorrhoeae: pathogenesis
piliation: most important; causes infection
plasmids: a lot in bacteria; 3 common types
cryptic plasmid: no one knows what is does
big conjugal plasmid: 1 out of 5; moves from the strain that has it to the stain that does not; gene on plasmid
beta-lactamase plasmid: destroys penecillin
infection sites: eyes, rectum, throat, & genetalia
symptoms: inflammation, production of pus *painful urination
sterility: if the infection if of the urinary tract & pt does not receive treatment, pt becomes sterile
*bacteremia: skin lesions
*gonococcal opthalmia neonatorum: eye infection in babies when the mothers secretion gets in the babies face/eye; AgNO3 and erythromycin treat this
*pelvic inflammatory disease: when disease is left untreated
neisseria gonorrhoeae: diagnostic tests
specimen: pus or secretion
smear: gram stain
culture: lab made AB to confirm
serology: look for gram-diplococci
neisseria gonorrhoeae: immunity
none
neisseria gonorrhoeae: treatment
penecillin (on sensitive organsism), tetracycline, and spectinomycin for PPNG
neisseria gonorrhoeae: epidemiology
worldwide
more common for man to get from a woman
neisseria meningitidis (meningococcous): background
meningitis: common name
very lethal
neisseria meningitidis (meningococcous): antigenic structure
capsule: contains
outer membrane proteins:
pili:
LPS: causes toxic effects
neisseria meningitidis (meningococcous): pathogenesis
host: person to person
portal of entry: nasopharynx
transience: lives in respiratory tract, then goes away
dissemination: bacteria causes disease
nasopharynx to bloodstream to upper respiratory tract: disease process
*petechiae:
waterhouse-friderichsen syndrome:
arthritis: rash;dotten
neisseria meningitidis (meningococcous): diagnostic tests
specimen: CSF, blood, nasopharyngeal swab, petechiae material
smear: gram stain
culture: pt should not have WBC in CSF
serology: AB tests
neisseria meningitidis (meningococcous): immunity
pt who has gotten infected will be immune to that specific chain
neisseria meningitidis (meningococcous): treatment
penecillin G
neisseria meningitidis (meningococcous): epidemiology
epidemics: military bases & colleges
hosts: people 80% carrier rate during epidemic
wakes: points where there is no outbreak then suddenly there is
neisseria meningitidis (meningococcous): control
rifampin: for when someone comes in contact with a carrier
crowding: disease is caused by crowding
vaccine: not common enough to make people get vaccines
moraxella catarrhalis: background
branhamrlla catarrhalis or neisseria catarrhalis
nucleic acid analysis: oxidase +, reasons for changing name
morphology:
identification:
location: upper respiratory tract
rich media: helps bacteria grow
*bronchitis and bronchopneumonia: shown in elderly
*sinusitis and otitis: shows in children
penecillin resistance: cant be used
transformation: good at exchanging genes
cephalosporin, erythromycin, tetracycline, and trimethoprim-sulfamethoxazole: treatment
other neisseria
COPD; 1/4 people die from COPD
Staph; 1/4 people die from staph
mycobacteria tuberculosis: background
tuberculosis: common name
morphology: rod
acid-fast: not gram + or -; stained cells cannot be decolorized with alcohol waxy
ziehl-neelsen technique: AKA acid fast
mycobacteria tuberculosis: culture
*simple synthetic media: large inoculum colonies grow in several weeks
*oleic acid-albumin medium: small sample of inoculum
tweens: disperses growth; related to soap
*complex organism media: small sample of inoculum (yak, serum, tissue extracts)
penecillin or malachite green: keeps other bacteria from knowing
lowenstein-jensen medium: complex organic medium always uses malachite green
mycobacteria tuberculosis: growth characteristics
aerobic: loves oxygen likes CO2
doubling time: 18 hours
mycobacteria tuberculosis: variation
different pigments/appearances
*cord factor: wax like drops
mycobacteria tuberculosis: physical and chemical agents
resistance: very resistant, lives a long time in saliva
mycobacteria tuberculosis: lipids
*causes disease (fatty acids)
cell walls: cause most tissue reaction
biochemistry: fatty acid & lipid are toxin
activity: allergic reaction to fatty acid
proteins and polysaccharides:
mycobacteria tuberculosis: pathogenesis
transmission: inhalation; eating
route of infection: mouth
toxins: lipids cause disease
*hypersensitivity: allergic reastion
*serpentine cords: bad infection; parallel chains
*cord factor: toxin; interferes w WBC
granulomas: site of infection filled with WBC
adjuvant: boosts immune response
mycobacteria tuberculosis: pathology
two principal lesions
exudative: inflammation lung tissue
productive (tuberculosis): chronic granulomas
mycobacteria tuberculosis: spread of organism in host
direction: lymph system –> blood stream –> organs (if consumed)
lesions in lung: if inhaled
throat –> stomach & intestinal tract –> lymph –> blood –> organs
mycobacteria tuberculosis: intracellular site of growth
inside of cells
location: WBC
drug treatment: if the bacteria is in the cell it is hard to treat
mycobacteria tuberculosis: two types of infection
*primary infection: ghon complex: first lesions; will heal but patient is TB+
*reactivation types
causes: bacteria that survive primary lesion
koch’s phenomenon: 2 injections
1st: slow to heal
2nd: rapid and dramatic response (created a sore); this led to the TB test
mycobacteria tuberculosis: tuberculin test
test for TB
mycobacteria tuberculosis: material
*old tuberculin (OT): 1st material filtrate of broth of TB; worked, but was painful
*purified protein derivative (PPD): new test
mycobacteria tuberculosis: dose of tuberculin
small volume: 1/10 mL (3 drops) injected into skin
large amount antigen: patient may have a dramatic response
mycobacteria tuberculosis: reaction to tuberculin
time: 2-3 days
no reactions: TB-
primary infection: contact with mycobacteria
edema, erythema, and necrosis: 3 characteristics of response (swelling, reddening, and dying of tissue)
positive test: come back in 1 month
time to test: 4-6 weeks
BCG vaccination: some countries require this; US does not
mycobacteria tuberculosis: interpretation of TB test
pt may have positive TB test but not have TB; pt may have previously had it, been exposed, or have the vaccine
mycobacteria tuberculosis: clinical findings
fatigue, weakness, weight loss; flu like
*coughing and spitting up blood
mycobacteria tuberculosis: diagnostic tests
specimen: sputum, urine, gastric washing
smear: zeal-neelson or acid fast
culture: takes many days
animal inoculation: wait a few weeks and test animals after inoculation
mycobacteria tuberculosis: treatment
rest: main treatment
isoniazid, ethambutol. rifampin, and streptomycin: drugs used
cure time: 6-12 months
mycobacteria tuberculosis: epidemiology
transmission: droplet nuclei & dairy products
other factors: overpopulation, crowding poverty, poor medical care, alcoholism, being elderly, and immunostasis
mycobacteria tuberculosis: prevention and control
*BCG (bacille, calmette, guerin): depending on country this vaccine is given
mycobacterium leprae: background
leprosy: disease caused (Hansen’s)
characteristics: exists in armadillos; acid fast
mycobacterium leprae: culture
media: no media
foots pads of mice or armadillos: exists naturally; grows to a certain degree
mycobacterium leprae: clinical findings
skin, nerves, nose, pharynx, eyes, and testicles
lesions: on skin
anesthesia: as disease progresses the infected tissue will not feel pain
disfiguration: absorption of tissue including bone
mycobacterium leprae: pathogenesis
*lepromatous: pt develops nodules; negative skin test
lepromin: type of lesion
tuberculoid: macule: flat lesion: + skin test
mycobacterium leprae: diagnosis
specimen: scraping or biopsy of earlobe
smear: acid fast
mycobacterium leprae: treatment
sulfones or rifampin: work really well
mycobacterium leprae: epidemiology
cases: 10 mil; in Asia
children: risk group; 10% of children who are exposed will get disease
incubation period: 2-10 years
mycobacterium leprae: prevention and control
identification: identify patient and those around them
prophylaxis: exposed patients receive this
mycobacterium leprae: other mycobacteria
pathogens
nonpathogens
m. phlei: environment
m. smegmatis: human excretions
treponema pallidum: background
syphilis
morphology: slender, long spirals; turn like a screw
culture: N/A
reiter stain: doesn’t causes disease; looks and acts like teponema
anaerobic: grown without O2
viability: lives for 24hrs in fridge
physical and chemical agents: sensitive; easy to kill
treponema pallidum: pathogenesis
-
treponema pallidum: acquired syphilis
transmission: sexual/physical contact with infected
primary lesion: takes 2 weeks-months after encounter
papule: sore on skin, mucous membranes, & genetalia
*hard chancre: swollen and hard sore
dissemination: spread through body –> sore –> lymph –> blood
secondary lesions: 2-10 weeks; after 1st lesion like a surprise
rash: surprise rash
pale papules: sometimes rash shows itself as this, can be axillary, oral, or genital areas
meningitis, hepatitis, and nephrtitis: can occur in this stage
recurring lesions: 3-5 years after 2nd
fate of host: after rash, patient carries disease does not transmit
complete cure: 1/3 of people
latent cases: dont show noticeable symptoms
*tertiary cases: classic syphilis in 1/3 of patients
granulomatous lesions: in bone skin or liver
nervous system or heart: spirochetes atatck
treponema pallidum: congenital syphilis
in babies
placenta: if mother to be has baby; the baby will acquire the disease in 10-15 weeks
fetus: will be affected
death, miscarriage, and still birth: may occur
childhood disease: baby will develop syphilis growing up
treponema pallidum: experimental disease
rabbits: animals used; can’t get disease
skin, testis and eye: where spirochete grows
chancre: will develop and be filled with spirochetes
fate: does not get sick & die
treponema pallidum: diagnostic tests
specimen: fluid from chancre & blood or serum
dark-field examination: looking for spirochete
immunofluorescence: fancier tests
serological tests: store well; not expensive; 1st time; 2 categories
nontreponemal ag tests: cheapest, cardiolipin mixture and antigens instead; see if pt makes antibodies
antigen: AB fights AG
cardiolipin mixture: beef fat from heart –> mixed and person who has Aby shows reaction
reagin: serum from the patient
veneral disease research laboratories (VDRL), rapid plasma reagin (RPR), waasermann (CF), and kolmer: other tests
*treponemal antigen tests: real spirochetes; grown in rabbit testes
antigen: rabbit testes
antibody: come from pt serum
fluorescent treponemal antibody (FTA), T. pallidum immobilization (TPI), t. pallidum (CF), and t, pallidum hemagglutination (TPHA)
treponema pallidum: treatment
penecillin: good treatment
jarisch-hexheimer reaction: cell explodes due to penicillin and spirochetes reactions to chemicals; released in pt blood stream; causes toxic reaction
treponema pallidum: epidemiology
high risk groups: promiscuous people; teenagers
control: good hygiene; prophylaxis
bejel, yaws, and pinta: background
tropics: where disease is found; identical to syphilis
skin: direct contact
treponemes:
borrelia recurrentis: background
relapsing fever: disease caused
morphology: large spirochete; few spirals
culture: grown in lab; media with blood
viability: blood keeps spirochetes alive for months
variation: during disease process bacteria changes Ag then patient gets better then patient relapse
surface antigens:
borrelia recurrentis: pathogenesis
incubation period: 10 days
symptoms: chills, fever, bacteria in blood
recurrences: 3-10 recurrences; 4-10 day breaks
pathology: spleen, liver, & spinal fluid
borrelia recurrentis: diagnostic tests
giemsa’s or wright’s stain: blue stain
animal inoculation: see if animal gets sick
complement fixation: best diagnosis
borrelia recurrentis: treatment
penicillin, tetracycline, and erythromycin
borrelia recurrentis: epidemiology
main reservoir: rodents
vectors: ticks & lice: cause epidemics
other: crowding, malnutrition, and cold water
borrelia recurrentis: control
1/3 of people who don’t get treated die
clean and use insectisides; no vaccine
borrelia burgdorferi: background
lyme: disease caused
connecticut: first recognized
arthralgia and lymphadenopathy: symptoms; don’t go away but get getter
neurologic symptoms and arthritis: long term symptoms; last years
vectors: ticks: bites –> rash—> symptoms
penicillin and tetracycline: kills bacteria
leptosepira interrogans: background
leptospirosis: disease caused
morphology: spirochete with hooks at end
aerobic: likes O2; grows in rich medium
embryonated eggs: grown
leptosepira interrogans: pathogenesis
transmission: food or water
incubation: 2 weeks
two phases
liver and kidneys: bacteria attacks
aseptic meningitis, nephritis, and hepatitis: bad cases
leptosepira interrogans: diagnostic tests
dark-field examination: sees growth
culture: blood or urine
animal inoculation: uses guinea pig to see if it gets the disease
serology: AB test
leptosepira interrogans: immunity
person can recover but get different strain
leptosepira interrogans: treatment
penicillin or tetracycline
leptosepira interrogans: epidemiology
hosts: rodents
environmental factor: water for a long time
high risk groups: people who work with water; sewer and fishermen
leptosepira interrogans: prevention
kill rodents
fusospirochetal disease: background
trench mouth, Vincent’s angina: disease caused
predisposing factors: poor oral hygiene, poor health
etiology
borrelia buccalis: main bacteria grows out of control
control: improve oral and overall health
risk group: teenagers 18-19 years old
transmission: cannot be caught; patients with oral herpes gets disease
