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Mechanisms of Disease Exam #3 > Bacterial Infections > Flashcards

Flashcards in Bacterial Infections Deck (141)
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1
Q

Which cell wall is thick with lots of cross-linking?

Whose is thine with simple cross-linking?

A

Gram+

Gram-

2
Q

How many layers does a Gram+ cell have?

What makes them up?

A

2 layers.

Outer layer is made of peptidoglycan, teichoic acid, polysaccharides and proteins (peptidoglycan cell wall).
The inner membrane is the cytoplasmic layer and it has proteins that may span the width of the lipid bilayer. It does NOT contain cholesterol.

3
Q

How many layers does a Gram- cell have?

What makes them up?

A

3 layers.

It has the same 2 layers as Gram+, but also contains a thin outer layer that has LPS.

4
Q

What is the periplasmic space?

What is the murein lipoprotein?

A

The periplasmic space is between the cytosolic layer and the cell wall of a Gram- cell. It contains proteins/enzymes.

Murein lipoprotein is between the cell wall and the outermost layer and helps bind the two together.

5
Q

What molecule is a marker for Gram+ cells?

A

Teichoic acid

6
Q

Which cells have porins?

A

Gram-

7
Q

Which cells have a high lipid content?

A

Gram-

8
Q

4 steps of performing a Gram stain

A
  1. Pour crystal violet onto slide and wait 60 s.
  2. Wash with water and flood w/ iodine. Wait 60 s.
  3. Wash with water and decolorize w/ 95% EtOH.
  4. Counter-stain w/ safranin. Wait 30 s. and wash.
9
Q

What are the 6 most medically relevant Gram+ bacteria and their group?

A

Strips of cocci: Streptococcus
Clusters of cocci: Staphylococcus
Spore forming rods: Bacillus and Clostridium
Non-spore forming rods: Corynebacterium and Listeria

10
Q

Which Gram- pathogen is spiral-shaped?

A

Spirochetes

11
Q

What is a facultative anaerobe?

What is an obligate anaerobe?

A

FA - they are actually aerobes but can function anaerobically if needed.

OA - these cannot grow in an environment with oxygen.

12
Q

Gram+ obligate aerobes (1)

A

Bacillus cereus

13
Q

Gram+ facultative anaerobes (4)

A

Staphylococcus
Bacillus anthracis
Corynebacterium
Listeria

14
Q

Gram+ microaerophilics (2)

A

Enterococcus

Streptococcus

15
Q

Gram+ obligate anaerobes (1)

A

Clostridium

16
Q

What is a microaerophilic bacteria?

A

It uses fermentation and has no ETC, but can function in places with low oxygen because they have SOD.

17
Q

Gram- obligate aerobes (5)

A
Neisseria
Pseudomonas
Bordatella
Legionella
Brucella
18
Q

Gram- microaerophilics (2)

A

Spirochetes (Treponema, Borrelia, Leptospira)

Campylobacter

19
Q

What is the catalase reaction?

A

2H2O2 –> 2H2O + O2

Used to tell which cells are aerobic, anaerobic, etc.

20
Q

What are examples of virulence factors?

A

Flagella
Pili
Capsules

21
Q

What is the function of a pilus?

A

Adhesion. Without it, the bug in unable to infect as it cannot grab ahold of its host.

22
Q

Most capsules are made of:

What is a major exception?

A

Simple sugar residues.

Bacillus anthracis - AA residues.

23
Q

Why are encapsulated bugs more virulent?

A

Because neutrophils and Mo cannot phagocytose them.

24
Q

What is the India ink stain?

A

Helps to determine if a bacteria has a capsule.
The capsule does not take up the stain and appears like a clear halo around the cell.

Used mostly on Cryptococcus.

25
Q

What is the Quelling reaction?

A

Helps to determine if a bacteria has a capsule.

Bacteria are mixed with Abs that bind to the capsule, causing it to swell with water.

26
Q

Which 2 bacteria are spore forming?

A

Gram+ –> aerobic Bacillus and anaerobic Clostridium.

27
Q

What is unique about endospores?

A

They are metabolically dormant bacteria that are resistant to heat, cold, drying and chemical agents.

They form when there is shortage of nutrients and need to be dormant for years.

28
Q

What 3 markers are associated with TSS?

A

TNF
IL-1
NO

29
Q

Transduction

Transformation

Conjugation

Transposons

A

Transduction - DNA is delivered by a bacteriophage.

Transformation - naked DNA is taken up by a bacterium by binding to the cell’s CM and is taken up. Usually the same species.

Conjugation - DNA is exchanged between bacteria through a sex pilus.

Transposons - jumping genes that can go from cell to cell.

30
Q

What is generalized transduction?

A

A virus infects a bacterium and produces its proteins, while damaging/degrading the host’s DNA. If a part of the host’s DNA is the right size, it can fit in a phage’s capsid head and be carrier to the next host cell upon lysis. Once the DNA is put into the next cell, it could disrupt a gene/protein and possibly inactivate an antibiotic.

It is more effective than specialized transduction because the free DNA is protected in the capsid head while it is transferred.

31
Q

What is specialized transduction?

A

A temperate phage can put its DNA into the host’s genome, causing the bacteria to be lysogenic. Once the phage is ready to be active, it can splice its genome out of the host. Errors in this allow for parts of bacterial DNA to be taken with the virus.

32
Q

4 major methods for identifying pathogens

A

Smears
Cultures
Molecular techniques
Serology

33
Q

Group A beta-hemolytic strep

Species name:
Virulence factors:

4 disease associations w/ local invasion and exotoxin release

2 disease associations w/ delayed Ab release

A

Streptococcus pyogenes
C carb, M protein, Strep O, Strep S, pyrogenic toxin

Pharyngitis, skin infections, Scarlet fever, TSS.

Rheumatic fever, acute post-streptococcus glomerulonephritis.

34
Q

What is most important in determining a rash?

A

Its distribution

35
Q

Group B strep
Species:

Which age group is most common?

What is the classic presentation?

A

Streptococcus agalactiae

Most common in children.

Nuchal rigidity, high fever, lethargy.

36
Q

What are the 3 most common pathogens associated w/ meningitis in neonates and infants <3 mo.?

A

Group B Strep
Listeria
E. coli

37
Q

Viridans group Streptococci is normal flora where? (3)

What infections are common? (3)

What is the hemolytic pattern?

A

Nasopharynx, gingiva and GI tract.

Subacute bacterial endocarditis, dental caries, occult abscesses (in brain or liver) due to Streptococcus intermedius.

Alpha.

38
Q

What are the 2 subtypes of group D Strep and their bacteria? (2)

A
  1. Enterococci
    - Strep faecalis
    - Strep faecium
  2. Non-enterococci
    - Strep bovis
    - Strep equinas
39
Q

Where are group D Strep normal flora?

What is are unique characteristics about them?

Where do they occur often?

Hemolytic pattern?

A

GI tract.

They can grow in areas w/ bile and salt.

At hospital and can be multiply drug resistant.

Gamma mainly.

40
Q

What bacterium has an association w/ colon cancer?

A

Grp 4 non-enterococci Strep bovis

41
Q

What are the 2 tests to identify pneumococci and how do they work?

A
  1. Quellung reaction: a smear is prepped / some anti-serum and methylene blue. If it is pneumococci, the capsule will swell.
  2. Optochin sensitivity: Strep viridans and pneumococci are both alpha hemolytic. Optochin is added to an agar plate and pneumococci should not grow, but Strep viridans will.
42
Q

Streptococcus pneumoniae is the most common cause of what infections?

A

Lobar pneumonia in adults
OM in kids
Bacterial meningitis in adults

43
Q

What are the 3 main bacteria involved in OM in kids?

A

Strep pneumoniae
Haemophilis influenzae
Moraxella catarrhalis

44
Q

What are some strains of Strep pneumoniae resistant to?

A

PCN

45
Q

Who should NOT get Pneumovax?

A

Immunocompromised pts (b/c it is encapsulated)
Pts w/o a spleen
Sickle cell pts.

46
Q

3 major Staph geuns/species

A

Staph aureus
Staph epidermidis
Staph saprophyticus

47
Q

Is Staph catalase positive?

Which type of Staph is coagulase positive?

A

Yes.

Staph aureus.

48
Q

What is the hemolytic pattern for Staph?

What is their morphology?

A

Beta.

Clusters of cocci.

49
Q

What are the virulence proteins in Staph aureus? (6)

A

Protein A: protects against opsonization.
Coagulase
Hemolysins
Leukocidins
*Beta-lactamase: disrupts PCN.
Novel PCN-binding protein/transpeptidase: needed for cell wall production.

50
Q

What are the enzymatic degrading proteins in Staph aureus that lead to necrosis? (4)

A

Hyaluronidase - breaks down CT
Staphylokinase - lyses fibrin clots
Lipase
Protease

51
Q

What diseases can ensue from exotoxin release in Staph aureus? (3)

A

Gastroenteritis
TSS - often from a tampon leading to significant TNF and IL-1 release which can lead to organ failure (kidneys and lungs).
Scalded skin syndrome - similar to TSS, but occurs in kids most often and those prone to skin infections.

52
Q

8 diseases resulting from direct organ activation of Staph aureus

A
Pneumonia superimposed on strep
Meningitis
Osteomyelitis
Acute bacterial endocarditis
Septic arthritis
Skin infections
Sepsis
UTI
53
Q

What is MRSA usually treated with, but now is showing signs of resistance?

A

Vancomycin

54
Q

In IVDUs, where can Staph end up?

A

Heart valves causing necrosis

55
Q

Staph epidermadis infections…

A

Can occur in hospital settings. It is a bug native to our skin, but due to lines, catheters, etc. it can be transmitted.

56
Q

Staph saprophyicus is the…

A

2nd leading cause (E. coli) of UTI in sexually-active young women.

57
Q

Bacillus anthracis

Reservoir:
Metabolism:
Virulence:
Exotoxins:
Clinical:
A

Reservoir: soil, herbivores.
Metabolism: facultative anaerobe.
Virulence: unique protein capsule, non-motile.
Exotoxins: edema factor (EF), lethal factor (LF), protective antigen (PA).
Clinical: cutaneous anthrax, pulmonary anthrax, GI anthrax, injectional anthrax.

58
Q

Bacillus cereus

Metabolism:
Virulence:
What kind of toxins?
Clinical

A

Metabolism: aerobic.
Virulence: no capsule, but motile.
What kind of toxins? Heat labile and heat stable enterotoxin.
Clinical: food poisoning (bacillary dysentery)

The toxins are pre-formed, so symptoms occur quickly.

59
Q

Clostridium have what type of metabolism? What about Bacillus?

A

Clostridium are anaerobes while bacilli are aerobes.

60
Q

Clostridium tetani

Reservoir:
Metabolism:
Virulence:
Toxins:
Clinical:
A

Reservoir: soil.
Metabolism: anaerobic.
Virulence: flagella.
Toxins: Tetanospasmin inhibits inhibitory NTs.
Clinical: muscle spasm, lockjaw, respiratory muscle paralysis.

61
Q

Clostridium perfringens

Reservoir:
Metabolism:
Virulence:
Toxins:
Clinical:
A
Reservoir: ubiquitous.
Metabolism: anaerobic.
Virulence: non-motile.
Toxins: alpha toxin (lecithinase).
Clinical: gangrene
62
Q

Clostridium difficile

Reservoir:
Metabolism:
Virulence:
Toxins:
Clinical:
A
Reservoir: GI tract, hospitals.
Metabolism: anaerobic.
Virulence: flagella.
Toxins: Toxin A and Toxin B.
Clinical: Pseudomembranous enterocolitis
63
Q

Corynebacterium diphtheriae

Morphology:
Metabolism:
Virulence:
Toxins:
Clinical:
A

Morphology: G+, non-spore forming rod, non-motile*.
Metabolism: facultative anaerobe, catalase positive.
Virulence: pseudomembrane forms in pharynx and allows toxin to be distributed.
Toxins: Exotoxin provided by a bacteriophage. Must be infected in order to be toxic.
Clinical: Diphtheria –> sore throat, myocarditis, neural involvement.

64
Q

Listeria monocytogenes

Morphology:
Metabolism:
Virulence:
Toxins:
Clinical:

Where is it found?

A

Morphology: G+ rods, non-spore-forming, motile*.
Metabolism: facultative anaerobe, catalase positive, beta hemolytic.
Virulence: flagella, hemolysin
Toxins: Listeria O and phospholipases allow for release from phagolysosomes of Mo.
Clinical: neonatal meningitis, meningitis in elderly, septicemia in pregnant women, placentitis.

Found intracellularly.

65
Q

What are the toxins provided by the following bacterium?

Bacillus anthracis 
Bacillus cereus
Clostridium tetani 
Clostridium perfringens
Clostridium difficile 
Corynebacterium diphtheria
Listeria
A

Bacillus anthracis: EF, LF, PA.
Bacillus cereus: heat labile and heat stabile toxin.
Clostridium tetani: tetanospasmin which inhibits inhibitory NTs.
Clostridium perfringens: alpha toxin (lecithinase).
Clostridium difficile: toxin A and toxin B.
Corynebacterium diphtheria: toxin is provided from a phage.
Listeria: Listeria O and phospholipase which allows for release from Mo.

66
Q

Hemolytic patterns for:

Grp A strep
Grp B strep
Grp D strep
Viridans
Strep pneumoniae 
Listeria
A
Grp A strep: beta
Grp B strep: beta
Grp D strep: gamma
Viridans: alpha
Strep pneumoniae: alpha 
Listeria: beta
67
Q

Motility of the following:

Bacillus anthracis
Bacillus cereus
Tetanus
Clostridium perfringens
Clostridium difficile
Corynebacterium diphtheria
Listeria monocytes
A
Bacillus anthracis: non-motile
Bacillus cereus: motile
Tetanus: motile
Clostridium perfringens: non-motile
Clostridium difficile: motile
Corynebacterium diphtheria: non-motile
Listeria monocytes: motile
68
Q

What are the only 2 major pathogenic Gram- cocci?

A

Neisseria meningitidis

Neisseria gonorrheae

69
Q

What is the morphology of Neisseria meningitidis and Neisseria gonorrheae?

A

G- diplococci

70
Q

What is the G+ diplococci to know?

A

Strep pneumoniae

71
Q

Which 2 bacteria need to be infected by a bacteriophage to become toxic?

A

Diphtheria

Grp A hemolytic strep

72
Q

What medium is required for growing Corynebacterium diphtheriae?

A

Loeffler’s medium

73
Q

What are symptoms of Neisseria meningitidis?

A

Meningococcemia - fevers, chills, arthralgia, myalgias and petechial rash.

Waterhouse-Friderichsen syndrome - BL adrenal hemorrhage. It can lead to DIC and coma.

Sepsis

74
Q

Which groups are considered high risk for Neisseria meningitidis?

A

Infants from 6 mo. to 2 yr.
Army recruits
College freshmen

75
Q

What are symptoms of Neisseria meningitidis?

A

Meningococcemia - fevers, chills, arthralgia, myalgias and petechial rash.

Waterhouse-Friderichsen syndrome - BL adrenal hemorrhage.

Sepsis

76
Q

What feature allows a doctor to make a presumptive DX of Neisseria meningitidis prior to a spinal tap?

A

The classic petechial rash

77
Q

What medium is required for Meisseria meningitidis?

A

Thayer-Martin VCN.

V - vancomycin to kill G+.
C - colistin to kill all other G-.
N - nystatin to kill fungi.

78
Q

What are the 4 virulence factors in Neisseria gonorrhea?

A

Pili
Outer membrane protein porins and opa proteins both for invasion and adhesion into epithelium.
LPS endotoxin

79
Q

How can men get Gonorrhea?

What are their SX?

A

MSM and rectal infections.

Purulent urethral discharge, epididymitis, prostatitis, urethral strictures. Can occasionally occur in the mouth.

80
Q

What are womens’ SX with Gonorrhea?

What are some complications?

A

Often asymptomatic, but mostly results in dysparenuria and PID.

Infertility, ectopic pregnancies, peri-hepatitis. Rarely tubo-ovarian abscess and peritonitis.

81
Q

What are other bugs that are part of the “greater Neisseria family”?

A

Moraxella catarrhalis**

Haemophilus**
Actinobacillus
Cardiobacterium
Eikenella
Kingella**
82
Q

How can ABX resistance occur in Gonorrhea?

A

Because in western society, babies born vaginally are given prophylactic ABX for Gonorrhea and Chylamidia.

83
Q

Which 4 species make up the enterics?

What is their role?

A

Enterobacteriaceae
Vibrionaceace
Psuedomonadaceae
Bacteriodaceae

They are normal GI flora and can occasionally cause GI infections.

84
Q

What is a novel TX for patients with C diff?

A

Fecal transplant (bacteriotherapy)

85
Q

What diseases can be caused by E. coli? (7)

A
Diarrhea
UTI
Neonatal meningitidis
ETEC
EHEC
Hemolytic-uremic syndrome (HUS)
EIEC
86
Q

ETEC vs. EHEC

A

ETEC - (toxigenic) traveler’s diarrhea. Toxins are heat labile toxin and heat stable toxin. Watery diarrhea. Does not breach epithelium

EHEC - (hemorrhagic) secretes Shiga-like toxin that inhibits 60s ribosome. Diarrhea is bloody. Breaches the epithelium.

87
Q

What is associated with Hemolytic-uremic syndrome?

A

Anemia
Thrombocytopenia
Renal failure (uremia)

It is a type of EHEC E coli infection.

88
Q

What is EIEC?

A

Enteroinvasive E Coli - also includes Shiga-like toxin. It invades epithelial cells and leads to fever, and diarrhea w/ WBCs.

89
Q

E. Coli can cause diarrhea that is indistinguishable from which other infections?

A

Shigella and Vibrio (cholera)

90
Q

Klebsiella pneumoniae is in which family?

What is the Ag? Is it motile?

What does it cause in hospitals?

What is it characterized by?

A

Enterobacteriaceae.

Encapsuled O Ag.

Sepsis.

Cavitory pulmonary lesions, thick sputum, hemoptysis and “red jelly” sputum.

91
Q

Proteus mirabilis is in which family?

What does it have a unique capability to do?

Is it motile?

What can it be cross-reactive with?

What is it a common cause of?

A

Enterobacteriaceae.

Cleave urea (NH3 + CO2)

Highly motile and makes culturing tough.

Can be cross-reactive with Rickettsia.

UTIs, often nosocomial.

92
Q

What family is Enterobacter serratia in?

A

Enterobacteriaceae.

93
Q

Shigella family:

How many spp.?

It is always…

Who are the only hosts?

What does it cause?

Where is it often found?

A

Enterobacteriaceae.

4 spp.

Always pathogenic, never normal flora.

Humans only hosts.

Causes cell damage, inflammation, ulceration, fever, diarrhea, purulent exudate. Main cause of dysentery.

Found often in nursing homes and the elderly. Also can affect very young pts.

94
Q

Salmonella is in which family?

What Ag is virulent?

Where is it found?

What is most common carrier in USA?

It is always…

4 DZ states:

A

Enterobacteriaceae.

Vi Ag.

Animal feces, contaminated water, zoonotic infection (except S. typhi).

Chicken and eggs.

Always pathogenic.

Typhoid fever - S. typhi and rose spots.
Carrier state - if infected prior, pts. can be lifelong carriers (typhoid Mary).
Sepsis - in lung, brain, bone and caused by S. choleraesius.
Diarrhea (gastroenteritis) - caused by any type of Salmonella.

95
Q

Rose spots are seen in which infection? What percentage?

When is onset?

What is it characterized by?

How big?

How long do they stay? What can they leave behind?

A

30% of S. typhi (commonly in those untreated).

2-4 wks.

5-15 bumps from nipples to umbilicus and occasionally on extremities.

2-8 mm.

3-5 days and may leave hyperpigmentation.

96
Q

Yersinia enterocolitica is related to:

How is it transmitted?

Where does it come from?

What is often the outcome of infection?

A

Yersinia pestis (Bubonic plague)

Fecal-oral route.

Animals.

Pseudoappendicitis - RLQ pain, fever, diarrhea, ulceration in terminal ileum.

97
Q

Vibrio cholerae is in what family?

How is it transmitted?

Where is it found?

What does it cause?

How does it cause death?

A

Vibrionaceae.

Fecal-oral route.

Fecally contaminated water.

Does not invade epithelium, but instead binds epithelial cells and triggers and increase in cAMP leading to “rice-water diarrhea”.

Causes death due to dehydration and electrolyte abnormalities.

98
Q

3 most common causes of diarrhea in the world

A

Campylobacter jejuni, ETEC, rotavirus

99
Q

Campylobacter jejuni is a _______ disease.

Transmitted?

SX?

Toxin?

Associated with?

A

Zoonotic DZ.

Fecal-oral route (animals and unpasteurized milk).

Fever, HA, loose and bloody stools/diarrhea.

LT toxin.

Reactive arthritis and Guillan-Barre syndrome.

100
Q

H. pylori is the most common cause of:

What is it associated with?

Where is it found in gastric BX?

A

Duodenal ulcers and chronic gastritis.

Gastric epithelial neoplasms and MALTomas**.

Localized to superficial gastric mucosal lining cells.

101
Q

99% of GI flora is composed of:

A

Obligate anaerobis G- rods of family Bacteriodes.

Also in mouth and vagina.

102
Q

Bacteriodes fragilis’ virulence:

A

Has a capsule but NO endotoxin or lipid A.

103
Q

GI flora is normally…

But it can…

A

Normally low virulence.

But it can cause secondary infection after trauma in some cases.

104
Q

What can Bacteriodes complicate? (3)

A

Abortion
Tubo-ovarian abscess
IUD erosions

105
Q

Bacteriodes melaninogenicus can cause:

What is it associated with?

A

Necrotizing anaerobic pneumonia following GI aspiration.

Associated w/ periodontitis.

106
Q

Fusobacterium can have similar SX as:

A

Bacteriodes melaninogenicus (pneumonia post GI aspiration), but also rarely OM.

107
Q

Peptostreptococcus is what kind of bacterium? (Gram, metabolism and shape)

Where is it found?

What 2 other bacterium can be found in this infection?

A

G+ anaerobic cocci.

Normally found in mouth, vagina and intestines.

Microaerophilics and Viridans grp strep.

108
Q

Pseudomonas aeruginosa features (6)

A

Serious complication in very ill, debilitated and hospitalized patient.
Resistant to many ABX.
Has a classic green-grey pigment which is easily visible.
Distinctive sweet/sour smell (fermented grapes, etc)
Can infect almost anything and cause sepsis anywhere.
Common in CF pts.

109
Q

Burkholderia (pseudomonas) cepacia is becoming a…

Acinetobacter species is similar to? Causes?

A

Rapidly becoming a similar threat as it is a relative of Pseudomonas aeruginosa.

Similar to pseudomonads and tends to cause nosocomial infections.

110
Q

3 bugs grouped together because of their common acquisition via the respiratory tract:

A

Hemophilus, Bordatella and Legionella

111
Q

Haemophilus influenzae subtypes:

Virulence?

Vaccine?

A

6 –> A, B, C, D, E, F.
All have a polyribitol ribose capsule. B subtype is worst. Some other varients may not have a capsule, but they are not powerful.

LPS lipid A.

Hib capsule vacc.

112
Q

2 bacteria can cause meningitis later in childhood and are not obtained via vaginal delivery. What are they?

What does it cause?

A

Neisseria meningitidis and Haemophilus influenzae. Abs to these infections are not obtained from approx 6 mo to 3 yrs and a window for infection is created.

Acute epiglottitis, septic arthritis (most common in infants), sepsis, meningitis (obviously).

113
Q

Haemophilus ducreyi is an:

SX:

What would be included in a DDX? (3)

A

STD.

Painful genital ulcer (chancroid), swollen/painful inguinal LNs.

Syphilis, Herpes, Lymphogranulomas.

114
Q

What are “clue cells”?

A

They are found in pts. with Gardnerella vaginalis, a common cause of vaginitis. They are vaginal epithelial cells with pleomorphic bacilli in the cytoplasm.

115
Q

Bordatella pertussis causes:

What are the 4 virulence factors?

A

Whooping cough.

Pertussis toxin - allows entry of A toxin.
Extra cytoplasmic AC - weakens phagocytosis.
Filamentous hemagglutinin (FHA) - helps binding to host.
Tracheal cytotoxin - destroys ciliated epithelium and is probable cause for cough in Whooping cough.

116
Q

Legionella pneumophilia has what metabolism?

Famous for?

Where does it like to live?

Is it often diagnosed?

A

Aerobic G- rod.

Outbreak in 1976 at an American Legion convention in Phi.

Water-lover.

Only correctly DX 3% of time.

117
Q

Pontiac fever vs. classic Legionnaire’s DZ

A

PF: HA, myalgias, fatigue, fever, chills and resolved in 1 wk or less.

Legionnaire’s: very high fevers and severe pneumonia.

118
Q

Yersinia, Francisella, Brucella and Pasteurella are all (2):

They can be the etiology of:

What is it possible to use these for?

Where is the usual site of contact? Where do they spread?

They are all generally:

A

G- rods and zoonotic.

Very aggressive/virulent disease.

Possible to use for weaponization.

Skin is typical site of contact and can spread to LNs and vital organs.

Facultative intracellular orgs.

119
Q

Yersinia pestis

Where is the DZ found?

Where is a focus for the DZ?

Gram stain and what staining pattern?

A

Rats harbor it, vectors are fleas.

SW US is the focus.

G- bipolar staining pattern.

120
Q

Francisella tularensis (Tularemia)

Can be mistaken for:

Found where?

Clinical manifestations (4)

A

Bubonic plague.

Found in ticks, deerflies and wild rabbits.

Ulceroglandular tularemia (hole in skin w/ black base), pneumonic tularemia (pneumonia), effects on eyes and GI (typhoidal tularemia).

121
Q

Brucella infects:

Where is it common?

Main SX:

Main bug of this family to know:

A

Goats, cows, pigs, dogs.

Not common in US, but found in parts of world.

Undulant fever.

Pasturella multocida: G- zoonotic that is associated w/ dog and cat bites.

122
Q

Chlamydia trachomatic infects:

Chlamydia psittaci and Chlamydia pneumoniae infect:

A

Eyes, genitals and lungs.

Respiratory system.

123
Q

Chlamydia trachomatis is the most…

What can it cause eventually?

Other SX (4)

A

Common STD in US.

Leading cause of preventable blindness in world.

Urethritis
Cervicitis
PID
Epididymitis (males)

124
Q

Reiter’s syndrome vs. Fitz-Hugh-Curtis syndrome

A

Reiter’s syndrome - inflammation of joints associated w/ Chlamydia infection.
Fitz-Hugh-Curtis syndrome - infection of liver capsule and causes RUQ pain.

125
Q

Rickettsia morphology:

What does it require? Where does it replicate?

Clinical manifestations:

A

Small G-, non-motile, coccobacillary.

Requires arthropod vector. Replicates freely in cytoplasm of endothelial cells.

Rash, high fevers and severe HA.

126
Q

What test is used to differentiate Rickettsia and Proteus vulgaris?

A

Weil-Felix reaction

127
Q

Rocky Mountain Spotted fever

Pathogen:

Vector/reservoir:

Clinical manifestations:

A

Rickettsia rickettsii.

Tick or dog tick.

Spots (due to hemorrhages in BVs and microthrombi), fever, palmar rash

128
Q

Epidemic typhus/Brill-Zinsser DZ

Pathogen:

Vector/reservoir:

Clinical manifestations:

A

Rickettsia prowazekii.

Lice.

Abrupt onset w/ fever and HA, then 2 wk incubation with rash (not on pals, soles like RMSF) and possible gangrene. Serious.

129
Q

Endemic or murine typhus

Pathogen:

Vector/reservoir:

Clinical manifestations:

A

RIckettsia typhi.

Fleas.

Incubates for 10 days, then fever, HA w/ flat or bumpy rash. Serious.

130
Q

Scrub typhus or Tsutsugamushi fever

Pathogen:

Vector/reservoir:

Clinical manifestations:

A

Rickettsia tsutsugamushi.

Larvae of mites.

2 wk incubation, then high fever, HA, and scab at original bite site.

131
Q

Rickettsia parkeri and Rickettsia africae are…

A

New Rickettsia spp.

132
Q

Bortanella infections’ common name:

Coxiella burnetti
Erlichia chaffeensis
Bartonella quintana
Bartonella henselae

A

Coxiella burnetti - Q fever, endospore former.
Erlichia chaffeensis - similar to RMSF.
Bartonella quintana - Trench fever.
Bartonella henselae - Cat scratch DZ, bacillary angiomatosis.

133
Q

What differentiates Rickettsia and Bortanella?

A

Rickettsia are obligate intracellular orgs.

134
Q

Spirochetes morphology:

What makes them challenging to work with?

3 genera:

A

Tiny G- spirals.

Hard to culture and must use darkfield micro, silver stains and serologic tests.

Treponema, Borrelia, Leptospira.

135
Q

Syphilis name:

1-3 stages

Tests for syphilis:

A

Treponema pallidum.

Primary: painless chancre in genitals 3-6 wks post contact.
Secondary: systemic organ involvement, rash.
Tertiary: develops over 6-40 yrs. Gummatous syphilis, CV syphilis and neuropsyphilis.

Treponemal tests.

136
Q

Borrelia morphology:

Associated with _______ and its stages (5)

A

Larger than treponemes and can usually be seen w/ light microscopy.

Lyme DZ.

  1. Bite
  2. Disseminated skin
  3. Wks - Facial/cardiac abnormalities
  4. 6 mo - 1 yr - septic arthritic sx.
  5. Chronic arthritis and increasing encephalopathy.
137
Q

Leptospiria morphology:

Found in:

A

Long, thin aerobic spirochetes.

Contaminated urine.

138
Q

What is Weil’s DZ?

A

Infectious jaundice caused by Leptospira interrogans

139
Q

Acid-fact mycobacteria morphology:

2 types:

Infect only:

A

Thin rods w/ lipid laden cell walls.

TB and Leprosy.

Only humans.

140
Q

What are Mycoplsma?

2 types

A

The smallest free-living orgs capable of self-replication. Do not have cell walls.

Mycoplasma pneumoniae and Ureaplasma urealyticum.

141
Q

2 types of Leprosy

A

Lepromatous and Tuberculoid