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Microbiology > Exam 3* > Flashcards

Exam 3* Flashcards

1
Q

vibrio cholerae: background

A

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

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2
Q

vibrio cholerae: antigenic structure

A

O antigen: LPS; H antigen: flagella

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3
Q

vibrio cholerae: enterotoxin

A

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

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4
Q

vibrio cholerae: pathogenesis

A

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

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5
Q

vibrio cholerae: clinical findings

A

incubation period: 1-4 days
symptoms: NVD, abdominal cramps
*rice water stools: no solid matter in stools

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6
Q

vibrio cholerae: diagnostic tests

A

*mucus flecks: taken from stool; clumps from intestine wall

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7
Q

vibrio cholerae: immunity

A

*gastric acid: in gastrointestinal tract; kills bacteria
serum antibodies: do not last long (gone after 6 months)

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8
Q

vibrio cholerae: treatment

A

*mortality rate: 50% of people without treatment
dehydration and salt depletion: causes death; important to replenish water and electrolytes.
antibiotic of choice: tetracycline

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9
Q

vibrio cholerae: epidemiology

A

*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

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10
Q

campylobacter jejuni: background

A

gram-negative rod; motile; comma-shaped

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11
Q

campylobacter jejuni: culture

A

atmosphere: low O2 more CO2 needed to grow
temperature: 42 degrees centigrade

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12
Q

campylobacter jejuni: selective media

A

media needed to grow
*skirrows medium: vancomycin, polymyxin B, and trimethoprim
*campy BAP medium: cephalothin
separate campylobacter from feces

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13
Q

campylobacter jejuni: colony variation

A

not all the same; vary from watery & spread to round & convex

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14
Q

campylobacter jejuni: biochemistry

A

does not like carbs

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15
Q

campylobacter jejuni: toxins

A

LPS & enterotoxin; small toxin; help cause disease

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16
Q

campylobacter jejuni: pathogenesis

A

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

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17
Q

campylobacter jejuni: clinical findings

A

abdominal pain, headache, malaise, *severely blood diarrhea

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18
Q

campylobacter jejuni: cases

A

2 million reported cases per year

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19
Q

campylobacter jejuni: diagnostic test

A

stool sample, gram stain, grows in lab

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20
Q

campylobacter jejuni: treatment

A

*self-limiting: goes away in 5-8 days in healthy patient
erythromycin: antibiotic treatment; makes disease get bad then good

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21
Q

campylobacter jejuni: control

A

stop contamination & stop sexual activity in gay people

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22
Q

helicobacter pylori: background

A

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

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23
Q

helicobacter pylori: pathogenesis

A

*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

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24
Q

helicobacter pylori: epidemiology

A

all people with gastritis

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25
Q

helicobacter pylori: transmission

A

person to person & sexual activity

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26
Q

helicobacter pylori: diagnostic tests

A

*biopsy:
*urease test:
*microaerophilic atmosphere: high CO2 atmosphere
serology: AB used to test for AG presence

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27
Q

helicobacter pylori: treatment

A

omeprazole, clarithromycin, amoxicillin, and metronidazole

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28
Q

legionella pneumophila: background

A

recognized in 1970s; aerobic
american legion convention: where disease was vastly spread
*fastidious: disease is difficult
basic fuschin: dye used; stains the bacteria

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29
Q

legionella pneumophila: culture

A

*buffered charcoal-yeast extract agar (BYCE): medium used to grow
air: humidity; 90%; takes 3 days
variation: speckles, shapes, sizes, & colors

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30
Q

legionella pneumophila: antigens

A

*gas-liquid chromatography: testing technique; differentiates stains
*fatty acids: proteases, phosphatases, lipase, DNASE, RNASE, hemolysis, and cytotoxin

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31
Q

legionella pneumophila: pathogenesis

A

environment: warm & moist (AC units, showerheads, respirators, machinery dealing with water)
host: lungs –> leads to pneumonia
*grows intracellularly: bacteria grows in lung

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32
Q

legionella pneumophila: individuals at risk

A

elderly, debilitated, immunosuppressed, diabetics, & smokers

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33
Q

legionella pneumophila: clinical findings

A

*symptoms: delirium & flu-like
mortality rate: 10% of those untreated

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34
Q

legionella pneumophila: diagnostic tests

A

bronchial washings, pleural fluid, lung biopsy, & blood
patient urine: AG will show (created by Dr Weeks)

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35
Q

legionella pneumophila: treatment

A

erythromycin

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36
Q

legionella pneumophila: epidemiology

A

not passed from person to person; inhalation/ingestion

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37
Q

legionella pneumophila: control

A

cleaning shower heads & machinery

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38
Q

yersinia, francisella, & pasteurella: background

A

not motile; gram-negative
facultative anaerobes: grows with or without presence of O2
bipolar staining: ends of rods stain better

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39
Q

yersinia pestis: background

A

*plague, black death: common name
rodents: rats; how bacteria causes disease
fleas: flea bites
*pandemic: bacteria causes pandemic

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40
Q

yersinia pestis: antigens and toxins

A

endotoxin: LPS
exotoxin: cardiotoxin
*V-W antigens: virulent (does something bad)
plasmid: gene is on plasmid
*coagulase: made in flea 28 C

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41
Q

yersinia pestis: pathogenesis

A

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

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42
Q

yersinia pestis: clinical findings

A

incubation: 2-7 days
symptoms: *buboes (swelling of armpit and groin)
*bubonic plague: caused by buboes
*lymphadenopathy: sore-like lymph nodes

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43
Q

yersinia pestis: diagnostic tests

A

specimen: sputum, CSF, blood
giemsa’s stain and immunofluorescent stains: dyes used
blood agar and macconkey: medium used

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44
Q

yersinia pestis: treatment

A

streptomycin or tetracycline
mortality: 50%

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45
Q

yersinia pestis: epidemiology

A

common in animals; south america, western US, mexico, india, asia, africa

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46
Q

yersinia pestis: control

A

surveys: of infected animals
formalin-killed vaccine: treats bubonic plague; recommended for forest rangers & lumberjacks

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47
Q

francisella tularensis: background

A

rabbit fever
*tularemia: medical name

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48
Q

francisella tularensis: culture

A

aerobic: likes O2
glucose cysteine blood agar & glucose blood agar: medium used; needs blood

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49
Q

francisella tularensis: two strain categories

A

jellison A: lethal to rabits; severe to people
jellison B: not lethal to rabbits; mild to people

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50
Q

francisella tularensis: immunology

A

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

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51
Q

francisella tularensis: pathogenesis

A

inoculum dose: 50 cells; used as warfare method
entry: skin break or inhalation
papule: pimple –> sore –> ulcer –> necrotic
inhalation: pneumonia
eye infection: rubbing eyes

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52
Q

francisella tularensis: clinical findings

A

fever, malaise, headache, flu-like symptoms

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53
Q

francisella tularensis: diagnostic tests

A

smears & culture
serology: most common test; looks for high titers
skin tests

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54
Q

francisella tularensis: prevention and control

A

rabbits or muskrats: don’t deal with them
ticks or deerflies: other way to get disease
immunization: only if you work with infections

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55
Q

pasturella: background

A

found in animals

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56
Q

pasturella: various species

A

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

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57
Q

pasturella: clinical findings

A

animal bite: bite or scratch (cat scratch fever)
lymphadenopathy: swelling of lymph nodes

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58
Q

haemophilus influenzae: background

A

coccobacilli: short rod
upper respiratory tract: where bacteria lives

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59
Q

haemophilus influenzae: culture

A

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:

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60
Q

haemophilus influenzae: transformation

A

ability to take DNA from one cell and use the genes, which are used for drug resistance

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61
Q

haemophilus influenzae: variation

A

some have capsule and some do not; the bacteria with the capsule harms the person

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62
Q

haemophilus influenzae: antigenic structure

A

capsule, LPS, protein

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63
Q

haemophilus influenzae: pathogenesis

A

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

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64
Q

haemophilus influenzae: diagnostic tests

A

specimen: pus sample, blood, CSF when meningitis is suspected.
*nasopharyngeal swab: key diagnostic test
identification: immunofluorescent, lab made Aby against bacteria

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65
Q

haemophilus influenzae: treatment

A

mortaility: 90% of untreated cases
ampicillin, chloramphenicol or cephalosporin: treatment for RTI

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66
Q

haemophilus influenzae: epidemiology

A

person to person; vaccine given to mothers to be

67
Q

haemophilus aegyptius: background

A

*contagious conjunctivitis: medical name
*pink eye: common name
caused by gram-negative rod

68
Q

haemophilus aphrophilus: background

A

respiratory tract infection
pneumonia and endocarditis: diseases caused by bacteria

69
Q

haemophilus ducreyi: background

A

vinerial disease
soft chancre: common name
erythromycin: treatment
swollen lymph nodes and ulcers

70
Q

haemophilus parainfluenzae: background

A

respiratory tract infection: not pathogen

71
Q

bordetella pertussis: background

A

*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

72
Q

bordetella pertussis: antigenic structure

A

*LPS:
*pertussis toxin: causes coughing
*two hemagglutinins: chemical on germs, sticks to blood cells

73
Q

bordetella pertussis: pathogenesis

A

transmission: air
trachea and bronchi: where bacteria grows
cilia: when infected, cilia do not work
blood:
*secondary invaders:

74
Q

bordetella pertussis: clinical findings

A

incubation period: 2 weeks
*paroxysmal stage: coughing & sneezing get worse
*whoop: cough noise

75
Q

bordetella pertussis: diagnostic tests

A

nasopharyngeal swab or cough plate: specimen is collected then a fluorescent AB test is done
smear:

76
Q

bordetella pertussis: treatment

A

erythromycin

77
Q

bordetella pertussis: immunity

A
78
Q

bordetella pertussis: prevention

A

DTP, given again later in life

79
Q

bordetella pertussis: epidemiology

A

children < 5; death occurs within 1st year of life

80
Q

bordetella pertussis: control

A
81
Q

bordetella parapertussis: background

A

similar to whooping cough, weaker colonies

82
Q

bordetella bronchiseptica

A

kennel cough and pneumoitis: whooping cough in dogs

83
Q

brucella: background

A

*brucellosis, undulant fever, and malta fever: names for bacterial disease
*b. melitensis, b. suis, b. abortus, and b. canis: species

84
Q

brucella: morphology and identification

A

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

85
Q

brucella: variation

A

virulent organism:
avirulent organism:

86
Q

brucella: antigenic structure

A
87
Q

brucella: pathogenesis

A

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

88
Q

brucella: clinical findings

A

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

89
Q

brucella: diagnostic tests

A

agglutination test; looks for high titers

90
Q

brucella: immunity

A

a person who has had the disease may have resistance but still get it

91
Q

brucella: treatment

A

tetracycline; can only fight outside of cell

92
Q

brucella: epidemiology

A

infection contact: animals/waste products
control: 4% of cattle are infected
government gets involved, kill sick animals, and vaccinate

93
Q

neisseria: background

A

*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

94
Q

neisseria gonorrhoeae: antigentic structure

A

*pili: help attact to tissue and keep WBC away
DNA rearrangement:
proteins: protease digests Aby
LPS: part of structure
variation: likes to change antigen

95
Q

neisseria gonorrhoeae: pathogenesis

A

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

96
Q

neisseria gonorrhoeae: diagnostic tests

A

specimen: pus or secretion
smear: gram stain
culture: lab made AB to confirm
serology: look for gram-diplococci

97
Q

neisseria gonorrhoeae: immunity

A

none

98
Q

neisseria gonorrhoeae: treatment

A

penecillin (on sensitive organsism), tetracycline, and spectinomycin for PPNG

99
Q

neisseria gonorrhoeae: epidemiology

A

worldwide
more common for man to get from a woman

100
Q

neisseria meningitidis (meningococcous): background

A

meningitis: common name
very lethal

101
Q

neisseria meningitidis (meningococcous): antigenic structure

A

capsule: contains
outer membrane proteins:
pili:
LPS: causes toxic effects

102
Q

neisseria meningitidis (meningococcous): pathogenesis

A

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

103
Q

neisseria meningitidis (meningococcous): diagnostic tests

A

specimen: CSF, blood, nasopharyngeal swab, petechiae material
smear: gram stain
culture: pt should not have WBC in CSF
serology: AB tests

104
Q

neisseria meningitidis (meningococcous): immunity

A

pt who has gotten infected will be immune to that specific chain

105
Q

neisseria meningitidis (meningococcous): treatment

A

penecillin G

106
Q

neisseria meningitidis (meningococcous): epidemiology

A

epidemics: military bases & colleges
hosts: people 80% carrier rate during epidemic
wakes: points where there is no outbreak then suddenly there is

107
Q

neisseria meningitidis (meningococcous): control

A

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

108
Q

moraxella catarrhalis: background

A

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

109
Q

other neisseria

A

COPD; 1/4 people die from COPD
Staph; 1/4 people die from staph

110
Q

mycobacteria tuberculosis: background

A

tuberculosis: common name
morphology: rod
acid-fast: not gram + or -; stained cells cannot be decolorized with alcohol waxy
ziehl-neelsen technique: AKA acid fast

111
Q

mycobacteria tuberculosis: culture

A

*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

112
Q

mycobacteria tuberculosis: growth characteristics

A

aerobic: loves oxygen likes CO2
doubling time: 18 hours

113
Q

mycobacteria tuberculosis: variation

A

different pigments/appearances
*cord factor: wax like drops

114
Q

mycobacteria tuberculosis: physical and chemical agents

A

resistance: very resistant, lives a long time in saliva

115
Q

mycobacteria tuberculosis: lipids

A

*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:

116
Q

mycobacteria tuberculosis: pathogenesis

A

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

117
Q

mycobacteria tuberculosis: pathology

A

two principal lesions
exudative: inflammation lung tissue
productive (tuberculosis): chronic granulomas

118
Q

mycobacteria tuberculosis: spread of organism in host

A

direction: lymph system –> blood stream –> organs (if consumed)
lesions in lung: if inhaled
throat –> stomach & intestinal tract –> lymph –> blood –> organs

119
Q

mycobacteria tuberculosis: intracellular site of growth

A

inside of cells
location: WBC
drug treatment: if the bacteria is in the cell it is hard to treat

120
Q

mycobacteria tuberculosis: two types of infection

A

*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

121
Q

mycobacteria tuberculosis: tuberculin test

A

test for TB

122
Q

mycobacteria tuberculosis: material

A

*old tuberculin (OT): 1st material filtrate of broth of TB; worked, but was painful
*purified protein derivative (PPD): new test

123
Q

mycobacteria tuberculosis: dose of tuberculin

A

small volume: 1/10 mL (3 drops) injected into skin
large amount antigen: patient may have a dramatic response

124
Q

mycobacteria tuberculosis: reaction to tuberculin

A

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

125
Q

mycobacteria tuberculosis: interpretation of TB test

A

pt may have positive TB test but not have TB; pt may have previously had it, been exposed, or have the vaccine

126
Q

mycobacteria tuberculosis: clinical findings

A

fatigue, weakness, weight loss; flu like
*coughing and spitting up blood

127
Q

mycobacteria tuberculosis: diagnostic tests

A

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

128
Q

mycobacteria tuberculosis: treatment

A

rest: main treatment
isoniazid, ethambutol. rifampin, and streptomycin: drugs used
cure time: 6-12 months

129
Q

mycobacteria tuberculosis: epidemiology

A

transmission: droplet nuclei & dairy products
other factors: overpopulation, crowding poverty, poor medical care, alcoholism, being elderly, and immunostasis

130
Q

mycobacteria tuberculosis: prevention and control

A

*BCG (bacille, calmette, guerin): depending on country this vaccine is given

131
Q

mycobacterium leprae: background

A

leprosy: disease caused (Hansen’s)
characteristics: exists in armadillos; acid fast

132
Q

mycobacterium leprae: culture

A

media: no media
foots pads of mice or armadillos: exists naturally; grows to a certain degree

133
Q

mycobacterium leprae: clinical findings

A

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

134
Q

mycobacterium leprae: pathogenesis

A

*lepromatous: pt develops nodules; negative skin test
lepromin: type of lesion
tuberculoid: macule: flat lesion: + skin test

135
Q

mycobacterium leprae: diagnosis

A

specimen: scraping or biopsy of earlobe
smear: acid fast

136
Q

mycobacterium leprae: treatment

A

sulfones or rifampin: work really well

137
Q

mycobacterium leprae: epidemiology

A

cases: 10 mil; in Asia
children: risk group; 10% of children who are exposed will get disease
incubation period: 2-10 years

138
Q

mycobacterium leprae: prevention and control

A

identification: identify patient and those around them
prophylaxis: exposed patients receive this

139
Q

mycobacterium leprae: other mycobacteria

A

pathogens
nonpathogens
m. phlei: environment
m. smegmatis: human excretions

140
Q

treponema pallidum: background

A

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

141
Q

treponema pallidum: pathogenesis

A

-

142
Q

treponema pallidum: acquired syphilis

A

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

143
Q

treponema pallidum: congenital syphilis

A

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

144
Q

treponema pallidum: experimental disease

A

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

145
Q

treponema pallidum: diagnostic tests

A

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)

146
Q

treponema pallidum: treatment

A

penecillin: good treatment
jarisch-hexheimer reaction: cell explodes due to penicillin and spirochetes reactions to chemicals; released in pt blood stream; causes toxic reaction

147
Q

treponema pallidum: epidemiology

A

high risk groups: promiscuous people; teenagers
control: good hygiene; prophylaxis

148
Q

bejel, yaws, and pinta: background

A

tropics: where disease is found; identical to syphilis
skin: direct contact
treponemes:

149
Q

borrelia recurrentis: background

A

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:

150
Q

borrelia recurrentis: pathogenesis

A

incubation period: 10 days
symptoms: chills, fever, bacteria in blood
recurrences: 3-10 recurrences; 4-10 day breaks
pathology: spleen, liver, & spinal fluid

151
Q

borrelia recurrentis: diagnostic tests

A

giemsa’s or wright’s stain: blue stain
animal inoculation: see if animal gets sick
complement fixation: best diagnosis

152
Q

borrelia recurrentis: treatment

A

penicillin, tetracycline, and erythromycin

153
Q

borrelia recurrentis: epidemiology

A

main reservoir: rodents
vectors: ticks & lice: cause epidemics
other: crowding, malnutrition, and cold water

154
Q

borrelia recurrentis: control

A

1/3 of people who don’t get treated die
clean and use insectisides; no vaccine

155
Q

borrelia burgdorferi: background

A

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

156
Q

leptosepira interrogans: background

A

leptospirosis: disease caused
morphology: spirochete with hooks at end
aerobic: likes O2; grows in rich medium
embryonated eggs: grown

157
Q

leptosepira interrogans: pathogenesis

A

transmission: food or water
incubation: 2 weeks
two phases
liver and kidneys: bacteria attacks
aseptic meningitis, nephritis, and hepatitis: bad cases

158
Q

leptosepira interrogans: diagnostic tests

A

dark-field examination: sees growth
culture: blood or urine
animal inoculation: uses guinea pig to see if it gets the disease
serology: AB test

159
Q

leptosepira interrogans: immunity

A

person can recover but get different strain

160
Q

leptosepira interrogans: treatment

A

penicillin or tetracycline

161
Q

leptosepira interrogans: epidemiology

A

hosts: rodents
environmental factor: water for a long time
high risk groups: people who work with water; sewer and fishermen

162
Q

leptosepira interrogans: prevention

A

kill rodents

163
Q

fusospirochetal disease: background

A

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

Microbiology (6 decks)

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