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Clinical Micro > Gram Negative Bacteria > Flashcards

Gram Negative Bacteria Flashcards

1
Q

Describe neisseria

A

Diplococci, gram negative

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2
Q

What are the virulence factors for neisseria meningitidis

A
  1. Capsule
  2. Endotoxin (LPS)
  3. IgA1 protease
  4. Extract iron from human cells
  5. Pili
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3
Q

High risk groups for neisseria meningitidis

A
  1. Infants aged 6 months to 2 years
  2. Army recruits
  3. College freshmen
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4
Q

Illness that causes petechial rash

A

Neisseria meningitidis

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5
Q

What are the 3 microorganisms that cause meningitis in babies under 3 months?

A

Listeria monocytogenes, e coli, group B strep

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6
Q

What are the organisms that cause meningitis in people older than 3 months

A

Neisseria meningitidis, haemophilus influenzae

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7
Q

What agar is used to grow Neisseria meningitis

A

Thayer Martin VCN- chocolate agar

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8
Q

Treatment for neisseria meningitis patient? Close contacts?

A

Penicillin G or ceftriaxone

Close contacts- rifampin or ciprofloxacin

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9
Q

Who should have the meningitis vaccine?

A

Certain high risk groups and during epidemics, serogroup B ages 10-25

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10
Q

Slow growing gram negative pathogens that cause endocarditis

A

HACEK group

Haemophilus influenzae
Actinobacillus species
Cardiobacterium species
Eikenella species
Kingella species

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11
Q

Describe moraxella catarrhalis

A

Gram negative diplococcis, Part of normal resp flora, causes otitis media in children, can cause respiratory infections and pneumo, exacerbates COPD, resistant to penicillin

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12
Q

What enterics ferment lactose

A

E. Coli, most enterobactericeae

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13
Q

What enterics do not ferment lactose

A

Salmonella, shigella, pseudomonas aeruginosa

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14
Q

Is e coli found outside of the intestine normally?

A

No

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15
Q

Describe Eosine methylene blue agar

A

Inhibits gram positive and lactose fermenters turn black, e coli turns metallic green

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16
Q

Describe macconkey agar

A

Inhibits gram positive bacteria and lactose fermenters turn pink/ purple

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17
Q

Antigens used to classify enterics

A

O antigen- outer layer LPS in membrane
K antigen- capsule (covers O antigen)
H antigen- flagella for mobile bacteria

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18
Q

Enterics that don’t invade cell but release exotoxins that causes watery diarrhea

A

Enterotoxogenic e coli and vibrio cholera

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19
Q

Enteroinvasive organisms

A

EHEC, shigella, salmonella enteritidis

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20
Q

What enterics can invade the lymph nodes and bloodstream?

A

Salmonella typhi, yersinia enterocolitica, campylobacter jejuni

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21
Q

What are examples of hospital acquired gram negative how can they be acquired?

A

E Coli
klebsiella pneumoniae
Proteus mirabilos
Enterobacte
serratia
pseudomonas aeruginosa

Invade Foley catheters, aspirate vomit, etc.

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22
Q

What are the main groups of enterics?

A

Enterobactericeae
Vibrionaceae
Bacteroidaceae
Psuedomonadacea

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23
Q

Example of bacteria that can ferment lactose

A

Escherichia coli

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24
Q

Examples of bacteria that cannot ferment lactose

A

Salmonella, shigella, pseudomonas aeruginosa

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25
Q

What are the biochemical classification methods for gram negative bacilli

A

Ability to ferment lactose and production of H2S

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26
Q

What agars are used to help classify enterics?

A
  1. EMB agar (Eosine methylene blue) - inhibit gram + growth and lactose fermenters become deep purple / black and e coli gets green sheen.
  2. Mackonkey agar - inhibit gram + a s lactose fermenters become pink purple color
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27
Q

Is E coli usually endogenous or exogenous?

A

Endogenous in the colon

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28
Q

3 surface antigens of enterics

A

1) o antigen
2) k antigen
3) H antigen

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29
Q

Describe the o atnigen

A

Part of enterics bacteria- outer most component of LPS, differs between the dif gram - bacteria

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30
Q

Describe K antigen

A

Capsule antigen (covers O antigen)

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31
Q

Describe H antigen

A

Makes up subunits of bacterial flagella. Only motile bacteria have this antigen.

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32
Q

Example of bacteria without h antigen

A

Shigella

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33
Q

Example of bacteria with h antigen

A

Salmonella- changes and protects from our antibodies

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34
Q

Describe non invasive enteric diarrhea

A

Bacteria bind to intestinal epithelial cells, but do not enter cell. Release exotoxins that cause watery diarrhea without systemic symptoms.

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35
Q

Examples of organisms that cause noninvasive enteric diarrhea

A

ETEC
Vibrio cholera

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36
Q

Describe pathogenesis of invasive enteric diarrhea

A

Bacteria with virulence factors that allow for binding and invasion of cell. Toxins released that kill cell. Leukocytes in stool and systemic symptoms + diarrhea.

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37
Q

Examples of enteroinvasive organisms

A

EIEC
Shigella
Salmonella enteritidis

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38
Q

Examples of enteric organisms that cause bacteriema

A

Salmonella typhi
Yersinia enterocolitica
Campylobacter jejuni

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39
Q

Two example situations when enterics normally part of our gut flora cause disease (hospital acquired gram negatives)

A

1) Foley catheter
2) patient aspirates vomit colonized with enterics

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40
Q

Examples hospital acquired gram negative organisms

A

E Coli
Klebsiella pneumoniae
Proteus mirabilis
Enterobacter
Serratia
Pseudomonas aeruginosa

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41
Q

What bacteria are in the family enterobactericeae?

A

E coli
Proteus mirabilis
Klebsiella pneumoniae
Enterobacter
Serratia
Shigella
Salmonella
Yersinia enterocolitica

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42
Q

What bacteria are in the family vibrionaceae?

A

Vibrio cholera
Vibrio parahaemolyticus
Campylobacter jejuni
Helicobacter pylori

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43
Q

What bacteria are in the family bacteroidaceae?

A

Bacteroides fragilis
Bacteroides melaninogenicus
Fusobacterium

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44
Q

How can normal gut flora e
Coli cause disease?

A

Obtain virulence factors through plasmid exchange, transduction, etc.

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45
Q

Virulence factors E coli can obtain

A

1) mucousal adherence and invasion factors
2) exotoxin production (heat liable and stable toxins, or shiga like toxin)
3) endotoxin : lipid A
4) iron binding ability

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46
Q

What diseases can E coli cause when virulence factors are present

A

1) diarrhea
2) UTI
3) neonatal meningitis
4) gram-negative sepsis

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47
Q

What diseases does enterotoxogenic E coli cause?

A

Traveler’s diarrhea

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48
Q

What virulence factors does ETEC have?

A

Colonization factor (pili to bind)
Exotoxins- heat liable toxin (LT) and heat stable toxin (ST) - causes water loss and stool to look like rice water (like cholera)

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49
Q

What virulence factors does Enterohemorrhagic E coli have?

A

-Colonization factor (pili to bind to cells)
-Shiga-like toxin (aka verotoxin) - causes intestinal epithelial cell death. Causes bloody diarrhea

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50
Q

Name for disease caused by EHEC

A

Hemorrhagic colitis

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51
Q

Disease and symptoms cause by E Coli O157:H7

A

Hemolytic uremic syndrome (HUS)
-anemia
-thrombocytopenia (decrease in platelets)
-renal failure

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52
Q

Describe the pathogenesis of enteroinvasive E coli

A
  • virulence factors shared on plasmid with shigella
  • invades epithelial cells and releases shiga- like toxin
    -inflammatory response with fever and bloody diarrhea
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53
Q

Bladder infection

A

Cystitis

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54
Q

Kidney infection

A

Pylenophritis

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55
Q

Most common organism for utis

A

E coli

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56
Q

Symptoms of uti

A

Dysuria (burn)
Frequency
Feeling fullness of bladder

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57
Q

Number of colonies needed to dx uti

A

100,000

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58
Q

Most common organism for gram - sepsis for hospitalized patients

A

E coli, sepsis due to lipid A toxin

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59
Q

Enteric common cause of neonatal meningitis

A

E coli

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60
Q

Most common disease causing Proteus species

A

Proteus mirabilis

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61
Q

Describe Proteus mirabilis

A

1) motile
2) splits urea

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62
Q

Cross reactivity for proteus

A

Rickettsia

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63
Q

Infections that Proteus spp cause

A

UTI
HAI

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64
Q

Dx for proteus UTI

A

Alkaline pH since it splits urea

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65
Q

Describe klebsiella pneumonia

A

-encapsulated (k antigen), non motile

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66
Q

Second most common cause of gram negative sepsis

A

Klebsiella (first e coli)

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67
Q

Organism commonly associated with UTIs in hospitalized patients with Foley catheters

A

Klebsiella pneumoniae

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68
Q

Risk factors for klebsiella pneumoniae pneumonia

A

Hospitalization
Alcoholics

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69
Q

Describe clinical outcomes of klebsiella pneumoniae pneumonia

A

Bloody sputum (red currant jelly), destroys lung tissue, produces cavities, high mortality rate

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70
Q

Characteristic trait of pneumonia causes by klebsiella pneumoniae

A

Sputum that looks like red currant jelly

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71
Q

Describe enterobacter

A

Part of normal intestinal flora, highly motile

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72
Q

Concern for enterobacter

A

Antibiotic resistance due to ampC (beta lactamase). Resistant to ampicillin and early generation cephalosporin, increasingly later generation cephalosporin.

If unsure use carbepenem

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73
Q

What color are serratia colonies in culture?

A

Bright red

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74
Q

What diseases can serratia cause?

A

UTI
Wound infections
Pneumonia

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75
Q

What are the 4 species of shigella?

A

Shigella dysenteriae
Shigella flexneri
Shigella boydii
Shigella sonnei

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76
Q

Describe basics of shigella

A

Non-motile
Does not ferment lactose
Does not produce H2S

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77
Q

Hosts for shigella

A

Humans

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78
Q

Population at risk for dysentery

A

Pre school age
Nursing homes

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79
Q

Is shigella part of the normal intestinal flora?

A

No

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80
Q

How is shigella transmitted?

A

Water, hands

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81
Q

Pathogenesis of shigella

A

Invades intestinal epithelial cells, releases shiga toxin which kills cells, inflammatory response, systemic infection and colon ulcers

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82
Q

Diarrhea presentation from shigella

A

Bright red flecks of blood and pus

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83
Q

Describe basics of salmonella

A

Motile
Non lactose fermenter

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84
Q

Distinguishing virulence factor salmonella

A

Vi antigen- polysaccharide capsule- protects from antibodies

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85
Q

Two main groups of salmonella

A

Typhoidal - typhi and paratypho
Non-typhoidal- salmonella enteritidis…

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86
Q

How does salmonella differ from other enterics in terms of reservoirs?

A

Lives in GI tract of animals, transmitted through animal feces

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87
Q

What type of salmonella only can be found in humans?

A

Salmonella typhi

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88
Q

Is salmonella part of the normal intestinal flora?

A

No, salmonella like shigella is always pathogenic

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89
Q

What are the 4 disease states of salmonella?

A

Typhoid fever
Carrier state
Sepsis
Gastroenteritis

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90
Q

Salmonella typhi can only survive intracellularly, so it is a …

A

Facultative intracellular parasite

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91
Q

Pathogenesis of typhoid fever

A

Salmonella typhi invades intestinal cells, then invades regional lymph nodes and seeds in organ systems. Evades phagocytosis

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92
Q

Incubation period salmonella typhi

A

1-3 weeks

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93
Q

Characteristic symptoms Salmonella typhi

A

Fever
Rose spots on belly
Pain in lower right quadrant
Enlarged spleen

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94
Q

Empiric therapy when salmonella typhi suspected

A

Ciprofloxacin or ceftriaxone

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95
Q

When people become salmonella typhi carriers, where does the salmonella live?

A

Gallbladder

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96
Q

What species of salmonella can cause systemic infection and does not involve GI tract

A

Salmonella choleraesuis

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97
Q

Populations more susceptible to salmonella infections

A

Sickle cell anemia and no speen

Reason: neutrophils in the spleen opsonize and phagositize encapsulated bacteria

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98
Q

What population is prone to salmonella osteomyelitis?

A

Sickle cell anemia

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99
Q

Clinical symptoms of diarrheal, non-typhoidal salmonella

A

Abdominal pain
Watery diarrhea (typically no blood)
Fever in half

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100
Q

What causes diarrhea from non-typhoidal salmonella?

A

Cholera-like toxin and/ or ileal inflammation

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101
Q

Basic description yersinia enterocolitica

A

Motile
Gram negative ros

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102
Q

Major source of yersinia enterocolitica infections

A

Animals - fecal oral food contamination

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103
Q

Clinical symptoms yersinia enterocolitica

A

Fever
Diarrhea
Abdominal pain in right lower abdomen
Mucousal ulceration

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104
Q

Pathogenesis of yersinia enterocolitica

A

1) invasion of intestinal epithelial cells, lymph nodes, and bloodstream (like salmonella)
2) secrete enterotoxin

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105
Q

General concern about survival of yersinia in food

A

Can live and reproduce in cold temps (concern for refrigeration)

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106
Q

Basic description vibrio cholera

A

Gram negative rod
Stains red
Single flagella

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107
Q

Does vibrion cholera invade epithelial cells?

A

No, releases cholera toxin (choleragen)

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108
Q

Population at greatest risk for vibrio cholera

A

Children in endemic areas
Us adult travelers

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109
Q

Clinical manifestations cholera

A

Watery diarrhea, loss of 1 liter of fluid per day

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110
Q

Pathogenicity of choleragen

A

Causes production of cAMP, throws off NaCl balance

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111
Q

Microscopic exam of vibrio reveals…

A

No leukocytes but fast darting rods

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112
Q

Leading cause of diarrhea in Japan from sushi

A

Vibrio parahaemolyticus

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113
Q

Basic description campylobacter jejuni

A

Gram negative rod
Single polar flagellum

One of the most common causes of diarrhea in the world

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114
Q

What are the reservoirs for campylobacter?

A

Wild and domestic animals
Poultry

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115
Q

Mode of transmission vibrio cholera

A

Fecal contaminated water

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116
Q

Common modes of transmission for campylobacter

A

Fecal contaminated water, unpasteurized milk

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117
Q

Population at highest risk campylobacter

A

Children

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118
Q

Clinical illness campylobacter jejuni

A
  • prodrome of fever and headache
  • abdominal cramps
  • bloody, loose diarrhea
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119
Q

Pathogenesis of campylobacter jejuni

A

Similar to salmonella typhi and yersinia enterocolitica - invades gi epithelial cells and spreads systemically.

Secrete LT toxin (similar to e coli) - destroys colon mucosal cells

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120
Q

Most common cause of duodenal ulcers and chronic gastritis

A

Helicobacter pylori

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121
Q

Treatment for helicobacter pylori

A

Bismuth salts (pepto-bismol) inhibit helicobacter pylori growth + antibiotics

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122
Q

Describe basics of the family bacteriodaceae

A
  • obligate anaerobes
  • gram negative rods
  • make up 99 percent of intestinal flora (mouth and vagina also have bacteroides)
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123
Q

Species of not bacteroidaceae

A

Bacteroides fragilis
Bacteroides melaninogenicus
Fusobacterium

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124
Q

basic description bacteroides fragilis

A
  • does not contain lipid A endotoxin like most gram negatives
  • capsule
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125
Q

Bacteroides fragilis are a normal part of intestinal flora, but can cause infection when…

A

There are tears, laceration, penetration. Of the intetine

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126
Q

This bacteria forms abcssses in the peritoneal cavity

A

Bacteroides fragilis

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127
Q

Bacteria associated with abdominal surgery

A

Bacteroides fragilis

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128
Q

What are the prophylaxis recommendations to prevent bacteroides fragilis after abdominal surgery?

A

Antibiotics for anaerobes
- metronidazole (flagyl)
- piperacillin/tazobactsm
- meropenem

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129
Q

Action if abscess forms in abdominal cavity?

A

Surgically drain

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130
Q

Disease caused by bacteroides melaninogenicus

A

Necrotizing anaerobic pneumonias from aspiration if sputum from the mouth

Periodontal disease

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131
Q

What bacteroides melaninogenicus looks like in culture

A

Black pigmented colonies

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132
Q

Where does bacteroides melaninogenicus normally live?

A

Mouth vagina, intestines

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133
Q

Diseases caused by fusobacterium

A

Periodontal disease
Aspiration pneumonia
Abdominal and pelvic abscesses
Otitis media

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134
Q

Strep that are often isolated from abdominal abscesses with other gram negative bacteria

A

Strep viridans group
(Strep anginosus and strep milleri)

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135
Q

Common general types of HAIs a s what they are associated with

A
  • pneumonia (endotracheal intubation and mechanical ventilation)
  • UTI (Foley catheters)
  • wound infections (recent surgery and implanted devices)
  • bloodstream infections ( IV and central lines)
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136
Q

Most common group of gram negative bacteria that cause HAIs

A

Enterobacteriaceae (E coli, klebsiella, enterobacter)

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137
Q

Types of gram negative bacteria with increases in MDR

A

Pseudomonads-
(Pseudomonas aeruginosa
Stentrophomonas maltophilia
Burkholderia cepacia)

Acinetobacter

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138
Q

Describe pseudomonas aeruginosa

A

-Obligate aerobe
-Non lactose fermenter
-Gram negative rod
-Gives colonies and wound dressings a green blue color
-grape smell

139
Q

Pathogenicity of pseudomonas aeruginosa

A

Doesn’t infect healthy people ( not very virulent)

Weakened patient :
- excretes exotoxon A (stops protein synthesis) and some have capsule to add in adhesion
- highly drug resistant

140
Q

Important pseudomonas aeruginosa infecitons

A
  1. Pneumonia
  2. Osteomyelitis
  3. Burn wounds infections
  4. Sepsis
  5. Urinary tract infections and pyelonephritis
  6. Endocarditis
  7. Malignant external otitis
  8. Corneal infections
141
Q

Patients with this disease are commonly colonized with pseudomonas aeruginosa. It progressively destroys their lungs.

A

Cystic fibrosis

142
Q

What patients are at highest risk for pneumonia from pseudomonas aeruginosa?

A

Cystic fibrosis
Immunocompromised patients

143
Q

Highest risk for osteomyelitis from pseudomonas aeruginosa

A
  • diabetic patients (from foot ulcers)
  • IV drug users
  • children with puncture wounds to foot
144
Q

Describe sepsis from pseudomonas aeruginosa

A
  • can occur in burn wounds patients
  • can come from infected lines, catheters, or secondary from other sites
  • high mortality
145
Q

Group at highest risk for UTI pseudomonas aeruginosa

A

Debilitated patients in nursing homes and hospitals
Foley catheters

146
Q

Two bacteria that are frequent causes of right heart valve endocarditis in IV drug users

A

Staphylococcus aureus
Pseudomonas aeruginosa

147
Q

Who is at risk for malignant external otitis from pseudomonas aeruginosa?

A

Elderly diabetic patients

148
Q

Who is at risk from corneal infections from pseudomonas aeruginosa

A

Contact lens wearers

149
Q

Basic description burkholderia cepacia

A

Oxidase positive
Aerobic
Gram negative brod
Grows in water, soil, plants, and animals
Highly drug resistant

150
Q

Burkholderia cepacia is most likely to cause infections in…

A

Burn and ventilated patients
Patients with cystic fibrosis (greatest risk)

151
Q

Disease burkholderia causes

A
  • Asymptomatic carriage
  • Bronchiectasis (dilated airways)
  • Rapidly progressing pneumonia with bacteremia
152
Q

Organism that is part of normal resp flora, but can cause pneumonia in hospitalized and immunocompromised persons

A

Stenotrophomonas maltophilia

153
Q

What is a risk factor for stenotrophomonas maltophilia pneumo?

A

Previous antibiotics

154
Q

Describe acinetobacter

A

Aerobic
Gram negative
Found in soil and water

155
Q

Most common acinetobacter isolated

A

Acinetobacter baumannii

156
Q

What infections does acinetobacter baumannii typically cause?

A

Hospital acquired pneumonia, line related bacteremia, burn infections, and Foley catheter associated UTIs

157
Q

What makes it difficult to dx acinetobacter baumannii under the microscope?

A

Take one different shapes and can look coccus, coco-bacillus, or like diplo cocci gram negative and get mixed with meningitis

158
Q

Acinetobacter baumannii treatment

A

Very difficult and may have some level of resistance to all antibiotics.

May be susceptible to aminoglycosides, carbepenems, poly ixins, tigecycline, and sulbactam

159
Q

Examples amonoglycosides

A

Gentamicin
Tobramycin
Amikacin

160
Q

Examples polymixins

A

Colistin
Polymyxin E
Polymyxin B

161
Q

Primary methods of prevention for gram negative HAIs

A

1) hand hygiene
2) limiting invasive devices
3) antimicrobial stewardship

162
Q

What does haemophilus influenza require for growth?

163
Q

Haemophilus influenzae typically co-infects with what disease?

164
Q

Does haemophilus have reservoirs besides humans?

A

No, obligate human parasite

165
Q

What makes haemophilus influenzae virulent?

166
Q

What are the 6 types of capsules for H influenza. Which one is typically associated with invasive disease?

A

A, b, c, d, e, f. Type b

167
Q

Describe non-encapsulated strains of Haemophilus influenzae

A

Non-typeable, colonize upper respiratory tract, only cause local infection

168
Q

What diseases do nontypeable haemophilus influenzae cause?

A
  • Otitis media in children
  • Resp disease in adults with preexisting lung disease (chronic bronchitis or recent flu)
169
Q

What diseases can HIB cause?

A

Meningitis
Epiglottis
Septic arthritis

170
Q

Who is at highest risk for nontypeable haemophilus influenzae disease?

A

Adults with COPD

171
Q

When are kids at highest risk for HIB?

A

6 months to 3-5 years old (no longer have moms antibodies but don’t have antibodies of their own yet)

172
Q

Long term effects of meningitis from HIB

A

Mental retardation, seizures, language delay, or deafness

173
Q

Concern for antibiotic use to treat meningitis from HIB

A

HIB releases LPS lipid A endotoxin, when bacteria killed causes inflammatory response that then kills neurons. Admin steroids before antibiotics

174
Q

3 bacteria that cause most meningitis cases in babies < 3 months

A

1) listeria monocytogenes
2) E coli
3) Group B strep

175
Q

Bacteria the cause meningitis > 6 months

A

1) neisseria meningitidis
2) haemophilus influenzae

176
Q

Describe the clinical symptoms of acute epiglottitis from HIB

A

Sore throat, fever, rapid swelling of epiglottis that obstructs airway and causes stridor (wheezing), child cannot swallow

177
Q

What is the most common cause of septic arthritis in infants?

A

Haemophilus influenzae type b

178
Q

Describe basics of Haemophilus influenzae

A

Pleomorphic rods
Gram negative

179
Q

What conditions put child at highest risk for sepsis from haemophilus influenzae?

A

No spleen
Sickle cell
Why? Encapsulated bacteria- opsonization happens in spleen

180
Q

What conditions put child at highest risk for sepsis from haemophilus influenzae?

A

No spleen
Sickle cell
Why? Encapsulated bacteria- opsonization happens in spleen

181
Q

What is the antibiotic of choice for less serious infections of Haemophilus influenzae?

A

Ampicillin or amoxicillin

182
Q

Treatment of choice for more serious haemophilus influenzae infections?

A

Third generation cephalosporin

183
Q

Severe manifestations of Haemophilus influenzae type b

A

1) meningitis
2) acute epiglottitis
3) septic arthritis
4) sepsis

184
Q

haemophilus influenzae vax recommendations

A

2, 4, 6, 15 months (given at same time as DPT and polio)

Eighth month of preganncy

185
Q

Describe haemophilus ducreyi

A

Gram negative cocobacilli
STI- chancroid, not systemic
Swollen lymph nodes that can rupture
Create break in skin that increase HIV risk

186
Q

Treatment for haemophilus ducreyi

A

Ceftriaxone or azithromycin

187
Q

Slow growing bacteria that cause endocarditis

A

HACEK

  1. Haemophilus spp (parainfluenzae, aphrophilus, paraphrophilus)
  2. Actinobacillus spp
  3. Cardiobacterium spp
  4. Eikenella spp.
  5. Kingella spp.
188
Q

What are the virulence factors for bordetella pertussis?

A

1) pertussis toxin
2) extra cytoplasmic adenylate cyclase
3) filamentous hemagglutinin (FHA)
4) tracheal cytotoxin

189
Q

Describe pertussis toxin

A

Exotoxin
Causes increase in cAMP

190
Q

What are the effects of pertussis toxin?

A

1) histamine sensitization
2) increase in insulin synthesis
3) promotion of lymphocytes production and inhibition of phagocytosis

191
Q

What is the role of the bordetella pertussis virulence factor extra cytoplasmic adenylate cyclase?

A

Weakens host’s ability to phagocytose and clear the bacteria

192
Q

What is the role of the bordetella pertussis virulence factor filamentous hemagglutinin (FHA)?

A

Pili to attach to epithelial cells if bronchi (doesn’t invade, adheres and release exotoxins)

193
Q

What is the role of bordetella pertussis virulence factor tracheal cytotoxin?

A

Responsible for violent cough, kills ciliated epithelial cells which disrupts body’s clearance mechanism

194
Q

Incubation period for whooping cough

A

Typically 1 week

195
Q

What are the 3 stages of bordetella pertussis

A

Catarrhal stage
Paroxysmal stag
Convalescent stage

196
Q

How long does the catarrhal stage last?

197
Q

Describe catarrhal stage of bordetella pertussis

A

1-2 weeks
Low grade fever, runny nose, sneezing, mild cough
Most contagious during this stage

198
Q

Describe the paroxysmal stage of bordetella pertussis

A
  • Bursts of no productive coughing (15-25 attacks per day)
  • Violent coughing followed by inspiratory gasp
  • patient may not be able to breathe during attack
  • posttussive commiting
199
Q

How do partially immunized/ immunized/ adults typically present?

A

Cough > 1 week

200
Q

Method to determine pertussis from non-infectious cough

A

Increase in lymphocytes

201
Q

Describe convalescent stage of bordetella pettussis

A

Cought less frequent over a month and patient no longer cotnageous

202
Q

What culture medium is used for bordetella pertussis?

A

Bordet gengou medium

203
Q

Treatment for bordetella pertussis

A

Erythromycin

204
Q

Considerations for bordetella pertussis prophylaxis

A

Erythromycin for household members

205
Q

When should the pertussis vax be given?

A

-2, 4, 6, 15-18 months, 4-6 years
-booster for adults

206
Q

Basic description legionella pneumophilla

A

Aerobic
Gram negative rod
Found in water
Facultative intracellular parasite

207
Q

Transmission of legionella

A

Inhalation

208
Q

Examples facultative intracellular parasites

A

Legionella pneumophilla
Mycobacterium tuberculosis

209
Q

Two ways that legionella pneumophilla protects itself

A

1) biofilm
2) parasite of free living amoebas, and gets encysted in tough conditions

210
Q

What are the two major illnesses that legionella pneumophilla can cause?

A

1) Pontiac fever
2) legionnaire’s disease

211
Q

Describe Pontiac fever

A

-Similar to flu
Headache, muscle aches, fatigue, fever, chills
- resolves quickly (less than 1 week)

212
Q

Describe legionnaire disease

A

Very high fever + severe pneumonia

213
Q

Common cause of community acquired pneumonia (estimated 2%)

A

Legionella pneumophilla

214
Q

Treatment legionella pneumophilla

A

Need to concentrate on macrophages
- macrolides
- tetracyclines
- quinolines

215
Q

These antibiotics do NOT concentrate inside macrophages well

A

Aminoglycosides
Beta-lactams

216
Q

These antibiotics concentrate well in macrophages

A

Macrolides
Quinolines
Tetracyclines

217
Q

Examples of macrolides

A

Erythromycin
Azithromycin
Clarithromycin

218
Q

Example of tatracyclines

A

Doxycycline

219
Q

Examples of quinolones

A

Ciprofloxacin
Leviflaxacin
Moxifloxacin

220
Q

What organisms cause atypical pneumonia?

A

Mycoplasma
Legionella
Chlamydia

221
Q

What antibiotics work for atypical pneumonia?

A

Macrolides, tetracyclines, quinolones

222
Q

Basic description yersinia

A

Gram negative rod
Poles of rod stain darker
Zoonotic
Virulent and can penetrate and tissue
Facultative intracellular organism that can survive in macrophages

223
Q

Basic description brucella

A

Gram negative rod
Zoonotic
Virulent and can penetrate and tissue
Facultative intracellular organism that can survive in macrophages

224
Q

Basic description pasteurella

A

Gram negative rod
Zoonotic

225
Q

Treatment for yersinia

A

Aminoglycosides and
Doxycycline for prolonged period

226
Q

Treatment for brucella

A

Aminoglycosides and
Doxycycline for prolonged period

227
Q

Virulence factors for yersinia pestis

A

1) Fraction 1 (capsule antigen with antiphagocytic properties
2) V and W antigens (unknown but unique to yersinia pestis)

228
Q

Pathogenesis of yersinia pestis

A

Flea bites, invade skin, reproduce intracellularly in macrophages, move to lymph nodes, extremely swollen lymph nodes, fever, headache, bloodstream infection, other organ invasion and failure, hemorrhaged under skin (black skin)

229
Q

Two types of yersinia pestis (diseases)

A

Bubonic plague - fleas, skin and lymph nodes, systemic

Pneumonic plague- person to person transmission by aerosolized bacteria, pneuminia

230
Q

High risk groups yersinia pestis

A

Camping, hiking, hunting southwest

231
Q

Mortality rate of yersinia pestis if untrested

232
Q

What spreads tuleremia?

A

Rabbits, ticks, deerflies but many animals (even cold blooded) carry tuleremia

233
Q

Where is tuleremia found?

A

All over the U.S.

234
Q

Diseases caused by francisella tularensis

A

Ulceroglandular tularemia
Pneumonic tularemia

235
Q

Describe clinical pathology of ulceroglandular tularemia

A

Bitten by tick or deerfly or contact with wild rabbit, demarcated hole in skin with black base, fever + systemic symptoms, local lymph nodes swollen, red, painful, bacteria spreads to blood and other organs

236
Q

Mortality rate ulceroglandular tularemia

237
Q

What disease does ulceroglandular tularemia resemble? How does it differ?

A

Bubonic plague. No skin ulcer in plague and mortality rate much lower

238
Q

Describe pneumonic tularemia

A

Starts at ulceroglandular and spreads to lungs

239
Q

How do people get pneumonic tuleremia?

A

1) ulceroglandular tularemia spreads to lungs
2) aerosolized bacteria during skinning / tanning

240
Q

Describe the infective dose for tularemia

A

Very low, only need 10 bacteria to cause disease

241
Q

What body systems can tularemia invade?

A

Skin
Lungs
Eyes
GI tract

242
Q

How to dx

A

No culture - dangerous.
Ppd ski test, clinical symptoms, antibodies

243
Q

How to dx

A

No culture - dangerous.
Ppd ski test, clinical symptoms, antibodies

244
Q

What animals can brucella infect?

A

Goats, cows, pigs, dogs

245
Q

How brucella is transmitted

A

Direct contact infected meat or placenta, ingestion of infected mil (pasteurization kills)

246
Q

Who is at risk for brucellosis?

A

-Meat packing industry (beef)
- Vet
- Farmer
- Traveler who drinks cow or goat milk in Mexico

247
Q

What organ systems does brucellosis effect?

A

Skin
Lungs
GI
Eyes

248
Q

Clinical pathologenesis of brucellosis

A

Starts with skin (but no ulcers), gi, eyes, or lungs. Spreads to macrophages and reproduces. Spreads systemically. Chronic but not fatal

249
Q

Symptoms of brucellosis

A

Fever (night)
Chills
Sweats
Loss of appetite
Backache
Headache
Lymphadenopathy

250
Q

Dx of brucellosis

A

Culture or serology
PPD test does not indicate active brucellosis, just shows exposure

251
Q

Basic description francella

A

Gram negative rod
Zoonotic
Virulent and can penetrate and tissue
Facultative intracellular organism that can survive in macrophages

252
Q

Organism that colonized the mouths of cats

A

Pasteurella multocida

253
Q

Bacteria that most commonly causes wound infections following a cat or dog bite

A

Pasteurella multocida

254
Q

Treatment for pasteurella multocida

A

Don’t close wound with sutures, treat with doxy or penicillin

255
Q

What makes Chlamydia and rickettsia different from other bacteria?

A

They cannot make their own energy and are obligated intracellular parasites

256
Q

Basic description of chlamydia

A

Gram negative
No peptidoglycan layer
No muramic acid (like other gram negative)

257
Q

Important chlamydia species

A

Chlamydia trachomatis
Chlamydophila psittaci
Chlamydophila pneumonia

258
Q

How to treat chlamydia

A

Doxycycline
Macrolides
Fluoroquinolones

259
Q

Lifecycle chlamydia

A

Elementary bodies enters cells that line mucous membranes, prevent phagocytosis, turn into initial body and reproduce

260
Q

What organs does chlamydia trachomatis impact?

A

Eyes and genitals

261
Q

Chronic conjunctivitis from chlamydia

262
Q

How trachoma spreads

A

Children reservoir, spread by hand to hand transmission of infected eye secretions or sharing contaminated clothing or towels

263
Q

Leading cause of preventable blindness in the world, disease of poverty

A

Chlamydia trachomatis

264
Q

Clinical pathogenesis of trachoma

A

Folds eyelid inward, inflammation, infection, and scarring of conjunctiva and cornea. Blindness in 10-15 years

265
Q

Treatment for trachoma

A

Oral azithromycin

266
Q

Conjunctival inflammation in 5-14 days of birth to mother with chlamydia trachomatis

A

Inclusion conjunctivitis

267
Q

Type of eye drops given at birth to prevent inclusion conjunctivitis

A

Erythromycin eye drops

268
Q

Diseases caused by chlamydia trachomatis

A

-Trachoma
-Inclusion conjunctivitis
-Infant pneumonia
-Urethritis
-Cervicitis and pelvic inflammatory disease
-Epididymitis
- reiters syndrome
- fitz-hough Curtis syndrome
- lymphogranuloma venereum

269
Q

STIs that typically cause urethritis

A

Neisseria Gonorrhea
Chlamydia trachomatis
Ureaplasma urealyticum

270
Q

Test for chlamydia

A

PCR preferred (cannot be cultures on non living media)

271
Q

How PID/ Cervicitis/ urethritis are treated

A

Likely gonorrhea or chlamydia or confection, so empiric therapy with shot of ceftriaxone followed by oral course doxy

272
Q

Inflammatory arthritis of large joints in men between ages 20-40

A

Reiters syndrome (associated with chlamydia)

273
Q

Infection of liver capsule. What organisms is the illness associated with?

A

Fitz high Curtis syndrome, chlamydia and gonorrhea

274
Q

How is chlamydia psittaci transmitted?

A

Inhaling chlamydia in dust from bird feathers or dried feces

275
Q

What disease does chlamydia psittaci caus

A

Psittacosis

276
Q

Who is at highest risk for psittacosis

A

Bird breeders vets, pet shop employees, poultry slaughterhouses

277
Q

Incubation period of psittacosis

278
Q

What is the clinical manifestation of psittacosis?

A

Atypical pneumonia

279
Q

What species of Chlamydia is spread person to person via the respiratory route

A

Chlamydia pneumoniae - TWAR (Tawain acute respiratory disease).

280
Q

Basic description rickettsia

A

Small
Gram negative
Non-motile
Rod to coccoid shape
Obligate intracellular parasite

281
Q

Tests for rickettsial infections

A
  • Weil-Felix agglutination (low specificity and sensitivity, uses proteus bacteria)
  • standard: Four fold titer increase via IFA, ELISA, complement fixation (CF)
282
Q

Antigens on rickettsia

A

OX-2, OX-9, OX-k

283
Q

What vectors spread rocky mountain spotted fever

A

Wood tick - dermacentor andersoni
Dog tick- dermacentor variabilis

284
Q

Causative agent of rocky mountain spotted fever

A

Rickettsia ricketsii

285
Q

Clinical symptoms rocky mountain spotted fever

A

Fever, conjunctival redness, severe headache, rash that spreads from wrists, ankles, soles, and palms to trunk

286
Q

Where is rocky mountain spotted fever most common

A

Southeast U.S.

287
Q

Time needed for tick to feed to transmit rocky mountain spotted fever

A

6-10 hours

288
Q

Preferred cells rickettsia rickettsii

A

Endothelial lining small blood vessels

289
Q

What is the causative agent for rickettsialpox?

A

Rickettsia akari

290
Q

Vector for ricketssialpox

A

Mites in house mice

291
Q

Clinical symptoms rickettsial pox

A

Mild, self-limited, papule at site of mite bite which later turns into blister, then later fever and headache and other vesicles appear on body

292
Q

Antibiotic for ricketsiallpox

293
Q

What is the causative organism for epidemic typhus?

A

Rickettsia prowazekii

294
Q

What causative agent is responsible for endemic types?

A

Rickettsial typhi

295
Q

What vector is responsible for epidemic typhus (rickettsia prowazekii)? Reservoir in U.S?

A

Lice
Reservoir- flying squirrel in Southern US

296
Q

Clinical symptoms epidemic typhus

A

Abrupt onset fever, headache, small pink macules on 5th day around upper trunk and spreads to body

297
Q

Incubation period epidemic typhus

298
Q

Treatment for epidemic typhis

A

Doxy and improved sanitation

299
Q

What is brill zinser disease

A

If not fully treated, epidemic typhus (ricketssia prowazekii) can become a latent infection, and when it becomes active less severe version of epidemic typhus

300
Q

What vector carries endemic typhus? Reservoir?

A

Flea, rodents

301
Q

Clinical symptoms endemic typhus and incubation period

A

10 days, headache, fever, maculopapular rash

302
Q

How to treat rickettsia typhi

A

Doxy, kill fleas and rats

303
Q

Diseases caused by rickettsia

A

Rocket mountain spotted fever
Rickettsialpox
Epidemic typhus
Endemic typhus
Scrub typhus
Trench fever (Bartonella)
Cat scratch fever (Bartonella)
Q fever
Ehrlichiosis

304
Q

What agent causes q fever

A

Rickettsia coxiella burnetii

305
Q

What organism causes q fever

A

Rickettsia coxiella burnetti

306
Q

What organism causes q fever

A

Rickettsia coxiella burnetti

307
Q

What is unique about coxiella burnetii compared to other rickettsia and gram negative bacteria?

A

Can form an endospore

-differs from rickettsia because passed to humans via inhaltion

308
Q

How is q fever transmitted?

A

Spores aerosolized from cow hiders or placentas and transmitted via inhalation

309
Q

Incubation and Clinical symptoms Q fever

A

Incubation 2-3 weeks, fever, soaking sweats, pneumonia

Only rickettsial disease that causes pneumonia and no rash

310
Q

Basic description spirochetes

A

Gram negative
Corkscrew shape
Second outer membrane
Periplasmic flagella

311
Q

3 genera of spirochetes

A
  1. Treponema
  2. borrelia
  3. Leptospira
312
Q

Agent responsible for syphilis

A

Treponema pallidum

313
Q

How can syphilis be spread between doctor and patient?

A

Skin contact with an ulcer

314
Q

What two organisms cause some acute meningitis with a predominance of lymphocytes?

A

Treponema pallidum
Mycobacterium tuberculosis

315
Q

Rule of 6s for syphilis

A

6 axial filaments
6 week incubation (3-6)
6 weeks for ulcer to heal
6 weeks after the ulcer heals secondary syphilis develops
6 weeks for secondary syphilis to resolve
66% of latent stage patients have resolution
6 years to develop tertiary syphilis

316
Q

Stages of syphilis

A

Primary syphilis
Secondary syphilis
Latent
Tertiary syphilis

317
Q

What are the manifestations of tertiary syphilis?

A

Gummas of the skin and bone
Cardiovascular syphilis
Neurosyphilis

318
Q

Pregnant mom is infected with syphilis
….

A

Passed through placental barrier, if untreated, high mortality rate. If baby lives will get early or late onset congenital syphilis

319
Q

Age for early congenital syphilis, symptoms

A

Under 2 years, rash, snuffles, lymph, liver and spleen enlargement,

320
Q

Complications late congenital syphilis

A
  • Neurosyphilis (deafness common)
  • Bone and teeth impacts (saddle nose, saber shins, Hutchinson’s teeth, mulberry molars)
  • eye disease
321
Q

How to prevent congenital syphilis

A

Test and treat mom before 4th month pregnancy

322
Q

Testing for syphillis

A

1) active - direct examination microscopy
2) not active - RPR (false positives so need to follow up with confirmatory test like FTA-ABS)
3) PCR

323
Q

Treatment for syphilis

A

Pennicillin

324
Q

What is jarisch-herxheimer phenomen

A

Patients that undergo treatment for spirochetes feel worse before they feel better

325
Q

What is unique about treponema

A

Does not release toxin, symptoms solely from body’s immune response

326
Q

What diseases do borrelia cause?

A

Lyme disease and relapsing fever

327
Q

Basic description of borrelia

A

Gram negative
Spirochete

328
Q

What tick spreads Lyme disease? How long does it need to be attached?

A

Ixodes
24 hours

329
Q

Regions with Lyme disease

A

Northeast, Midwest, northwest

330
Q

Reservoirs for Lyme disease

A

White footed mouse and whit tail deer

331
Q

What are the stages of Lyme disease?

A

1) early localized stage
2) early disseminated stage
3) late stage

332
Q

Incubation period Lyme diseases

333
Q

Describe early localized stage Lyme disease

A

Lasts 4 weeks, skin lesion at site of bite, erythema migrans, flu like illness, regional lymphadenopathy

334
Q

Describe the early disseminated phase of Lyme disease

A

Borrelia burgeorferi disseminates to the skin (lesions), nervous system (meningitis, bells palsy), heart (heart block), and joints (migratory arthritis)

335
Q

Describe latent Lyme disease

A

10% untreated patients develop chronic arthritis

Can develop neurological symptoms like memory impairment, irritability, etc.

336
Q

Describe relapsing fever

A

Caused by 18 species of borella
Gram negative
Spirochete
Used antigenic variation to evade immune system
Causes a relapsing fever, need to culture while febrile

337
Q

Basic description leotospira

A
  • Gram negative
  • Aerobic
  • Spirochetes wound in tight coil
  • Lives in urine if dogs, rats livestock, wild animals
338
Q

What species of leptospira causes dksease

A

Leptospira interrogans

339
Q

Transmission of letospirisis

A

Swimming through urine contaminated waters or direct contact with urine

340
Q

First phase of leptospira

A

Letpspiremic phase
Bacteria invade blood and CSF
Abrupt onset high fever
Headache
Malaise
Severe muscle aches
Red conjunctiva
Photophobia
Lasts 1 week

341
Q

What is the second phase of letospirisis?

A

Immune phase
IgM antibodies appear
Meningismus
Elevated WBC in CSF

342
Q

What is weils disease

A

Infectious jaundice cause by leptospira
Renal failure
Hepatitis
Hemorrhage

343
Q

Dx and treatment of leptosporisis

A

PCR most immediate, or culture when febrile.

Treat with doxy or penicillin

Clinical Micro (12 decks)

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