(SOME) Zoonoses Flashcards Preview

Micro Exam #2 > (SOME) Zoonoses > Flashcards

Flashcards in (SOME) Zoonoses Deck (105)
Loading flashcards...
1
Q

Describe the physical structure of Bacillus.

A

G+ Rods
Large, Fat, Square Ends
Chains, Palisades, Clumps

2
Q

Bacillus response to adversity?

A

Sporulation

3
Q

Oxygen metabolism of Bacillus.

A

Aerobic

Some species have butanediol or lactate ferm pathways.

4
Q

Where can Bacillus be found primarily?

A

Soil and on Leaf Surfaces

5
Q

Two types of Bacillus we covered?

A

Bacillus cereus

Bacillus anthracis

6
Q

Bacillus cereus is typically seen in what context?

A

Food Poisoning

7
Q

Describe the physical appearance of Bacillus cereus spores.

A

Subterminal

8
Q

Describe the physical appearance of Bacillus cereus colonies on agar plates.

A

Large, flat, rough

9
Q

What two varieties of Bacillus cereus are seen clinically?

A

Emetic Variety

Diarrheal Variety

10
Q

Describe the clinical presentation of emetic variety Bacillus cereus.

A

Very Acute Onset (1-6 hrs)
Recovery in 12 hours
Nausea, Vomiting, Cramps

11
Q

Describe the clinical presentation of the diarrheal variety of Bacillus cereus.

A

Slow onset (8-16 hrs)
Profuse Diarrhea, Cramps
No Vomiting

12
Q

How do people get Bacillus cereus?

A

Cooked rice and pasta that has been cooled too slowly?

13
Q

Why the fuck does it matter how slowly my rice cools?

A

Cooling slowly allows spores to germinate and produce the toxin

14
Q

How many toxins are associated with Bacillus cereus?

A

4 (1 emetic toxin and three enterotoxins)

15
Q

What does the emetic toxin of Bacillus cereus do?

A

K+ Ionophore

16
Q

What are the three enterotoxins associated with Bacillus cereus?

A

Hemolytic
Non-hemolytic (pore-formers)
Cytotoxin (Activates Ad cyclase)

17
Q

Unique physical characteristics of Bacillus anthracis?

A

Central Spores
“Cut glass” colonies on blood agar
Poly-D-glutamate capsule

18
Q

Clinical presentation of Bacillus anthracis?

A

Papule (12-36 hrs) becomes a large necrotic eschar
Disseminates and becomes systemic
May infect any organ

19
Q

What is an eschar?

A

a dry, dark scab or falling away of dead skin

20
Q

Three most common causes of diarrhea (not necessarily in order)

A

Norovirus
S Aureus
B cereus

21
Q

How is Bacillus anthracis typically contracted?

A
  • Animals ingest/carry spores from soil
  • Human handles infected animal materials
  • Spore contacts mucous membranes or enter through abrasions
  • Germinate in Macrophages after engulfment
22
Q

How long are Bacillus anthracis spores viable?

A

more than 50 years

23
Q

Four ways (even though they may kind of overlap..) that Bacillus anthracis can get into the body

A

Contact Mucus Membrane
Abrasion
Inhalation
Ingestion

24
Q

Why should we give a shit about Bacillus anthracis if it comes up less than once a year in the whole world?

A

Possibly comes up in bioweaponization

25
Q

What do spores do upon entering the host?

A

Enter macrophages

Germinate in the phagolysosome (upon O2 radical exposure)

26
Q

Can Bacillus anthracis spores be found in blood smears?

A

No

27
Q

Describe the Bacillus anthracis toxin

A

Tripartite AB-type (A2B) toxin

28
Q

What are the three components of Bacillus anthracis toxin?

A

Binding (Protective Antigen)
Lethal Factor
Edema Factor

29
Q

What does Bacillus anthracis Lethal Factor do?

A

It is a MAP Kinase Protease responsible for necrosis

30
Q

What does Bacillus anthracis Edema factor do?

A

It is a calmodulin-dependent adenyl cyclase

It makes cAMP, which causes H2O secretion into tissues

31
Q

Both virulence factors of Bacillus anthracis (______, ________) are encoded by ______.

A

(Toxin, Capsule)

Plasmid Encoded

32
Q

How do you treat Bacillus anthracis?

A

Penicillin (cutaneous), Doxycycline, Ciprofloxacin

33
Q

How is Bacillus anthracis controlled?

A

Live pXO2 vaccine
PA toxoid vaccine (military)
Livestock vaccine

34
Q

Describe the physical structure of Brucella

A

G-

Aerobic Coccobacillus

35
Q

T or F. Brucella is dangerous due to its rapid growth rate.

A

F. Very Slow growing (5 days on plate)

36
Q

Growth site of Brucella in host?

A

Facultative Intracellular parasite

37
Q

Four species of Brucella that affect humans?

A
Brucella melitensis (goats)
Brucella abortus (cattle)
Brucella suis (swine)
Brucella canis (dogs)
38
Q

In what animal population is Brucella becoming more common?

A

Dogs – spreading through animal shelters

Up to 10% prevalence in kennels

39
Q

Clinical presentation of Brucella?

A
1-6 week incubation
Undulant Fever
May become chronic -- weakness
Granulomas (Liver, Spleen, LN, bone)
Psychoneuroses
40
Q

What is an Undulant Fever?

A

Fever that goes up and down on a regular basis

rise in afternoon, drop w/ profuse sweating in evening

41
Q

How may Brucella present in livestock (esp cattle)?

A

Bacteria bind erythritol in testes, placenta, or mammary tissue
If on placenta, form foci that detach microvilli
Abortion Storm

42
Q

What is an abortion storm?

A

Large scale abortions throughout an animal population

43
Q

How is Brucella in cattle so common out West?

A

Wild animals (Bison, goats, elk, sheep) carry it
Male transmits in semen
Abortion storm contaminates pasture grass

44
Q

How do humans acquire Brucella?

A

Infected milk
Handling Infected Animal
Lab Accident

45
Q

How is Brucella diagnosed?

A

Blood Sample
Serology
Culture

46
Q

Pathogenesis of Brucella?

A

Intracellular survival in PMNs/Macrophages
Spreads to lymphatics and bloodstream
Infects liver, spleen, BM – Forms granulomas
Bacterial growth – Inflamm. response

47
Q

So…what actually causes the undulant fever?

A

Bacterial release from macrophages

Brought back down as it is taken back in by macrophages

48
Q

How can Brucella be controlled?

A

Pasteurize Milk
Eradicate from herds/Segregate from wild herds
Testing/Slaughter of Infected Animals

Human Live Vaccine in Russia

49
Q

Why don’t Americans vaccinate for Brucella?

A

We don’t want to deal with the whole LPS toxicity thing.

U-S-A, U-S-A, U-S-A

50
Q

How is Brucella treated?

A

Doxycycline + Rifampin +/- Streptomycin

51
Q

Why might treatment tend to be ineffective?

A

Intracellular pathogen

52
Q

If you see an elevated erythrocyte sedimentation rate and C-Reactive Protein, what should you suspect?

A

Inflammation is happening

53
Q

Describe the structure of Francisella tularensis?

A

Small G- Coccobacillus
Pleomorphic
Slow Growth

54
Q

Francisella tularensis have a fastidious requirement of…

A

Cysteine

55
Q

Clinical Presentation of Francisella tularensis?

A

2-6 days Incubation
Inflamed, Ulcerated Papule at Infection Site
High Fever, Severe Toxemia
Abscess Formation in Liver, Spleen, LN, Lungs

56
Q

Francisella tularensis is commonly found on what part of the body?

A

Hands (from skinning animals)

57
Q

Reservoirs for Francisella tularensis?

A

Type A – Rabbits (Most Severe)

Type B – Beaver/Rodents (Milder)

58
Q

Area of the country that looks like its got Francisella tularensis all over it?

A

Missouri, Arkansis, Oklahoma

59
Q

Three methods of human acquisition of Francisella tularensis?

A

Skinning Infected Animals (and aerosol inhalation of carcass)
Ticks/Deerflies (maybe other biters)
Laboratory Hazards (Ingestion, Inhalation)

60
Q

How infection is Francisella tularensis?

A

Infectious dose = 10 bacteria

Need P3 containment lab to grow it

61
Q

Pathogenesis of Francisella tularensis?

A

Capsule resists complement
Take up by mphages by coiling phago.
Prevents oxidative burst, grows intracellularly
T4SS + effectors that prevent phagolyso fusion
LPS and PG release

62
Q

How is Francisella tularensis treated?

A

Doxycycline, Cipro, gentamycin

63
Q

Ways of controlling Francisella tularensis spread?

A

Strict isolation of lab organisms
Care while skinning rabbits
live cel vaccine for military

64
Q

Francisella tularensis has a PAI with 17 genes. What is a PAI?

A

Pathogenic Island in the genome that contains genes that mediate pathogenicity

65
Q

Describe the structure of Pasteurella multocida?

A

Small G- coccobacilli

Bipolar Staining

66
Q

Oxygen requirements of Pasteurella multocida?

A

Facultative Anerobe

67
Q

How many capsular antigen types of Pasteurella multocida are there?

A

4

68
Q

Clinical presentation of Pasteurella multocida in humans?

A

Local or disseminated edematous soft tissue abscess
Occurs within a few hours of animal bite
Rapidly progressive cellulitis

You see proximal streaking along a lymph tract

69
Q

Significance of Pasteurella multocida in the animal kingdom?

A

Fowl cholera (pneumonia) – wipes out flocks
Shipping Fever (cattle) – Copious nasal discharge,
septicemia, acute pneumonia, death
Snuffles (rabbits) – progress to lethal hemorrhagic pneumonia

70
Q

How does Pasteurella multocida typically spread to humans?

A
Animal bites (Carried by 90% cats and 70% of dogs)
Sometimes fomites (dust -- chicken shed workers)
71
Q

Pathogenesis of Pasteurella multocida?

A

Antiphagocytic Capsule
Pili, Adhesion Proteins, Fe-binders
Adhere to mphage, but not engulfed
Growth and abscess formation

72
Q

What is unique about the growth of Pasteurella multocida?

A

in vivo is as fast as in vitro

Grows too fast for immune system to keep up very well.

73
Q

Is Pasteurella multocida very susceptible to antibiotics? Why?

A

No – Grows too fast

74
Q

How is Pasteurella multocida treated?

A

Multiple Drugs

Pen/Amp or Ceph + Tetra

75
Q

Remember, most animal bites are….

A

Polymicrobial

76
Q

Describe the physical structure of Bartonella henselae.

A

Gram negative small rod

77
Q

Difference between Bartonella henselae and Rickettsia?

A

Bartonella henselae can grow on Lab Media

78
Q

What does Bartonella henselae attach to in cats? humans?

A

Cats – RBCs

Humans – Endothelial Cells (Intracellular)

79
Q

Describe the clinical presentation of Bartonella henselae.

A

Cat Scratch disease
Papule at inoculation site, local swelling, fever
Regional Lymph Node Involvement
Occasionally “Culture Negative” Endocarditis

80
Q

Describe the clinical presentation of Bartonella quintana.

A

Trench Fever/Homeless Fever
5 day recurring fever
Headache, lymphadenopathy

81
Q

What is Bacillary angiomatosis?

A

Proliferation of small spherical blood vessels in an inflamed endothelial background (blood vessel tumor)
May occur as papular/tumoral lesion or in organs

82
Q

What bacterium cause Bacillary angiomatosis?

A

Bartonella henselae
Bartonella quintana
Bartonella bacilliformis

83
Q

Who is more likely to get Bacillary angiomatosis?

A

Immunocompromised/AIDS patients

84
Q

What causes Bartonella henselae.

A
Cat Scratches or Bites
#1 Cause of localized lymph node swelling in children
85
Q

How is Bartonella quintana is spread by…

A

..human head and body lice.

86
Q

Describe Bartonella pathogenesis.

A

Outer Membrane Binding Protein
T4SS + Effector Protein
Produces Cell-Stimulating Factor

87
Q

What does Effector Protein do?

A

Ruffling of the membrane to promote endocytosis

Stops Phag-lys fusion

88
Q

What does Cell-stimulating factor do?

A

Stimulating NF-kB and induces apoptotic pathways

89
Q

How would you typically treat Cat Scratch disease?

A

You wouldn’t

90
Q

What can you use to treat Bartonella?

A

Azithromycin +/- Rifampin

91
Q

Elevated Liver enzymes are typically indicators of what two things.

A

1) Liver Involvement

2) Muscle Breakdown/Rhabdomyolysis

92
Q

What would you expect to see change in a CBC if you have cellulitis and nothing else.

A

No major CBC changes.

93
Q

Two common polymicrobial infections.

A

Animal Bites

Abscess

94
Q

Why do you take Ab levels early in an infection?

A

As a baseline

95
Q

Describe the structure of Leptospira interrogans.

A

Exceedingly this spirochete
Seen on SEM
Endoflagella

96
Q

Describe the difficulty in growing Leptospira interrogans.

A

Pretty easy for a spirochete – 6 days to visible col.

97
Q

How do Leptospira interrogans get energy.

A

Long-chain F.A.

No glycolysis

98
Q

Clinical presentation of Leptospira interrogans initial stage.

A

Fever from bacteremia
Capillary Vasculitis and edema
leakage of RBCS and Serum (Petechiae, Bleeding)
Bac eliminated everywhere but liver, kidneys, CNS, eyes

99
Q

Clinical presentation on Leptospira interrogans secondary

A
Weil's Disease
 - Jaundice from liver failure
 - Nitrogen retention in Kidney Medulla Destruction
Bloodshoot, Ooozing Eyes
Meningitis
100
Q

How is Leptospira interrogans typically contracted?

A

Shed into water from infected kidneys
Persists in fresh water and is ingested
Also spread in rat and dog urine

101
Q

Describe the pathogensis of Leptospira interrogans.

A

Intracellular growth possible
Pathogenesis from endothelial damage in capillaries
– Highly perfused organs more affected (liver, kidneys)

102
Q

How is Leptospira interrogans treated?

A

Antibiotics are of limited control

Macrolides or Quinolones can be used

103
Q

How is Leptospira interrogans controlled?

A

Prophylactic Doxycycline by the military
Avoid rat-contaminated water
Vaccinate dogs

104
Q

What does ANP indicate

A

Heart Damage (should be under 100)

105
Q

Treatment for cellulitis.

A

Clindamycin, Keflex

Penicillin for likely MRSA coinfection