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Infectious Disease > Gram Negative Bacteria of Medical Significance > Flashcards

Gram Negative Bacteria of Medical Significance Flashcards

1
Q

Whats the difference in the cell wall of gram pos and neg bacteria?
2

A

Thin peptidoglycan layer of the cell wall (Gram + have a much thicker peptidoglycan layer) is sandwiched between an inner cytoplasmic cell membrane and the bacterial outer wall membrane

Do not form spores

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2
Q

All have a lipopolysaccharide outer membrane of cell wall. What does this often act as?

A

endotoxin

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3
Q

Medically relevant gram negative cocci include three species responsible for:

A

Gonorrhea
Meningitis
Pneumonia

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4
Q

Medically relevant gram negative bacilli include a multitude of species responsible for:
3

A

Respiratory illness
Urinary infections
GI problems
….and many other ailments

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5
Q

If gram neg bacteria enter the blood stream, the LPS can cause a toxic reaction which results in what?
3

What could this lead to?

A

fever, increased respiratory rate, low blood pressure

endotoxic sepsis and shock

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6
Q

The presence of LPS also triggers what?

A
  1. an innate immune response and

2. production of cytokines, which in turn, leads to inflammation, which can also produce host toxicity

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7
Q

Gram Negative Cocci

2 genera?

A

Neisseria

Moraxella catarrhalis

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8
Q

Where does M. cat reside (1)and what can it cause?2

A

resides in respiratory tract

-causes tracheobronchitis and pneumonia

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9
Q

Describe Neisseria species?
movement?
grouping?
oxygen?

A

Non-motile, Gram negative
Usually diplococci
Aerobic

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10
Q

Neisseria meningitidis causes?2

Neisseria gonorrhea causes?

A

Neisseria meningitidis - Meningitis/septiceimia

Neisseria gonorrheae - Gonorrhea

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11
Q

Gonorrhea causes what in women and what in men?

1 in each and 2 shared

A

Infection of cervix
Infection of urethra (men, inflammatory response => purulent discharge)

Pain and fever

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12
Q

Gonorrhea infections in men can extend to what?

In women can extend to what?

A

Male infection may extend to prostate and epididymis, causing sterility

Can extend to fallopian tubes and create scar tissue and ectopic pregnancy

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13
Q

Gonnorrhea can Progresses to systemic disease:
3

Neonatuem

A

arthritis, endocarditis, meningitis

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14
Q

Only natural reservoir for Neisseria meningitidis?

How is it transferred?

A

human nasopharyngeal mucosa

direct contact or droplet

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15
Q

Describe the Subclinical/minimal disease of Neisseria meningitidis?

A

transient meningococcemia, short febrile flu-like episode, cleared spontaneously

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16
Q

Describe Fulminant meningeal sepsis (FMS)?

Will the blood culture be pos?

Symtpoms?
9

A

massive and rapid proliferation in bloodstream
blood culture positive, usually also involves meninges
rapid clinical deterioration

Fever, 
severe headache, 
vomiting, 
neck/back pain, 
stiffness, 
petechial rash, 
altered mental status, 
shock, 
organ failure
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17
Q

Describe the symtpms of meningitis?

7

A 
Fever, 
headache, 
vomiting, 
neck/back pain, 
irritability, 
skin rash, 
AMS
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18
Q

What does bacteria invade in menigitis?

What products cause much of the damage in menigitis?

A

bacterial invasion of meninges, rapid proliferation in CSF

Endotoxins and PMN products/inflammatory mediators

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19
Q

FMS/Meningitis shock is when what happens?

4

A

endotoxin

causes capillary leakage, poor vascular tone, intravascular microthrombi, myocardial dysfunction

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20
Q

FMS/Meningitis caused DIC can lead to what? 2

What two things are released that causes this?

A

endothelial damage => hemorrhages, microthrombi

Endotoxin AND cytokines

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21
Q

Early diagnosis of FMS or meningitis is difficult, but crucial
What are the later stages of FMS?

What are the later stages of menigitis?

A

skin lesions appear after 6 - 12 h, easier to recognize disease

Meningitis: skin lesions 12 - 18 h after onset, no lesions in 20% of patients

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22
Q

Bacteriologic diagnosis of
FMS?

Bacteriologic diagnosis of menigitis?

A

FMS: Gram stain of skin lesion biopsy specimen

Meningitis: only CSF positive

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23
Q

Most important therapeutic principles of meningitis?

2

A
  1. therapy should never be delayed by diagnostic procedures

2. antibiotics are the most important part of treatment

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24
Q

What is the first line treatment for menigitis?3

How would we treat pts in contanct with menigitis prophylactically?

A

Cefotaxime or ceftriaxone plus vancomycin

Patients in contact……………prophylactic ABX Rocephin (cefatriaxone)

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25
Q

Mortality with treatment for meningitis?

without treatment?

A
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26
Q

Neurological sequelae in 8 - 20% of survivors: What are these?
3

A

deafness,

mental retardation, concentration disturbances

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27
Q

Moraxella catarrhalis
is a gram negative cocci that causes infections of what?
5

A
  1. Upper and lower respiratory
  2. Middle ear
  3. Eye
  4. CNS
  5. Joints
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28
Q

Moraxella catarrhalis infections of the upper and lower respiratory tract are particularly important in what populations?2

A

particularly important cause of bronchopulmonary infection in elderly,
patients with chronic lung disease

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29
Q

Moraxella catarrhalis is resistant to what?

3

A

Resistant to PCNs, SMX/TMP, tetracyclines

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30
Q

What should we treat M. Cat with?

4

A

Treated with fluoroquinolones,
most 2nd and 3rd ceph, macrolides and
Augmentin

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31
Q

Name the Aerobic Gram-Negative Nonenteric Bacilli?

7

A
  1. Pseudomonas and
  2. Burkholderia – an opportunistic pathogen
  3. Brucella and
  4. Francisella – zoonotic pathogens
  5. Bordetella and
  6. Legionella – mainly human pathogens
  7. Alcaligenes – opportunistic pathogen
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32
Q

What are Small Gram-negative rods with a single polar flagellum?

A

pseudomonas

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33
Q

pseudomonas bacteria are freeliving. Where can they be found?
4

A

primarily in soil,
sea water, and
fresh water;
also colonize plants and animals

Important decomposers and bioremediators in nature

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34
Q

Where is pseudomonas a frequent contaminant in?

2

A

homes and clinical settings

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35
Q

What does pseudomonas produce?

3

A

Produce oxidase and catalase

water soluable pigments

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36
Q

Pseudomonas aeruginosa

is a common inhabitant of what?

A

soil and water?

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37
Q

pseudomonas is an intestinal resident in what percent of poeple?

What is it resistant to?6

A

10%

Resistant to soaps, dyes, quaternary ammonium disinfectants, drugs, drying

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38
Q

Pseudomonas is a Frequent contaminant of what in hospitals?

3

A

ventilators,
IV solutions,
anesthesia equipment

Opportunistic pathogen

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39
Q

Common cause of nosocomial infections in hosts with?3

A

burns,
neoplastic disease,
cystic fibrosis

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40
Q

Complications caused by pseudomonas cause?

8

A 
pneumonia, 
UTI, 
abscesses, 
otitis, and 
corneal disease
Endocarditis, 
meningitis, bronchopneumonia
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41
Q

What kind of odor and pigment does pseudomonas have?

A

Grapelike odor

Greenish-blue pigment (pyocyanin)

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42
Q

What do we treat pseudomonas with?

6

A

Treated with

  1. cephalosporins,
  2. aminoglycosides,
  3. carbenicillin,
  4. polymixin,
  5. quinolones (for ear infections), and
  6. monobactams
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43
Q

Brucella and Brucellosis
are shaped how?

What are its two species?

Brucellosis is spread how?

How does it present?

How do we treat it?3

A

Tiny Gram-negative coccobacilli

Brucella abortus (cattle)
Brucella suis (pigs)

a zoonosis transmitted to humans from infected animals

Fluctuating pattern of fever……weeks to a year
UNDULANT FEVER

Treated with combination of tetracycline and rifampin or streptomycin

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44
Q

The bacteria can spread to humans with contact with what?

3

A
  1. infected meat or
  2. the placenta of infected animals, or from
  3. unpasteurized milk or cheese.
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45
Q

Brucellosis in humans is usually associated with the consumption of what?

Clinically manifests how?

A

unpasteurized mildk and soft cheeses made from the milk of infected animals.

Can be insidious and may present in many atypical forms
UNDULANT FEVER
but may persist and progress to a chronically incapacitating disease with severe complications.

46
Q

Francisella tularensis and Tularemia is shaped how?

How is it transmitted?3

Clinical manifestations?

10% death rate in which forms? 2

Treatment?3

A

facultative intracellular coccobacillus

a zoonotic disease. Transmitted by contact with infected animals, water and dust or bites by vectors

Headache, backache, fever, chills, malaise and weakness

in systemic and pulmonic forms

Tx: gentamicin or tetracycline
Attenuated vaccine

47
Q

Bordetella pertussis
shape?

What does it cause?

Who is it most dangerous in?

Transmission?2

A

Minute, encapsulated coccobacillus

Causes pertussis or whooping cough, a communicable childhood affliction
Acute respiratory syndrome

Often severe, life-threatening complications in babies
Reservoir – apparently healthy carriers

Transmission by direct contact or inhalation of aerosols

48
Q

Bordetella pertussis
virulence factors?
2

A
  1. receptors that recognize and bind to ciliated respiratory epithelial cells
  2. toxins that destroy and dislodge ciliated cells
49
Q

What is the pathology of Bordetella pertussis?

Treatment?

A

Loss of ciliary mechanism leads to buildup of mucus and blockage of the airways.

Treatment- macrolides….Azithromycin

50
Q

Legionella pneumophila and Legionellosis is widely distributed where?

Tranmitted?

They live in close association with what?

Other names for Legionella pneumophila and Legionellosis? 2

Who is it most prevavalent in?

Its a nosocomial disease in who?

A

water

Organisms inhaled in aerosolized mist

Live in close association with amoebas

Legionnaires disease and Pontiac fever

Most prevalent in males over 50

Nosocomial disease in elderly patients

51
Q

Clinical manifestations of Legionella pneumophila and Legionellosis?
5

Fatality Rate?

What should we treat with?

A 
Fever, 
cough, 
diarrhea, 
abdominal pain, 
pneumonia

fatality rate of 3-30%

Treat with azithromycin

52
Q

What is The Most Prevalent Enteric Bacillus?

Most common aerobic and non-fastidious bacterium in gut?

A

Escherichia coli

Its needs are few

53
Q

Some E. Coli have developed virulence through ?

2

A

plasmid transfer, others are opportunists.

54
Q

Enterotoxigenic E. coli causes what?

Due to what?

What is a characteristic of the structure of this E. Coli?

A

severe diarrhea

due to heat-labile toxin and heat-stable toxin – stimulate secretion and fluid loss;

also has fimbriae (attachment pili)

55
Q

Enteroinvasive E. coli causes what?

A

inflammatory disease of the large intestine.

56
Q

Enteropathogenic E. coli linked to what?

A

wasting form infantile diarrhea

57
Q

Enterohemorrhagic E. coli, O157:H7 strain, causes ?

2

A

hemorrhagic syndrome and kidney damage

58
Q

Greatest cause of mortality among babies?

A

Pathogenic strains frequent agents of infantile diarrhea

59
Q

Causes ~70% of what?

Causes 50-80% of what?

A

traveler’s diarrhea

UTI

60
Q

What is Coliform count?

A

indicator of fecal contamination in water

61
Q

Most strains of E. Coli will respond to what?

3

A

SMX/TMP, nitrofurantoin, fluoquinolones

62
Q

Klebsiella pneumoniae is a normal inhabitant of where?

What should we know about its structure?

What does it cause?5

A

normal inhabitant of respiratory tract,

has large capsule,

cause of 
nosocomial pneumonia, meningitis, 
bacteremia, 
wound infections and 
UTIs
63
Q

Enterobacter sp. infects what?2

A

UTIs, surgical wounds

64
Q

Serratia marcescens produces what?

Causes what5

A

produces a red pigment;

causes 
pneumonia, 
burn and wound infections, septicemia and 
meningitis
UTIs
65
Q

Citrobacter sp. cause what?

2

A

opportunistic

UTIs and bacteremia

66
Q

Yersenia Pestis (Plague) is spread by what?

What areas are hardest hit right now?

A

fleas through rodents

Eastern African nations are hardest hit.

67
Q

Yersinia pestis and Plague
enteric or nonenteric?

Shape?

Virulence factors?3

A

nonenteric

Tiny, Gram-negative rod, unusual bipolar staining and capsules

  1. capsular and envelope proteins protect
    against phagocytosis and foster intracellular growth
  2. coagulase,
  3. endotoxin, murine toxin
68
Q

Describe the pathology of Yersinia pestis?

Where does it replicate?
What does this cause and what does it block?

A

bacteria replicates in gut, coagulase causes blood clotting that blocks the esophagus;

flea becomes ravenous

69
Q

Where does the plague enter after the flea bite?

What does this cause and what is it called?

A

lymph, causes necrosis and swelling called a bubo in groin or axilla

70
Q

How does the plague become systemic?

2

A
  1. Septicemic – progression to massive bacterial growth; virulence factors cause intravascular coagulation subcutaneous hemorrhage and purpura – black plague
  2. Pneumonic – infection localized to lungs, highly contagious;

fatal without treatment

71
Q

Diagnosis of plague depends on what?
3

Treatment?
4

How do we prevent it?2

A

history, symptoms, and lab findings from aspiration of buboes.

streptomycin, tetracycline or chloramphenicol
vaccine avilable

Prevention by quarantine and control of rodent population in human habitats

72
Q

Yersinia enterocolitica is found where?

How does this infect the host?

How do they avoid the host defenses?

Clinical manifestation can resemble?

A

domestic and wild animals, fish, fruits, vegetables, and water

bacteria enter small intestinal mucosa, some enter lymphatics and

survive in phagocytes;

inflammation of ileum can mimic appendicitis

73
Q

Y. pseudotuberculosis clinically manifests how?

2

A

localized tissue necrosis and granulomas in the spleen, liver and lymph nodes

TB symtpoms

74
Q

Y. enterocolitica causes what?

A

more lymph node inflammation

75
Q

Pasteruella multocida
(Avian Cholera) found in what?

What kind of infection is it in humans?

How is it transmitted and where does it spread (3)?

Who is at greatest risk

How do we treat?

A

normal flora in animals
-Follows bird migration

Opportunistic infections in humans
Animal bites or scratches cause local abscess that can spread to joints, bones, and lymph nodes.
Immunocompromised are at risk for septicemia and complications.
Treatment: penicillin and tetracycline

76
Q

Haemophilus
shape?

What kind of agar does it grow on?

A

tiny Gram-negative pleomorphic rods

Chocolate agar

77
Q

H. influenzae causes what?
6

What has really helped with this infection?

A 
acute bacterial meningitis, epiglottitis, 
otitis media, 
sinusitis, 
pneumonia, and 
bronchitis

subunit vaccine Hib

78
Q

H. aegyptius causes?

A

–conjunctivitis, pink eye

79
Q

H. ducreyi causes?

A

STD

80
Q

H. parainfluenzae and H. aphrophilus are find where normally (2) and what does it cause when it becomes pathogenic?

A

normal oral and nasopharyngeal flora;

infective endocarditis

81
Q

What do you treat H. Flu with?

5

A

Treated with
amoxicillin,
azithromycin,
cephalosporins, fluoroquinolones and clarithromycin

82
Q

Most pathogenic anaerobes are usually commensals and originate where?

Predisposing Conditions?4

A

Originate from our own flora

1. Breeches in the mucocutaneous barrier 
→ displace normal flora
2. Compromised vascular supply	
3. Trauma with tissue destruction	
4. Antecedent infection
83
Q

Clues to Anaerobic Infection

6

A
  1. Infections in continuity to mucosal surfaces
  2. Infections with tissue necrosis and abscess formation
  3. Putrid odor
  4. Gas in tissues
  5. Polymicrobial flora
  6. Failure to grow in the lab
84
Q

Classification of bacteria based on previous experiments allowing fast identification is called what?

What other tool is used in diagnosis of anaerobes?

A

API SYSTEM

GAS CHROMATOGRAPHY

85
Q

Bacteroides fragilis
is most noted when?

Does it form spores?

A

Major disease causing strict anaerobic after abdominal surgery

no

86
Q

Describe how Bacteroides fragilis evades body defenses?

3

A

Prominent capsule

  • anti-phagocytic
  • abscess formation
87
Q

Bacteroides fragilis has an endotoxin affect but low toxicity. Why?

A

structure different than other lipolysaccharide

88
Q

A leading cause of bacterial diarrheal illness?

How is it transmitted?

What is this bacteria associated with? 3

What should we treat with (what is it becoming resistant with)?

A

Campylobacter jejuni

oral/fecal route, ingestion of contaminated food and water, uncooked meat

Associated with feed lots, chicken houses, raw milk

Treated with azithromycin, increasing resistance to fluoroquinolones

89
Q

What is Borrellia burgdorferi?

Early symtpoms include?4

(whats the buzz word?)

A

Lyme disease

fever, headache, and fatigue, bull’s eye rash

90
Q

If lyme disease is left untreated later symptoms may involve what?
3

Usually treated by what well?

A

the joints, heart and central nervous system.

DOXY or Amox (2-4 weeks)

91
Q

How do we diagnose Lyme?

3

A

Unique bull’s eye rash
Elisa
Western Blot

92
Q

What should we treat Chlamydia trachomatis with?

3 options

What is a complication that could arise?

A

Treat both partners with azithromycin,
doxycycline or
ofloxocin

blindness

93
Q

What is Lymphogranuloma venereum(LGV)?

What system does it affect?

A

Uncommon sexually transmitted infection caused by three invasive serovars of Chlamydia trachomatis

Chronic long term infection of the lymphatic system

94
Q

Symptoms of Lymphogranuloma venereum(LGV)?

6

A
  1. Swollen inguinal nodes
  2. Drainage through the skin from buboes or abscesses in inguinal nodes
  3. Painful bowel movements (tenesmus)
  4. Small painless sore on the genitals
  5. Swelling of the labia
  6. Blood or pus from the rectum
95
Q

HOw do we Lymphogranuloma venereum(LGV)?

How do we treat?
3 options

A

Diagnosis usually made serologically and by exclusion of other causes of inguinal adenopathy or genital ulcers

doxycycline, erythromycin, azithromycin

Buboes may require incision and drainage

96
Q

Lymphogranuloma venereum(LGV) prognosis is more favorable with?

Untreated chronic condition may cause?

A

Prognosis more favorable with early treatment

Untreated chronic condition may cause fistulas of the penis, urethra, vagina, uterus, rectum

97
Q

Psittacosis is transmitted how?

Symptoms in humans range from what?2

A

zoonotic disease caused by Chlamydia pssitaci, contracted from parrots, pigeons, ducks, chickens, gulls

range from unapparent to systemic illness with severe pneumonia

98
Q

Psittacosis may mimic what?

What are the symptoms?
7

As it progresses what does it mimic?

A 
May mimic typhoid in early stages: 
high fever, 
arthralgias, 
diarrhea, 
conjunctivitis, 
epistaxis and 
neutropenia, 
splenomegaly

pneumonia as it progresses: dyspnea, high fever, cough, patchy infiltrates or whiteout on CXR

99
Q

Psittacosis diagnosis. What is key??
3

Treatment?

A
  1. Diagnosis: exposure history is paramount!
  2. Microbiological cultures from respiratory secretions or
  3. serology from blood cultures

Doxycycline and chloramphenicol

100
Q

What are the two types of Relapsing Fever?

What bacteria is it caused by?

Where is each one found most and which one is more severe?

What are the symtpoms?

A

Two types: tick borne (TBRF) and louse borne (LBRF)

Caused by Borellia spirochetes

TBRF occurs in western US, linked to sleeping in rustic, rodent infested cabins in mountainous areas
LBRF is transmitted by the human body louse and is generally restricted to refugee settings in third world. Occurs in epidemics, more severe than TBRF

Flu-like symptoms: sudden fever, chills, headaches, arthralgias, nausea. May develop a rash

101
Q

HOw do we diagnose and treat relapsing fever?

2

1

One big thing to remember

A

Diagnosis on blood smear…spirochetes
Treatment: doxycycline.

May cause Jarisch-Herxheimer reaction in over half of those treated

102
Q

Describe the strcuture of Salmonella sp.?

A

Motile, flagellated gram-neg

103
Q

What can Salmonella sp. cause? 2

Whats the most common form?

Whats the main reservoir and how can it spread?

A

Common Salmonella gastroenteritis (diarrhea, abdominal cramps, fever) to enteric fevers (including typhoid fever) which can be life threatening

Most common form AKA “food poisoning” presents with uncomplicated gastroenteritis, usually self-limited disease

animals are main reservoir, usually food borne illness, can spread from person to person

104
Q

Enteric Typhoid Fever-severe systemic disease, any species of salmonella may cause, S. typhi most studied.
What are the symtpoms? 6

How do we diagnose?3

How should we treat?3

A

N/V/D
septicemia
Fever, anorexia, headache, myalgias

Dx: stool and/or blood cultures, serology for antibodies

Often fatal if not treated
Replace fluids by oral or IV
Pain control and treating nausea and vomiting
Antibiotics…..ciprofloxacin

105
Q

What is Shigella (clinical manifestations)?

What demographic is it commonly seen?

How is it transmitted?

Diagnosis?

Treatment?3

A

Intestinal disease
Bloody diarrhea, may have abdominal pain or cramps, fever

children 2-4

Passed through direct contact with stool

Dx: stool studies

Replace lost fluids, water or Pedialyte, may need IV fluids

Increasing resistance to abx…. ciprofloxocin or cefixime should be used if abx indicated

106
Q

Vibrio sp. has two distinct groups?

Most non-cholera vibrio infections are associated with what?

A

Cholera infections
Non-cholera

improperly cooked contaminated food or eating raw shellfish

107
Q

Non-cholera (vibro) wound infection or septicemia will need what for treatment?

A

doxycycline or a quinolone, aggressive fluid replacement, vasopressors for hypotension, fasciotomy, debridement of infected wound

108
Q

Vibrio cholerae
buzzword?

Treatment?

A

profuse watery diarrhea

doxycycline or a quinolone, aggressive fluid replacement

109
Q

Acinetobacter baumanni buzzword?

3 things

A

Commonly isolated from the hospital environment and hospitalized patients
Often cultured from sputum, respiratory secretions, wounds, urine….colonization vs infection

HOSPITAL ACQUIRED OFTEN

CULTURED FROM SECRETIONS

ICU

110
Q

Acinetobacter baumanni treatment?

A

Multi-drug resistance……including carbapenems

Infectious Disease (29 decks)

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