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Bacteria flashcards

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1
Q

readily stained organisms fall into four categories

A

1) Gram + cocci
2) Gram - cocci
3) Gram + rods
4) Gram - rods

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2
Q

Of the four readily stained organisms, which ones further subdivide?

A

Gram - rods

1) Organisms associated w/the enteric tract
2) Organisms associated w/the respiratory tract
3) Organisms from animal sources

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3
Q

Organisms associated with the enteric tract further subdivide into?

A

1) Pathogens both inside and outside the enteric tract
2) Pathogens inside the enteric tract
3) Pathogens outside the enteric tract

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4
Q

Campylobacter causes?

A

Enteric tract disease but frequently has an animal source

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5
Q

Organisms that are not readily gram stained fall into six major categories

A

1) Mycobacterium species (acid-fast rods)
2) Mycoplasma species (no cell wall)
3 & 4) Treponema & Leptospira species (spirocetes too thin to be seen)
5 & 6) Chlamydia and Rickettsia species (stain well w/Giema stain or other special stains but poorly with gram

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6
Q

Chlamydia and Rickettsia species are ________ __________ __________, whereas members of the other four genera are not

A

Obligate intracellular parasites

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7
Q

Anaerobes are characterized by their ability to grow in an?

A

Atmosphere containing less than 20% oxygen. i.e. they grow poorly if not at all in room air

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8
Q

Anaerobes are a heterogeneous group composed of a variety of bacteria, from those that?

A

Can barely grow in 20% oxygen to those that can grow in less than 0.02% oxygen

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9
Q

The obligate aerobes, such as Pseudomonas aeruginosa, grow best in?

A

The 20% of O2 of room air & not at all under anaerobic conditions

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10
Q

Facultative anaerobes such as Escherichia coli can grow well under?

A

Either circumstance (anaerobic and aerobic)

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11
Q

Aerotolerant organisms such as Clostridium histolyticum can grow to some extent in?

A

Air but mult. much more rapidly in lower O2 concentration.

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12
Q

Microaerophilic organisms such as Campylobacter jejuni require a?

A

Reduced oxygen concentration (approx. 5%) to grow optimally

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13
Q

The obligate anaerobes such as Bacteroides fragilis and Clostridium perfringens require an?

A

Almost total absence of O2.

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14
Q

Many anaerobes use ___ instead of ___ as their final electron acceptor

A

nitrogen instead of oxygen

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15
Q

The main reason why the growth of anaerobes is inhibited by oxygen is?

A

The reduced amount (or absence) of catalase and superoxide

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16
Q

In addition to O2 concentration, the oxidation-reduction potential (Eh) of a tissue is an important determinant of the growth of anaerobes. Areas with low Eh such as the peridontal pocket, dental plaque and colon do what?

A

Support the growth of anaerobes well. Crushing injuries that result in devitalized tissue caused by impaired blood supply produce a low Eh allowing anaerobes to grow & cause disease

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17
Q

Anaerobes of medical interest include

A

Both rods and cocci & both gram + and gram - organisms. The rods are divided into the spore formers, i.e. Clostridium, & the non spore formers, e.g. Bacteroides

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18
Q

Streptococcus is a genus of major pathogens consisting of?

A

Both anaerobic & facultative organisms

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19
Q

Many of the medically important anaerobes are part of the normal human flora. As such, they are nonpathogens in their normal habitat & cause disease when?

A

Only when they leave those sites. The two prominent exceptions are Clostridium botulinum and Clostridium tetani, the agents of botulism & tetanus, which are soil organisms

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20
Q

Diseases caused by members of the anaerobic normal flora are characterized by?

A

Abscesses, which are most frequently located in the brain, lungs, female genital tract, bilary tract, & other intra-abdominal sites. Most abscesses contain more than one organism, either multiple anaerobes or a mixture of anaerobes plus facultative anaerobes

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21
Q

Three important findings of physical examination that arouse suspicion of an anaerobic infection are?

A

A foul-smelling discharge, gas in the tissue, and necrotic tissue. In addition, infections in the setting of pulmonary aspiration, bowel surgery, abortion, cancer, or human & animal bites frequently involve anaerobes

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22
Q

Two aspects of microbiological diagnosis of an anaerobic infection are important even before the specimen is cultured

A

1) Obtaining the appropriate specimen
2) Rapidly transporting the specimen under anaerobic conditions to the laboratory.
An appropriate specimen is one that does not contain members of the normal flora to confuse the interpretation. Example, such specimens as blood, pleural fluid, pus, & transtracheal aspirates are appropriate, but sputum & feces are not

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23
Q

Laboratory diagnosis: In the lab, the cultures are handled & incubated under _________ conditions

A

anaerobic

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24
Q

There are two medically important genera of gram-positive cocci

A

Staphylococcus and Streptococcus

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25
Q

Staphylococci & Streptococci are?

A

Non-motile & do not form spores

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26
Q

Both staphylococci & streptococci are gram-positive cocci, but they are distinguished by two main criteria

A

1) Microscopically, staphylococci appear in grapelike clusters, whereas streptococci are in chains
2) Biochemically, staphylococci produce catalase (i.e. they degrade hydrogen peroxide), whereas streptococci do not

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27
Q

Staphylococccus aureus causes what?

A

Abscesses, various pyogenic infections (e.g. endocarditis, septic arthritis, & osteomyelitis), food poisoning, scalded skin syndrome, & toxic shock syndrom. One of the most important causes of hospital acquired pneumonia, septicemia, & surgical wound infections. It is an important cause of skin infections, such as folliculitis, cellulitis, & impetigo. Most common cause of bacterial conjunctivitis

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28
Q

Kawasaki syndrome is a disease of unknown etiology that may be caused by?

A

Certain strains of Sta. aureus

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29
Q

Staphylococci are what type of shape and arrangement?

A

Spherical gram-positive cocci arranged in irregular grapelike clusters

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30
Q

Staphylococci produce?

A

Catalase, whereas no streptococci do (catalase degrades H2O2 into O2 & H20). Catalase is an important virulence factor because H202 is microbial & its degradation limits the ability of neutrophils to kill. Mostly aerobic. Can switch from aerobic to fermentation easily

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31
Q

Three species of staphylococci are human pathogens

A

Staphylococci aureus, Staphylococci epidermidis, and Staphylococci saprophyticus. Of the three Sta. aureus is by far the most important

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32
Q

Staphylococci aureus is distinguished from the others primarily by?

A

Coagulase production. This is an enzyme that causes plasma to clot by activating prothrombin to form thrombin. Thrombin then catalyzes the activation of fibrinogen to form the fibrin clot. Sta. epidermidis and Sta. saprophyticus are often referred to as coagulase-negative staphylococci

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33
Q

Sta. aureus produces a carotenoid pigment called?

A

Staphyloxanthin which imparts a golden color to its colonies. This pigment enhances the pathogenicity of the organisms by inactivating the microbial effect of superoxides & other reactive O2 species w/in neutrophils. Sta. epidermidis does not synthesize this pigment & produces white colonies

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34
Q

The virulence of Sta. epidermidis is?

A

Significantly less than that of Sta. aureus

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35
Q

Microorganisms not readily stained with gram

A
  • Mycobacteria (acid-fast)
  • Mycoplasma (no cell wall, walking pnemonia)
  • Treponema and Leptospira (not visible with gram, too thin)
  • Chlamydia and Rickettsia (not stained with gram, intracellular bacteria)
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36
Q

What are the 5 major pathogens

A

1) Chlamydial genital infections (most common, 1 million cases every year)
2) Gonorrhoea (1/2 million cases every year)
3) Salmonellosis
4) Syphilis ( 1-2% increase every year)
5) Lyme disease

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37
Q

3 characteristics of anaerobic bacteria

A

1) Growth in atmosphere w/less than 20% O2. Range from 0.02% to <20%
2) Many use N as their final electron acceptor
3) Catalase activity is minimal or absent in anaerobic bacteria. Survival is favored in environment with low reduction potential (periodontal pocket, dental plaque, colon, crushing injuries)

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38
Q

Classification of anaerobic bacteria

A

Rods
-Spore forming
* Gram positive- Clostridium
* Gram negative- None
- Non spore forming
* Gram positive- Actinomyces, Lactobacillus, Eubacteria
* Gram negative- Bacteroides, Fusobacteria
Cocci
- Gram positive- Streptococcus, peptococcus
- Gram negative- Veillonella

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39
Q

What are the clinical manifestations of anaerobic bacteria

A

1) Part of the normal flora
2) Non pathogenic in the natural site, pathogenic in other sites.
- Clostridium botulinum
- Clostridium tetani
- Clostridium perfringens
3) Abcesses- Brain, lungs, female genital tract, bilary tract

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40
Q

Gram positive cocci

A

2 medically important Genera:
1) Staphylococcus
2) Streptococcus
2 most important human pathogens:
1) Staphylococcus aureus (grapelike arrangements)
2) Streptococcus pyogenes (line or groups of 2)

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41
Q

You isolated a bacteria from a pyogenic infection of the throat with the following features

    Cocci
    Cell arrangement - diplococci
    Gram negative
    Oxidase positive
     Absence capsule
A

Neisseria gonorrhoeae

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42
Q

Your patient has a grey biofilm in the back of the throat and you isolate a microorganism with the following features

Bacilli
Gram Positive
No endospore
A

Corynebacterium diphtheriae

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43
Q

True or False: The position of the endospore in relation to the bacterial cell is an important criteria for bacterial classification

A

True

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44
Q

You isolated a bacteria from a wound of your patient with the following features

    Bacilli
    Gram Positive
    Terminal endospores
    Anaerobic microorganism
     When the toxin produced by the bacteria is injected in mice, the animals show flaccid paralysis of skeletal muscles
A

Clostritium botulinum

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45
Q

You isolated a bacteria from a wound of your patient with the following features

    Bacilli
    Gram Positive
    Terminal endospores
    Anaerobic microorganism
     When the toxin produced by the bacteria is injected in mice, the animals show rigid or spastic paralysis of skeletal muscles
A

Clostridium tetani

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46
Q

What bacteria would be sucessfuly stained with Acid Fast?

A

Mycobacterium vaccae

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47
Q

Which genus of bacteria most commonly produce endospores?

A

Bacillus & Clostridium

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48
Q

You isolated a bacteria from the throat of you patient with the following features

Cocci
Cell arrangement - strings of bacterial cells
Gram Positive
Catalase negative
alpha hemolysis when placed in blood agar
A

Streptococcus pneumoniae

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49
Q

Agar is classified as:

A

Carbohydrate

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50
Q

You isolated a bacteria from the throat of you patient with the following features

Cocci
Cell arrangement - strings of bacterial cells
Gram Positive
Catalase negative
Beta hemolysis when placed in blood agar
A

Streptococcus pyogenes

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51
Q

Your patient presents vomiting and diarrhea. You isolated a bacteria from a sample of food consumed by this patient with the following features

Bacilli
Gram Positive
Terminal endospores
Anaerobic microorganism
A

Clostridium perfringens

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52
Q

Inhalation of endospores of 1. ______ _______ can lead to bacterial infection with mortality close to 100%.

Contamination of rice with endospores of 2) ________ _________ is an important cause of food intoxication.

Most bacteria in the genus 3) _______ are aerobic, while 4) ________ are anaerobic

A
  1. ) Bacillus anthracis
  2. ) Bacillus cereus
    3) Bacillus
    4) Clostridium
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53
Q

The best method for preventing Staphylococcus pneumonia is?

A

A vaccine

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54
Q

The best method for preventing Bacillus anthracis is?

A

Incineration of infected animals

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55
Q

The best method for preventing Staphylococcus aureus is?

A

Hand washing

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56
Q

The best method for preventing Listeria monocytogenes is?

A

Avoid raw vegetables

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57
Q

The best method for preventing Neisseria gonorrhoea is?

A

Condoms

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58
Q

Your patient presents a bacterial biofilm on the intestinal linings. You isolated a bacteria from a stool sample with the following features

Bacilli
Gram Positive
Terminal endospores
Anaerobic microorganism
A

Clostridium dificille

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59
Q

The melting and solidifying temperatures for agar are_______ and ______.

A

95C, 45C

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60
Q

You isolated a bacteria from the throat of your patient with the following features

    Cocci
    Cell arrangement - diplococci
    Gram negative
    Oxidase positive
     Presence capsule
A

Neisseria meningitidis

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61
Q

Gram negative cocci

A

Neisseria

  • Neisseria meningitidis
  • Neisseria Gonohrreae
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62
Q

Most important cause of hospital pneumonia, septicemia and surgical infections

A

Staphylococcus aureus

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63
Q

What does Staphylococcus aureus cause?

A

1) Abcesses
2) Pyogenic infections
3) Food poisoning (toxic manifestation)
4) Scalded skin syndrome (toxic manifestation)
5) Toxic shock
6) Foliculitis

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64
Q

All Staphylococcus produce?

A

Catalase, mostly aerobic. Can switch from aerobic to fermentation easily

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65
Q

Staphylococcus has coagulase which?

A

Causes plasma to clot, important virulence factor. Important method of disguise, induces blood clotting system to be activated. Prevents being recognized by WBC’s

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66
Q

Staphylococcus aureus ferments?

A

Mannitol

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67
Q

Staphylococcus has staphyloxantin which is?

A

Golden color, prevents WBC’s from killing bacteria. Antioxidant

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68
Q

Staphylococcus aureus also has?

A

Protein A which helps bacteria to evade body responses. Prevents recognition by WBC, makes pores on the walls of the WBC’s will kill WBC by this

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69
Q

90% of Staph. aureus isolates have plasmids that?

A

Code for B Lactamase (resistance to penicillin)

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70
Q

What is MRSA?

A

Methacillin Resistant S. aureus. 50% of isolates in US. Most common is USA300

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71
Q

Vancomycin resistance is ___%. What are the two types?

A

2%
VRSA- Complete resistance
VISA- Intermediate resistance

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72
Q

What are the other species of staphylococcus that are less pathogenic than aureus?

A

Staphylococcus epidermidis- Heart infection. Does not produce protein A or coagulase
Staphylococcus saprophyticus- Urinary infection. 2nd major cause, first is E. coli

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73
Q

S. aureus- staphyloxantine, a?

A

Yellow pigment

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74
Q

Catalase for Gram positive cocci

A

Staphylococcus is catalase +

Streptococcus is catalase -

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75
Q

Coagulase for Staphylococcus

A

S. aureus is coagulase +
S. saprophyticus is coagulase -
S. epidermidis is coagulase -

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76
Q

Transmission of Staphylococcus aureus

A
  • 30% of individuals carry S. aureus in the nose. Because bacteria has a preferred environment, in the nose it varies from 25 degrees to 30 degrees
  • Disease is caused by the combination of heavy contamination and debilitated immune response
  • Severe Necrotizing disease- homeless & drug users
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77
Q

Mechanisms of disease of Stapylococcus aureus

A

1) Abcesses- S. aureus protein A inhibits elimination of bacteria (Leukocidin, enzymes)
2) Toxic shock syndrome- S. aureus (TSST) peptidoglycan has LPS like effects
3) Food poisoning- Toxins (Enterotoxin)
4) Scalded skin- Toxins (Exfoliatin)

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78
Q

Prevention of Staphylococcus

A
  • No vaccine
  • Cleanliness to avoid spread of microorganisms
  • Intranasal antibiotics for carriers
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79
Q

Transmission of Staphylococcus

A
  • Contact- direct contact will increase risk
  • Crowded environments- boarding schools, military
  • Cleanliness
  • Cuts or abrasions- presence of entry port
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80
Q

Most common streptococcus

A

Streptococcus pyogenes- pharingitis (strep throat) and heart infection

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81
Q

Important features of Streptococcus

A
  • Catalase negative- most anaerobic
  • Hemolysis
    1) a hemolysis (alpha)
    2) B hemolysis (beta) complete hemolysis
    3) y hemolysis (gamma)
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82
Q

B hemolytic streptococcus groups

A

1) Group A- pharingitis (strep throat)
2) Group B- Streptococcus agalactiae, common bacteria that can colonize vaginal tract, can become problem when giving birth
3) Group D- Enterococci (Vancomycin resistance)

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83
Q

Non B hemolytic streptococcus

A

1) Str. pneumoniae- pneumonia- alpha hemolytic bacteria

2) Str. mutans- dental decay (Viridans Group) alpha hemolytic

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84
Q

Features of B hemolytic streptococcus

A
  • C carbohydrate located in the cell wall, prevents recognition by WBC’s
  • M protein- most important virulence factor. Rheumatic fever.
    Enzymes that degrade protein
    Toxins
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85
Q

Transmission of Streptococcus

A

Part of the natural flora, cause disease when reaches the blood and tissues. Some can be transmitted through oral contact. Have a few dozen species in the mouth. Direct contact can transfer

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86
Q

Mechanisms of disease for streptococcus

A

Production of enzymes and toxins (Streptolysin O- SLO, Protein M, hyaluronidase)

  • Toxic- can produce food poisoning and shock
  • Pyogenic
  • Immunologic
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87
Q

Protein M for streptococci is?

A

An important virulence factor, similar to proteins we find in our body

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88
Q

DNAse is what for streptococci?

A

An important virulence factor

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89
Q

Post streptococcal diseases

A

Production of antibodies against streptococcal proteins (M protein, streptolysin O- SLO) can cross react with tissue

  • Heart & joints- Rheumatic fever
  • Kidneys- glomerulonephytis (kidney inflammation)
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90
Q

Major cause of sepsis in neonates and of peritonitis in patients with renal failure who are undergoing peritoneal dialysis through an indwelling catheter. It is the most common bacterium to cause cerebrospinal fluid shunt infections

A

Staphylococcus epidermidis

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91
Q

Strains of Sta. epidermidis that produce a glycocalyx are more likely to?

A

Adhere to prosthetic implant materials & therefore are more likely to infect these implants than strains that do not produce a glycocalyx

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92
Q

Major reservoir for antibiotic resistant strains of Sta. epidermidis

A

Hospital personnel

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93
Q

Cultures of Sta. aureus typically yeild?

A

Golden-yellow colonies (staphyloxantine, yellow pigment) that are usually B-hemolytic

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94
Q

Cultures of coagulase negative staphylococci typically yield what type of colonies?

A

White colonies that are non hemolytic

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95
Q

The two coagulase-negative staphylococci are distinguished by their reaction to the?

A

Antibiotic novobiocin: Sta. epidermidis is sensitive, whereas Sta. saprophyticus is resistant

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96
Q

In the U.S., 90% or more of Sta. aureus strains are resistant to?

A

Penicillin G. Most of these strains produce B-lactamase

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97
Q

Those most susceptible to infections of Sta. epidermidis is?

A

Intravenous drug users, newborns, and elderly, & those using catheters or other artificial appliances

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98
Q

Severe necrotizing skin and soft tissue infections are caused by?

A

MRSA strains that produce P-V leukocidin. These infections are typically community acquired. These are a common cause of infection among the homeless & intravenous drug users. Athletes who engage in close personal contact are also at risk

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99
Q

Hospital acquired MRSA (HA-MRSA) cause?

A

50% of all nosocomial Sta. aureus infections

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100
Q

Main biological features of Sta. aureus:

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Coagulase
  • Typical hemolysis
  • Catalase
A
  • Cell shape: Cocci
  • Arrangement: Irregular grape-like clusters
  • Gram stain: +
  • Endospores: No
  • Capsule: Thin capsule
  • Unusual features: Protein A on surface
  • Typical hemolysis: Beta
  • Coagulase production: +
  • Catalase: positive
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101
Q

Clinical manifestation of Sta. aureus (Diseases produced by this microorganism)

A

1) Abcesses
2) Pyogenic infections
3) Food poisoning
4) Scalded skin syndrome
5) Toxic shock
6) Folliculitis
Most common cause of hospital acquired pneumonia, septicemia, & surgical wound infections, most common cause of bacterial conjunctivitis

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102
Q

Mechanisms of disease for Sta. aureus

A

Pyogenic and toxin-mediated
Pyogenic: Skin infections, septicemia, endocarditis, osteomyelitis, post surgical wound infections, pneumonia, conjunctivitis
Toxin-mediated: Food poisoning, toxic shock syndrome, scalded skin syndrome

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103
Q

Transmission of Sta. aureus

A

Humans are reservoir

  • nose is main site. People who are carriers in nose have higher risk.
  • Skin (especially hospital personnel & patients)
  • Vagina of 5% of women
  • Shedding from lesions
  • Heavily contaminated environment
  • Comprised immune system
  • Diabetes & intravenous drug users
  • Patients w/chronic granulomatous disease
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104
Q

Prevention of Sta. aureus

A
  • No vaccine
  • Cleanliness
  • Frequent hand washing
  • Aseptic management of lesions
  • For nose, oral antibiotics or intranasal mupirocin
  • Shedders removed from high risk areas
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105
Q

Treatment of Sta. aureus

A
  • More than 90% are resistant to penicillin G. These produce B-lactamase. Can be treated w/ B-lactamase resistant penicillins.
  • 20% are methicillin resistant or nafcillin resistant. Can be treated w/vancomycin or daptomycin.
  • Toxic shock treatment: Correction of shock by using fluids, pressor drugs, & inotropic drugs: administration of a B-lactamase resistant penicillin: removal of tampon
  • Skin infections: Topical antibiotic
  • Abscess: drainage
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106
Q

Resistanct strains of Sta. aureus

A

90% strains resistant to penicillin G, 20% resistant to methicillin or nafcillin-resistant (MRSA or NRSA), strains w/intermediate resistance to vancomycin (VISA), complete resistance (VRSA)

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107
Q

Main biological features of Sta. epidermidis:

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Coagulase
  • Typical hemolysis
  • Catalase
A
  • Cell shape: Cocci
  • Arrangement: Irregular grape-like clusters
  • Gram stain: +
  • Endospores: No
  • Capsule:
  • Unusual features: Sensitive to nobobiocin, opportunistic pathogen, non-motile
  • Coagulase production: negative
  • Typical hemolysis: none
  • Catalase: Positive
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108
Q

Clinical manifestation of Sta. epidermidis

A

Can cause endocarditis & prosthetic joint infections. Heart infection. Infection of prosthetic heart valves & hips; common member of skin flora

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109
Q

Mechanism of disease for Sta. epidermidis

A

Almost always hospital acquired. Part of the normal human flora on the skin & mucous membranes but can enter the bloodstream (bacteremia) & cause metastatic infections, especially at site of implants. Commonly infects intravenous catheters & prosthetic implants. Highly antibiotic resistant. Most strains produce B-Lactamase & many are methicillin, & nafcillin resistant due to altered penicillin-binding proteins. PYOGENIC

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110
Q

Transmission of Sta. epidermidis

A

Found primarily on the human skin & can enter the blood stream at the site of intravenous catheters that penetrate through the skin

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111
Q

Prevention of Sta. epidermidis

A

No vaccine. Cleanliness to avoid spread

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112
Q

Treatment for Sta. epidermidis

A

Highly antibiotic resistant. Most strains produce B-lactamase and many are methicillin-/nafcillin resistant due to altered penicillin binding proteins. Drug of choice is vancomycin. Removal of the catheter or other device.

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113
Q

Main biological features for Sta. saprophyticus:

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Typical hemolysis
A
  • Cell shape: Cocci
  • Arrangement: Grape-like clusters
  • Gram stain: Positive
  • Endospores: No
  • Capsule:
  • Unusual features: Resistant to novobiocin
  • Coagulase: Negative
  • Catalase: positive
  • Typical hemolysis: None
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114
Q

Clinical manifestations for Sta. saprophyticus

A

Urinary tract infections particularly in sexually active young women. Most women with this infection have had sexual intercourse within the previous 24 hours.

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115
Q

Kawasaki syndrome is a disease of unknown etiology that may be caused by certain strains of?

A

Sta. aureus

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116
Q

Mechanism of disease for Sta. saprophyticus

A

Pyogenic

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117
Q

This organism is second to Escherichia coli as a cause of community acquired urinary tract infections in young women.

A

Sta. saprophyticus

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118
Q

Transmission for Sta. saprophyticus

A

Found primarily on the mucosa of the genital tract in young women and from that site can ascend into the urinary bladder to cause urinary tract infections

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119
Q

Prevention for Sta. saprophyticus

A

No vaccine. Lower sexual activity

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120
Q

Treatment for Sta. saprophyticus

A

Can be treated with a antibacterial drugs such as quinolone, such as norfloxacin, or with trimethoprim-sulfamethoxazole

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121
Q

Main biological features for Streptococcus phygenes:

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Typical hemolysis
  • Catalase
A
  • Cell shape: Coccus (spherical)
  • Arrangement: Chains or pairs
  • Gram stain: Positive
  • Endospores: No
  • Capsule: Hyaluronic acid capsule that is antiphagocytic
  • Unusual features: Group A because it displays antigen A on its cell wall. Flesh eating bacteria
  • Typical hemolysis: Beta
  • Catalase: negative
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122
Q

One of the most important characteristics for identification of streptococci is?

A

The type of hemolysis

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123
Q

Types of hemolysis:

1) Green zone
2) Clear halo
3) No hemolysis

A

1) Alpha (a)
2) Beta (B)
3) Gamma (y)

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124
Q

Clinical manifestations of Str. pyogenes

A

Causes 3 types of disease:
1) Pyogenic diseases such as pharyngitis & cellulitis
2) Toxigenic diseases such as scarlet fever and toxic shock syndrome
3) Immunologic diseases such as rheumatic fever and acute glomerulonephritis
Most common bacterial cause of sore throat.

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125
Q

Pharyngitis is characterized by?

A

Inflammation, exudate, fever, leukocytosis, and tender cervical lymph nodes. If untreated, spontaneous recovery occurs in 10 days, but rheumatic fever may occur. Untreated pharyngitis may extend to the middle ear, the sinuses, the mastoids, or the meninges

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126
Q

Mechanism of disease for Str. pyogenes

A

Can cause disease by three mechanisms:

1) Pyogenic inflammation, which is induced locally at the site of the organism in tissue
2) Exotoxin production, which can cause widespread systemic symptoms in areas of the body where there are no organisms
3) Immunologic which occurs when antibody against a component of the organism cross reacts w/normal tissue or forms immune complexes that damage normal tissue. Can cause inflammation

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127
Q

Group A streptococci (Str. pyogenes) produce three important inflammation-related enzymes

A

1) Hyaluronidase
2) Streptokinase
3) DNase

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128
Q

What does the enzyme Hyaluronidase do?

A

Enzyme produced by Group A streptococci. Degrades hyaluronic acid, which is the ground substance of subcutaneous tissue. Hyaluronidase is known as spreading factor because it facilitates the rapid spread of Str. pyogenes in skin infections (cellulitis)

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129
Q

What does the enzyme Streptokinase do?

A

Produced by Group A streptococci (Str. pyogenes).
Fibrinolysin. Activates plasminogen to form plasmin, which dissolves fibrin in clots, thrombi, and emboli. Can be used to lyse thrombi in the coronary arteries of heart attack patients

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130
Q

What does DNase (streptodornase) do?

A

Produced by Group A.
Degrades DNA in exudates or necrotic tissue. Antibody to DNase B develops during pyoderma; this can be used for diagnostic purposes

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131
Q

Transmission of Str. pyogenes

A

Most part of normal flora of the human throat, skin, and intestines but produce disease when they gain access to tissues or blood. Found on the skin & in the oropharynx in small numbers. Can be caught through air via coughing or sneezing. Direct contact

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132
Q

Describe the importance of coagulase for Sta. aureus

A

Causes plasma to clot; important virulence factor method of disguise. Induce blood clotting system to be activated & prevent being recognized by WBC’s

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133
Q

Sta. aureus has staphyloxantin which is?

A

Gives the colonies a golden color, prevents WBCs from killing bacteria (antioxidant)

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134
Q

The protein A (toxin A) for Sta. aureus helps?

A

The bacteria to evade body response. Prevents recognition by WBC, makes pores on the walls of WBC’s, will kill WBC by this

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135
Q

Staphylococcus heart infection disease

A

Sta. epidermidis

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136
Q

Staphylococcus urinary tract infection disease

A

Sta. saprophyticus

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137
Q

Catalase:
Staphylococcus?
Streptococcus?

A

Staphylococcus- Catalase positive

Streptococcus- Catalase negative

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138
Q

Bacteria gains access to dermal tissue (fascia) grows fast destroying tissue as it progresses

A

Severe Necrotizing Disease- homeless & drug users

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139
Q

Prevention of Str. pyogenes

A

No vaccine. Rheumatic fever can be prevented by prompt treatment of group A streptococcal pharyngitis w/ penicillin. Usually with benzathine penicillin once each month for several years in persons who have had rheumatic fever to prevent recurrence. Penicillin is effective. Antibodies against the M protein of one strain provide no protection against other strains

140
Q

Treatment for Str. pyogenes

A
  • Penicillin G or amoxicillin, but neither rheumatic fever no AGN patients benefit from penicillin treatment after the onset of the diseases
  • In mild group A oral penicillin V can be used
  • In penicillin allergic patients, erythromycin or one of its derivatives can be used, however erythromycin resistant strains have emerged that may limit the effectiveness of the macrolide class of drugs in the treatment of streptococcal pharyngitis
141
Q

Streptococcus b (beta) hemolytic group

A

Group A- pharingitis (strep throat)
Group B- Streptococcus agalactiae
Group D- Enterococci (vancomycin resistant)

142
Q

Non b (beta) hemolytic of streptococci

A

Primarily 2

1) Str. phneumoniae- pneumonia (alpha hemolytic bacteria)
2) Str. mutans- dental decay (viridans group) (alpha hemolytic bacteria)

143
Q

Main biological features of Str. Viridans group:

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Typical hemolysis
  • Catalase
A
  • Cell shape: Cocci spherical
  • Arrangement: chains or pairs
  • Gram stain: Positive
  • Endospores: No
  • Capsule:
  • Unusual features:
  • Typical hemolysis: alpha
  • Catalase: negative
144
Q

Clinical manifestation of Str. viridans

A

Most common cause of endocarditis (infection of inner lining of heart). Dental manipulation & dental disease w/the associated bacteremia are most common predisposing factors. Str. mutans & Str. sanguis are odontopathogens responsible for formation of dental plaque

145
Q

Mechanism of disease for Str. viridans

A

Pyogenic. Most common cause of endocarditis. Enters the blood stream (bacteremia) from the oropharynx, typically after dental surgery. Also cause brain abscesses, often in combination w/ mouth anaerobes. Dental surgery is an important predisposing factor to brain abscess because it provides a portal for the viridans & the anaerobes in the mouth to enter the blood stream & spread to the brain

146
Q

Transmission of Str. viridans

A

Found chiefly in the oropharynx. Endogenous

147
Q

Prevention of Str. viridans

A

No vaccine. In patients w/damaged heart valves who undergo invasive dental procedures, endocarditis can be prevented by using amoxicillin perioperatively

148
Q

Treatment of Str. viridans

A

Curable by prolonged penicillin treatment.

100% fatal unless effectively treated with antimicrobial agents

149
Q

Main biological features of Str. agalacteae

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Typical hemolysis
A
  • Cell shape: Cocci spherical
  • Arrangement: Chains or pairs
  • Gram stain: Positive
  • Endospores: No
  • Capsule:
  • Unusual features: Usually bacitracin-resistant, hydrolyzehippurate
  • Typical hemolysis: Beta
150
Q

Clinical manifestations of Str. agalacteae

A 
Causes:
Most in neonates
* neonatal sepsis 
* meningitis
* neonatal pneumonia
In adults
* Pneumonia
* Endocarditis
* Arthritis
* Osteomyelitis
* Postpartum endometritis
Diabetes is the main predisposing factor for adults
151
Q

Mechanisms of disease for Str. agalacteae

A

Pyogenic

  • Main predisposing factor is prolonged (longer than 18 hours) rupture of the membranes in women who are colonize w/ the organism.
  • Children born prior to 37 weeks gestation have higher risk of disease, also children whose mothers lack antibody to group B.
152
Q

Transmission for Str. agalacteae

A

Occurs in vagina and colon. 10-30% of women have it in their genital tracts, although normally a resident of GI tract. During birth, it can colonize the baby via amniotic fluid or the mucous membranes & produce early onset infection24-48 hours after birth. Late onset cases 1-3 months after birth may be contracted by contact w/ the mother or environment

153
Q

Treatment of Str. agalactiae

A

NO vaccine. 20% mortality rate in neonates. The incidence of neonatal sepsis can be reduced by a two-pronged approach
1) All pregnant women at 35-37 weeks gestation should be screened by doing vaginal and rectal cultures, if positive then penicillin G (or ampicillin) should be administered intravenously at time of delivery.
2) If patient has not had cultures done, then penicllin G should be administered intravenously at time of delivery to women who experience prolonged (18 hrs) rupture of membranes, whose labor begins before 37 weeks gestation, or who have fever at time of labor
If allergic to penicillin use cefazolin or vancomycin

154
Q

Main biological features of Str. enterococcus

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Typical hemolysis
  • Catalase
A
  • Cell shape: Coccus spherical
  • Arrangement: Chains or pairs
  • Gram stain: Positive
  • Endospores: No
  • Capsule:
  • Unusual features:
  • Typical hemolysis: Beta
  • Catalase: Negative
155
Q

Clinical manifestations of Str. enterococcus

A
  • Hospital acquired urinary tract infections and endocarditis. Members of normal flora of the colon & noted for ability to cause urinary, biliary, & cardiovascular infections.
  • Urinary catheters & urinary tract instrumentation important predisposing factors
  • Abdominal & pelvic infections
156
Q

Treatment for Str. enterococcus

A

Enterococci resistant to mult. drugs e.g penicillins, aminoglycosides, and vancomycin have emerged. Resistance to vancomycin is mediated by cassette of genes that encode the enzymes that substitute D-lactase for D-alanine in peptidoglycan. Vancomycin resistant enterococci (VRE) are now an important cause of nosocomial infections. No reliable antibiotic therapy for these organisms. There are 2 drugs that are being used to treat infections caused by VRE.
Nonenterococcal group D are not highly resistant & can be treated with penicillin G

157
Q

Mechanism of disease for Str. enterococcus

A
  • Urinary tract infections especially in hospitalized patients. Indewelling urinary catheters & urinary tract instrument are important predisposping factors.
  • Also cause endocarditis in patients undergone GI or urinary tract surgery or instrumentation
  • Cause intra-abdominal & pelvic infections
158
Q

Transmission for Str. enterococcus

A

Located in the colon (normal flora), produce disease when they gain access to tissues or blood.

159
Q

Prevention of Str. enterococcus

A
  • No vaccine
  • Patients with damaged heart valves who undergo GI or urinary tract procedures, endocarditis can be prevented by using ampicillin and gentamicin.
  • To avoid unnecessary use of antibiotics only give to patients at higher risk & who undergo high risk dental procedures
160
Q

Main biological features for Str. pneumoniae

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Typical hemolysis
  • Catalase
A
  • Cell shape: Cocci spherical (oval w. pointed ends)
  • Arrangement: Pairs (diplococci) or short chains
  • Gram stain: Positive
  • Endospores: No
  • Capsule: Polysaccharide capsules of more than 85 antigenically distinct types
  • Unusual features: Lysed by bile or deoxycholate & their growth is inhibited by optochin. Capsules are virulence factors
  • Typical hemolysis: Alpha
  • Catalase: Negative
161
Q

Describe the capsules of Str. pneumoniae

A
  • Polysaccharide capsules of more than 85 antigenically distinct types
  • With specific antigen serum capsules swell (quellung reaction), this can be used to identify type
  • Virulence factors (interfere w/phagocytosis, favor invasiveness)
  • Specific antibody to the capsule opsonizes the organism, facilitates phagocytosis, promotes resistance. Such antibody develops in humans as a result of infection or of administration of polysaccharide vaccine
  • Capsular polysaccharide elcits a B-cell response
162
Q

Important properties of Str. pneumonia

A

1) Polysaccharide capsules

2) C- substance (carbohydrate in cell wall)

163
Q

Clinical manifestations of Str. pneumonia

A

Pneumococci is a prominent cause of:

1) Pneumonia
2) Otitis media
3) Sinusitis
4) Mastoiditis
5) Conjunctivitis
6) Purulent bronchitis
7) Pericarditis
8) Bacterial meningitis
9) Sepsis

164
Q

Pneumonia often begins with a?

A

Sudden chill, fever, cough, & pleuritic pain. Sputum is a red or brown “rusty” color. Bacteremia occurs in 15-25% of cases. Spontaneous recovery may begin in 5-10 days & is accompanied by development of anticapsular antibodies

165
Q

Mechanisms of disease for Str. pneumonia

A

Pyogenic. Lypoteichoic acid activates complement & induces inflammatory cytokine production, contributes to the inflammatory response & to the septic shock syndrome that occurs in some immunocompressed patients. Mult. in tissues and cause inflammation. When they reach alveoli there is an outpouring of fluid & red and white blood cells

166
Q

Transmission for Str. pneumonia

A
  • Humans natural host for pneumococci, no animal reservoir.
  • 5-50% of healthy pop. harbor virulent organisms in oropharynx, pneumonococcal infections not considered communicable
  • Resistance high in healthy young people
  • Disease results when predisposing factors present
167
Q

Predisposing factors for Str. pneumonia

A

1) Alcohol or drug intoxication or other cerbral impairment that can depress cough reflex & increase aspirations of secretions
2) Abnormality of respiratory tract, pooling of mucus, bronchial obstruction, & respiratory tract injury caused by irritants
3) Abnormal circulatory dynamics
4) Splenectomy
5) Certain chronic diseases
Pneumonal meningitis predisposing factors
1) Trauma to head causes leakage of spinal fluid through the nose

168
Q

Prevention for Str. pneumonia

A
  • There is a vaccin (polyvalent polysaccharide vaccine) provides 5 yrs protection.
  • Booster dose for people older than 65 & people between ages 2 & 64 yrs who are asplenic, HIV infected, getting chemo, or immunosupressive drugs to prevent transplant rejection
  • Oral penicillin given to young children w/hypogammaglobulinemia or splenectomy
  • Another vaccine containing pneumoccal polysaccharide coupled (conjugated) to a carrier protein for children younger than 5
169
Q

Treatment for Str. pneumonia

A
  • Most susceptible to penicllins & eryhtromycin
  • Severe infections: penicillin G
  • Mild infections: Oral penicillin V
  • Penicillin allergic patients: Erythromycin or one of its long-acting derivative
  • Penicillin resistanct: Vancomycin
  • Strains tolerant to vancomycin & mult. drugs have emerged
    Mortality: High in elderly, immunocompressed, or debilitated persons
170
Q

Main biological features for Neisseria meningitidis

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Catalase
A
  • Cell shape: Cocci
  • Arrangement:
  • Gram stain: Negative
  • Endospores:
  • Capsule: No
  • Unusual features: Mult. serotypes based on antigenic variation. Endotoxin in outer membrane
  • Catalase:
  • Oxidase: Positive
171
Q

Clinical manifestation of Neisseria gonohrreae

A

1) Gonohrreae
2) Neonatal conjunctivitis
3) Pelvic inflammatory disease (PID)

172
Q

Mechanism of disease for Neisseria gonohrreae

A

Pyogenic:

1) Local: gonohrreae
2) Ascending: Pelvic inflammatory disease (PID)
3) Disseminated: disseminated gonococcal infection
4) Neonatal: Conjunctivitis

173
Q

Transmission of Neisseria gonohrreae

A
  • Humans natural host
  • Transmitted sexually; newborns infected during birth
  • Sexual transmission favors survival
  • Symptomatic in men, asymptomatic in women
  • Genital tract infections most common source
  • Pili important virulence factor (attachment)
  • Virulence factors in cell walls (LOS & outer membrane proteins
174
Q

Prevention of Neisseria gonohrreae

A

Use of condoms & prompt treatment of of symptomatic patients & their contacts. Must report to public health department & follow up. Newborn prevention by use of erythromycin ointment. No vaccine.

175
Q

Treatment for Neisseria gonohrreae

A
  • Ceftriaxone is treatment of choice in uncomplicated infections
  • Oral cefixime alternate drug
  • Follow up culture should be performed one week after completion of treatment
  • Complicated infections requires hospitalization
  • Some resistant strains have emerged
176
Q

Main biological features for Neisseria meningitidis

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Oxidase
A
  • Cell shape: Cocci spherical
  • Arrangement:
  • Gram stain: Negative
  • Endospores:
  • Capsule: Polysaccharide capsule
  • Unusual features: Divided into 13 serological groups on basis of antigenicity of capsular polysaccharides. Endotoxin in outer membrane (LPS)
  • Oxidase: Positive
177
Q

Clinical manifestations of Neisseria meningitidis

A

1) Meningitis

2) Meningococcemia: Most severe life-threatening is Waterhouse-Friderichsen syndrome

178
Q

Mechanisms of disease for Neisseria meningitidis

A

Pyogenic.

* Humans natural host

179
Q

Transmission of disease for Neisseria meningitidis

A
  • Airborne droplets
  • Colonize nasopharynx membranes & become part of transient flora of upper respiratory tract
  • Carriers asymptomatic
  • From nasopharynx can enter bloodstream & spread to specific sites
  • 5% chronic carriers & source of infection for others
  • Carriage rate high in close contact
180
Q

Meningococci have 3 important virulence factors

A

1) Polysaccharide capsule
2) Endotoxin LPS
3) Immunoglobulin A (IgA) protease

181
Q

Prevention for Neisseria meningitidis

A

Drugs (Chemoprophylaxis) & immunization are both used. There is also a vaccine

182
Q

Treatment for Neisseria meningitidis

A
  • Penicillin G

* Strains resistant to penicillin rarely emerged, but sulfonamide resistance is common

183
Q

Main biological features for Mycobacteria tuberculosis

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
  • Oxidase
A
  • Cell shape: Baccilli rods
  • Arrangement:
  • Gram stain: Neither
  • Endospores:
  • Capsule:
  • Unusual features: acid fast, grows slow, obligate aerobe
  • Oxidase:
184
Q

Bacteria that are not readily Gram stained are?

A

1) Mycobacteria
- M. tuberculosis
- M. leprae
- M. atypical mycobacteria
* M. avium/M. intracellulare
2) Chlamydia
- Chl. thracomatis
- Chl. psitacci
3) Treponema
- T. pallidum

185
Q

Clinical manifestations of Mycobacteria tuberculosis

A

Tuberculosis, worldwide it causes more deaths than any other single microbial agent. One-third of the worlds pop. is infected. Each year 1.7 million people die & 9 million new cases occur. 500,000 people are infected with a multidrug resistant strain.

186
Q

Mechanism of disease for Mycobacteria tuberculosis

A

?

187
Q

Transmission of M. tuberculosis

A
  • Transmitted from person to person by respiratory aerosol, & its initial site of infection is the lung
  • Humans natural reservoir
  • Resides chiefly w/in reticuloendothelial cells
  • Some animals can be infected but they are not reservoirs for human infection
  • Most transmission occurs by aerosols generated by the coughing of “smear positive” people, 20% are infected by “smear negative” people
  • In U.S. most cases associated w/reactivation in elderly malnourished men
  • Risk highest among socioeconomically disadvantaged people who have poor housing and poor nutrition
188
Q

What does M. tuberculosis infect?

A

Macrophages & other reticuloendothelial cells. It survives & multiplies w/in a cellular vacuole (phagosome). Produces exported repetitive protein which prevents the phagosome from fusing w/lysosome. Allowing the organism to escape the degradative enzymes in the lysosome

189
Q

Lesions of M. tuberculosis have two types of lesions

A

1) Exudative lesions: Acute inflammatory response, occurs chiefly in lungs at initial site of infection
2) Granulomatous lesions: has central area of giant cells containing tubercle bacilli surrounded by zone of epithelioid cells. These giant cells called “Langhan’s giant cells” are important

190
Q

Gram-positive cocci

A

Staphylococcus, Streptococcus, Enterococcus

191
Q

Gram-negative cocci

A

 Neisseria

192
Q

Gram-positive rods

A

Corynebacterium, Listeria, Bacillus, Clostridium, Actinomyces, Nocardia

193
Q

Gram-negative rods, Enteric tract organisms.

Pathogenic inside and outside tract

A

Escherichia, Salmonella

194
Q

Gram-negative rods, enteric tract organisms, pathogenic primarily inside tract

A

Shigella, Vibrio, Campylobacter, Helicobacter

195
Q

Gram-negative rods, enteric tract organisms.

pathogenic outside tract

A

lebsiella-Enterobacter-Serratia group, Pseudomonas,

Proteus-Providencia-Morganella group, Bacteroides

196
Q

Gram negative rods, enteric tract organisms, Respiratory tract organisms

A

Haemophilus, Legionella, Bordetella

197
Q

Gram negative rods, enteric tract, organisms from animal sources

A

Brucella, Francisella, Pasteurella, Yersinia

198
Q

There are four medically important genera of gram-positive rods: .

A

Bacillus, Clostridium, Corynebacterium, and Listeria.

199
Q

Members of the genus Bacillus are _______, whereas those of the genus Clostridium are ________

A

Members of the genus Bacillus are AEROBIC, whereas those of the genus Clostridium are ANAEROBIC

200
Q

Gram-positive rods: Bacillus

There are two medically important Bacillus species

A

Bacillus anthracis and Bacillus cereus

201
Q

Prevention for Mycobacterium tuberculosis

A
  • Has decreased rapidly due to better housing and nutrition, which have improved host resistance
  • prevention of the spread of the organism depends largely on the prompt identification and adequate treatment of patients who are coughing up the organism.
  • use of masks and other respiratory isolation procedures to prevent spread to medical personnel
  • Contact tracing of individuals exposed to patients with active pulmonary disease who are coughing
  • PPD skin test to detect recent converters and to institute treatment for latent infections
  • test, called Quantiferon- TB (QFT)
  • BCG vaccine can be used to induce partial resistance to tuberculosis
  • Pasteurization of milk and destruction of infected cattle are important in preventing intestinal tuberculosis.
202
Q

Groups that should be screened with the PPD skin test include people with?

A

HIV infection, close contacts of patients with active tubercu- losis, low-income populations, alcoholics and intravenous drug users, prison inmates, and foreign-born individuals from countries with a high incidence of tuberculosis.

203
Q

Treatment for Mycobacterium tuberculosis

A
  • Multidrug therapy is used to prevent the emergence of drug- resistant mutants during the long (6- to 9-month) duration of treatment
  • Isoniazid (INH), a bactericidal drug
  • Treatment for most patients with pulmonary tuberculosis is with three drugs
  • Treament of latent (asymptomatic) infections consists of I H taken for 6 to 9 months
  • Strains of M. tuberculosis resistant to multiple drugs (MDR strains) have emerged, primarily in AIDS patients
204
Q

Main biological features for Mycobacterium leprae

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
A
  • Cell shape: Bacillus
  • Arrangement: single
  • Gram stain: Neither
  • Endospores:
  • Capsule:
  • Unusual features: has not been grown in the laboratory, either on artificial media or in cell culture. It can be grown in the mouse footpad or in the armadillo
205
Q

Clinical manifestations of M. leprae

A

Leprosy (Hansen’s disease)

206
Q

Mechanism of disease for M. leprae

A

?

207
Q

Transmission of M. leprae

A
  • Infection is acquired by prolonged contact with patients with lepromatous leprosy, who discharge M. leprae in large numbers in nasal secretions and from skin lesions.
  • leprosy occurs primarily in Texas, Louisiana, California, and Hawaii
  • disease occurs worldwide, with most cases in the tropical areas of Asia and Africa
208
Q

Pathogenesis of M. leprae

A
  • The organism replicates intracellularly, typically within skin histiocytes, endothelial cells, and the Schwann cells of nerves
  • The nerve damage in leprosy is the result of two processes: damage caused by direct contact with the bacterium and dam- age caused by CMI attack on the nerves
  • There are two distinct forms of leprosy-tuberculoid and lepromatous-with several intermediate forms between the two extremes
209
Q

Prevention of M. leprae

A

Isolation of all lepromatous patients, coupled with chemopro- phylaxis with dapsone for exposed children, is required. There is no vaccine.

210
Q

Treatment for M. leprae

A
  • The mainstay of therapy is dapsone (diaminodiphenylsulfone), but because sufficient resistance to the drug has emerged, com- bination therapy is now recommended.
  • Treatment is given for at least 2 years or until the lesions are free of organisms
211
Q

Main biological features for atypical mycobacteria M. avium/M. intracellular

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
A
  • Cell shape:
  • Arrangement:
  • Gram stain:
  • Endospores:
  • Capsule:
  • Unusual features: M. avium-intracellulare complex (MAl, MAC) is composed of two species, M. avium and M. intracellulare, that are very dif- ficult to distinguish from each other by standard laboratory tests.
212
Q

Clinical manifestations of atypical mycobacterium avium/intracellular

A
  • cause pulmonary disease clinically indistinguish- able from tuberculosis, primarily in immunocompromised patients such as those with AIDS who have CD4 cell counts of less than 200/ J-LL.
  • They are highly resistant to anti- tuberculosis drugs, and as many as six drugs in combination are frequently required for adequate treatment.
213
Q

Main biological features for chlamydia thracomatis

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
A
  • Cell shape: coccoi or rod shaped
  • Arrangement
  • Gram stain: neither
  • Endospores
  • Capsule
  • Unusual features: grow only within cells
214
Q

Clinical manifestations of chlamydia thracomatis

A
  • causes eye (conjunctivitis, trachoma), respiratory (pneumonia), and genital tract (urethritis, lymphogranuloma venereum infections
  • associated with Reiter’s syndrome, an autoimmune disease
215
Q

Mechanism of disease for Chl. thracomatis

A

?

216
Q

Transmission of disease for Chl. tracomatis

A
  • c. trachomatis infects only humans and is usually transmitted by close personal contact, e.g., sexually or by passage through the birth canal. Individuals with asymptomatic genital tract infections are an important reservoir of infection for others. In trachoma, C. trachomatis is transmitted by finger-to-eye or fomite-to-eye contact
  • Sexually transmitted disease caused by C. trachomatis occurs worldwide, but trachoma is most frequently found in develop- ing countries in dry, hot regions such as northern Africa. Tra- choma is a leading cause of blindness in those countries
  • Patients with a sexually transmitted disease are coinfected with both C. trachomatis and Neisseria gonorrhoeae in approx- imately 10% to 30% of cases.
217
Q

Prevention of Chl. trachomatis

A
  • No vaccine
  • limit transmission by prompt treatment of both the patient and the sexual partners, including persons who are asymptomatic
  • Sexual contacts should be traced, and those who had contact within 60 days should be treated
  • Oral erythromycin given to newborn infants of infected mothers can prevent inclusion conjunctivitis and pneumonitis caused by C. trachomatis
218
Q

Treatment for Chl. trachomatis

A

All chlamydiae are susceptible to tetracyclines, such as doxycy- cline, and macrolides, such as erythromycin and azithromycin. The drug of choice for C. trachomatis sexually transmitted dis- eases is azithrornycin. Because the rate of coinfection with gonococci and C. trachomatis is high, any patient with a diagnosis of gonorrhea should also be treated for C. trachomatis with azithromycin.

219
Q

Main biological features for Chl. psitacci

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
A
  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features: obligate intracellular bacteria.
220
Q

Clinical manifestation for Chl. psitacci

A

psittacosis (pneumoniae)

221
Q

Mechanism of disease for Chl. psitacci

A

?

222
Q

Transmission for Chl. psitacci

A
  • infects birds, e.g., parrots, pigeons, and poultry, and many mammals. Humans are infected primarily by inhaling organ- isms in dry bird feces
223
Q

Prevention for Chl. psitacci

A
  • No vaccine
  • controlled by restricting the importation of psittacine birds, destroying sick birds, and adding tetracycline to bird feed. Domestic flocks of turkeys and ducks are tested for the presence of C. psittaci
224
Q

Treatment for Chl. psitacci

A
  • All chlamydiae are susceptible to tetracyclines
  • The drug of choice for C. psittaci and C. pneumoniae infections and for lymphogran- uloma venereum is a tetracycline, such as doxycycline
225
Q

Main biological features for Treponema palladium

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
A
  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
226
Q

Main biological features for Listeria monocytogenes

  • Cell shape
  • Arrangement
  • Gram stain
  • Endospores
  • Capsule
  • Unusual features
A
  • Cell shape: Bacillus rods V or L shaped formations
  • Arrangement:
  • Gram stain: positive
  • Endospores: No
  • Capsule:
  • Unusual features: grows well at cold temperatures, so storage of cont- aminated food in the refrigerator can increase the risk of gas- troenteritis. This paradoxical growth in the cold is called “cold enhancement”
  • Typical hemolysis: narrow zone of B hemolysis
227
Q

There are four medically important genera of gram-positive rods. Which ones form spores?

A

Bacillus, Clostridium, Corynebacterium, and Listeria. Bacillus and Clostridium form spores, whereas Corynebacterium and Listeria do not.

228
Q

Members of the genus Bacillus are _______, whereas those of the genus Clostridium are ________

A

Members of the genus Bacillus are aerobic, whereas those of the genus Clostridium are anaerobic

229
Q

There are two medically important Bacillus species

A

Bacillus anthracis and Bacillus cereus

230
Q

Clinical manifestations of Listeria monocytogenes

A

Causes meningitis and sepsis in newborns, pregnant women, and immunosuppressed adults.outbreaks of febrile gastroenteritis

231
Q

Mechanisms of disease for Listeria monocytogenes

A

Pygogenic. Invasion of cells is mediated by internalin made by Listeria and E-cadherin on the surface of human cells. The ability of Listeria to pass the placenta, enter the meninges, and invade the gastrointestinal tract depends on the interaction of internalin and E-cadberin on those tissues.Upon entering the cell, the organism produces listeri- olysin, which allows it to escape from the phagosome into the cytoplasm, thereby escaping destruction in the phagosome. Because Listeria preferentially grows intraceilularly, ceil-mediated immunity is a more important host defense than humoral immunity. Suppression of cell-mediated immunity predis- poses to Listeria infections. L. monocytogenes can move from cell to ceil by means of actin rockets-filaments of actin polymerize and propel the bacteria through the membrane of one human ceil and into another.

232
Q

Transmission of disease for Listeria monocytogenes

A
  • occur primarily in two clinical settings: (1) in the fetus or in a newborn as a result of transmission across the placenta or during delivery and (2) in pregnant women and immunosuppressed adults, especially renal trans- plant patients
  • organism is distributed worldwide in animals, plants, and soil. From these reservoirs, it is transmitted to humans primarily by ingestion of unpasteurized milk products, under- cooked meat, and raw vegetables. Contact with domestic farm animals and their feces is also an important source.
  • primarily a foodborne disease asso- ciated with eating unpasteurized cheese and delicatessen meats.
  • The pathogenesis of Listeria depends on the organism’s ability to invade and survive within cells.
233
Q

Prevention of Listeria monocytogenes

A
  • No immunization
  • Limiting the exposure of pregnant women and immunosuppressed patients to potential sources such as farm animals, unpasteurized milk products, and raw vegetables recommended
  • Trimethoprim-sulfamethoxazole given to immuno- compromised patients to prevent Pneumocystis pneumonia can also prevent listeriosis.
234
Q

Treatment for Listeria monocytogenes

A
  • Treatment of invasive disease, such as meningitis and sepsis, consists of trimethoprim-sulfamethoxazole
  • Combinations, such as ampicillin and gentamicin or ampicillin and trimethoprim-sulfamethoxazole, can also be used
  • Resistant strains rare
235
Q

Main biological features for Corynebacterium diphteriae

A
  • Cell shape: rod club shaped
  • Arrangement:
  • Gram stain: positive
  • Endospores: No
  • Capsule
  • Unusual features
236
Q

Mechanism of disease for Corynebacterium diphteriae

A

Toxigenic

237
Q

Clinical manifestation of Corynebacterium diphteriae

A

causes diphtheria. Other Corynebacterium species (diphtheroids) are implicated in opportunistic infec- tions.

238
Q

Transmission for Corynebacterium diphteriae

A
  • Humans only natural host
  • Both toxigenic and nontoxigenic organisms reside in the upper respiratory tract and are transmitted by airborne droplets
  • The organism can also infect the skin at the site of a preexisting skin lesion. This occurs primarily in the tropics but can occur worldwide in indigent persons with poor skin hygiene
239
Q

Prevention for Corynebacterium diphteriae

A
  • Rare in U.S. because children are immunized with diphtheria toxoid (DTaP)
  • Diphtheria toxoid is prepared by treating the exotoxin with formaldehyde. This treatment inactivates the toxic effect but leaves the antigenicity intact. Immunization consists of three doses given at 2, 4, and 6 months of age, with boosters at 1 and 6 years of age. Because immunity wanes, a booster every 10 years is recommended. Immunization does not prevent nasopharyngeal carriage of the organism.
240
Q

Treatment for Corynebacterium diphteriae

A
  • The treatment of choice is antitoxin, which should be given immediately on the basis of clinical impression because there is a delay in laboratory diagnostic procedures
  • toxin binds rapidly and irreversibly to cells and, once bound, cannot be neutralized by antitoxin
  • Treatment with penicillin G or an erythromycin is also rec- ommended, but neither is a substitute for antitoxin. Antibi- otics inhibit growth of the organism, reduce toxin production, and decrease the incidence of chronic carriers.
241
Q

Main biological features for Bacilli anthraces

  • Cell shape:
  • Arrangement
  • Gram stain:
  • Endospores:
  • Capsule:
  • Unusual features:
A
  • Cell shape: Rods
  • Arrangement
  • Gram stain: Positive
  • Endospores: Yes
  • Capsule:
  • Unusual features:
  • O2 requirement: aerobic
242
Q

Clinical manifestations for Bacilli anthracis

A

anthrax, which is common in animals but rare in humans. Human disease occurs in three main forms: cutaneous, pulmonary (inhalation), and gastrointestinal. In 2001, an outbreak of both inhalation and cutaneous anthrax occurred in the United States. The outbreak was caused by sending spores of the organism through the mail. As of this writing, there were 18 cases, of whom 5 died

243
Q

Mechanisms of disease for Bacilli anthracis

A

Toxigenic.
Pathogenesis is based primarily on the production of two exo- toxins, collectively known as anthrax toxin. The two exotoxins, edema factor and lethal factor, each consist of two proteins in an A-B subunit configuration. The B, or binding, subunit in each of the two exotoxins is protective antigen. The A, or active, subunit has enzymatic activity.

244
Q 
Organism: Bacilli anthracis
Disease:
Transmission/predisposing factor
Action of toxin
Prevention
A

Disease: Antrax
Transmission/predisposing factor: Cutaneous anthrax, pores in soil enter wound. Pulmonary anthrax pores inhaled into lungs
Action of toxin: Exotoxin has 3 components: 1) protective antigen binds to cell; 2) edema factor is an
Prevention: Vaccine contains protective antigen as the immunogen

245
Q

Transmission for Bacilli anthracis

A

1) Spores persist in soil for years. Humans often infected cutaneously at time of trauma to skin, which allows spores on animal products, such as hides, bristles, and wool, to enter
2) Spores can also be inhaled into the respiratory tract. Pulmonary (inhalation) anthrax occurs when spores are inhaled into the lungs. Inhalation anthrax is not communicable from person-to- person. After being inhaled into the lung, the organism moves rapidly to the medi- astinallymph nodes, where it causes hemorrhagic mediastinitis. Because it leaves the lung so rapidly, it is not transmitted by the respiratory route to others.
3) Gastrointestinal anthrax occurs when contaminated meat is ingested

246
Q

Prevention for Bacilli anthracis

A

1) Ciprofloxacin or doxycycline was used as prophylaxis in those exposed during the outbreak in the United States in 2001
2) People at high risk can be immunized with cell-free vaccine con- taining purified protective antigen as immunogen. vaccine is weakly immunogenic, and six doses of vaccine over an 18-month period are given. Annual boosters are also given to maintain protection
3) Incinerating animals that die of anthrax, rather than burying them, will prevent the soil from becoming contaminated with spores

247
Q

Treatment for Bacilli anthracis

A

Ciprofloxacin is the drug of choice. Doxycycline is an alternative drug. No resistant strains have been isolated clinically.

248
Q

Main biological features for Bacilli cereus

  • Cell shape:
  • Arrangement
  • Gram stain:
  • Endospores:
  • Capsule:
  • Unusual features:
A
  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Positive
  • Endospores: Yes
  • Capsule:
  • Unusual features:
    O2 requirement: Aerobic
249
Q

Clinical manifestation for Bacilli cereus

A

Causes food poisoning:
There are two syndromes: (1) one has a short incubation
period (4 hours) and consists primarily of nausea and vomiting, similar to staphylococcal food poisoning; (2) the other has a long incubation period (18 hours) and features watery, non-bloody diarrhea, resembling clostridial gastroenteritis

250
Q

Mechanism of disease for Bacilli cereus

A

Toxin mediated:

* produces two enterotoxins

251
Q

Transmission for Bacilli cereus

A

Spores on grains such as rice survive steaming and rapid fry- ing. The spores germinate when rice is kept warm for many hours (e.g., reheated fried rice). The portal of entry is the gas- trointestinal tract

252
Q

Prevention for Bacilli cereus

A

No vaccine. No specific means of prevention. Rice should not be kept warm for long periods.

253
Q

Treatment for Bacilli cereus

A

Only symptomatic treatment is given

254
Q 
Organism: Bacilli cereus
Disease:
Transmission/predisposing factor
Action of toxin
Prevention
A

Disease: Food poisoning
Transmission/predisposing factor: Spores germinate in reheated rice, then bacteria produce exotoxins which are ingested
Action of toxins: 2 exotoxins (enterotoxins): 1)
Prevention

255
Q

Main biological features for Clostridium tetani

  • Cell shape:
  • Arrangement
  • Gram stain:
  • Endospores:
  • Capsule:
  • Unusual features:
A
  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Positive
  • Endospores: Yes
  • Capsule:
  • Unusual features:
  • O2 requirements: Anaerobic
256
Q

There are four medically important species of Clostridium

A

1) Clostridium tetani
2) Clostridil!m botulinum
3) Clostridium perfringens
4) Clostridium difficile

257
Q

Clinical manifestations of Clostridium tetani

A

causes tetanus (lockjaw)

258
Q

Mechanism of disease for Clostridium tetani

A

Toxic-mediated

259
Q

Transmission of disease for Clostridium tetani

A

1) Spores widespread in soil
2) Entry portal usually wound site (nail penetrates foot, skin popping by drug addicts)
3) Germination of spores is favored by necrotic tissue and poor blood supply in the wound
4) Neonatal tetanus, in which the organism enters through a contaminated umbilicus or circumcision wound

260
Q

Prevention for Clostridium tetani

A

1) Immunization with tetanus toxoid in childhood and every 10 years thereafter. Usually given to children in combination with diphtheria toxoid and the acellular pertussis vaccine (DTaP)
2) When trauma occurs, the wound should be cleaned and debrided and tetanus toxoid booster should be given
3) If the wound is grossly contaminated, tetanus immune globulin, as well as the toxoid booster, should be given and penicillin administered
4) Tetanus immune globulin (tetanus antitoxin) is made in humans to avoid serum sickness reactions that occur when antitoxin made in horses is used
5) administration of both immune globulins and tetanus toxoid (at different sites in the body) is an example of passive-active immunity

261
Q

Treatment for Clostridium tetani

A

1) Tetanus immune globulin (tetanus antitoxin) used to neu- tralize toxin
2) role of antibiotics uncertain
3) If antibiotics are used, either metronidazole or penicillin G can be given
4) adequate airway must be maintained and respiratory support given
5) Benzodiazepines, e.g., diazepam (Valium), should be-given to prevent spasms
6) A high mortality rate is associated with this disease

262
Q

Clostridium tetani is characterized by?

A
  • Strong muscle spasms (spastic paralysis, tetany). Specific clinical features include lockjaw (trismus) due to rigid contraction of the jaw muscles, which prevents the mouth from opening, and exaggerated reflexes.
  • Opisthotonos, a pronounced arching of the back due to spasm of the strong extensor muscles of the back
  • Respiratory failure ensues
263
Q

In tetanus, _____ paralysis occurs, whereas in botulism, _______ paralysis occurs.

A

in tetanus, spastic paralysis (strong muscle contractions) occurs, whereas in botulism, flaccid paralysis (weak or absent muscle contractions) occurs

264
Q

Main biological features for Clostridium botulinum

  • Cell shape:
  • Arrangement
  • Gram stain:
  • Endospores:
  • Capsule:
  • Unusual features:
A
  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Positive
  • Endospores: Yes
  • Capsule:
  • Unusual features:
  • O2 requirements: Anaerobic
265
Q

Clinical manifestations of Clostridium botulinum

A

causes botulism

266
Q

Mechanism of disease for Clostridium botulinum

A

Toxin-mediated & proteolytic:

  • Botulinum toxin is absorbed from the gut and carried via the blood to peripheral nerve synapses, where it blocks release of acetylcholine
  • Minute amounts of the toxin are effective in the treatment of certain spasmodic muscle disorders such as torticollis, “writer’s cramp:’ and blepharospasm
  • Two special clinical forms occur: (1) wound botulism, in which spores contaminate a wound, germinate, and produce toxin at the site and (2) infant botulism, in which the organisms grow in the gut and produce the toxin there.
  • Ingestion of honey containing the organism is implicated in transmission of infant botulism
  • Affected infants develop weakness or paralysis and may need respiratory support but usually recover spontaneously
267
Q

Transmission for Clostridium botulinum

A
  • Spores, widespread in soil, contaminate vegetables and meats
  • When these foods are canned or vacuum-packed without adequate sterilization, spores survive and germinate in the anaerobic environment
  • Toxin is produced within the canned food and ingested preformed
  • The toxin is relatively heat-labile; it is inacti- vated by boiling for several minutes. Thus, disease can be pre- vented by sufficient cooking
268
Q

Prevention for Clostridium botulinum

A

Proper sterilization of canned & vacuum packed foods. Food must be adequately cooked to inactivate toxin. Swollen cans but be discarded (Clostridial proteolytic enzymes form gas, which swells cans)

269
Q

Treatment for Clostridium botulinum

A
  • Trivalent antitoxin given along w/ respiratory support

* Antitoxin made in horses & serum sickness occurs in about 15% of antiserum recipients

270
Q

Main biological features for Clostridium perfringens

  • Cell shape:
  • Arrangement:
  • Gram stain:
  • Endospores:
  • Capsule:
  • Unusual features:
  • O2 requirements:
A
  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Positive
  • Endospores: Terminal endospores
  • Capsule:
  • Unusual features:
  • O2 requirements: Anaerobic
271
Q

Clinical manifestation for Clostridium perfringens

A

Causes two diseases, gas gangrene and food poisoning depending on the entry port

272
Q

Mechanism of disease for Clostridium perfringens

A

Toxic mediated:

  • Gas gangrene
    • Grow in traumatized tissues & produce variety of toxins (most important alpha toxin)
    • Degradative enzymes produce gas in tissues
273
Q

Transmission of disease for Clostridium perfringens

A

Gangrene
* Spores in soil
* Vegatative cells members of normal flora of colon & vagina
* Gas gangrene associated w/war wounds, auto & motorcycle accidents & septic abortions
Food poisoning
* Spores in soil can contaminate food
* Heat resistant spores survive cooking & germinate
* Grow in large numbers in reheated foods

274
Q

Prevention for Clostridium perfringens

A 
Gangrene
- Wounds should be cleaned & derided 
- penicillin may be given 
- No vaccine
Food poisoning
- No specific measures
- Food should be adequately cooked to kill the organism.
275
Q

Treatment for Clostridium perfringens

A 
Gangrene
- High mortality rate for gangrene
- Antibiotic (Penicillin G)
- Wounds derided 
Food poisoning
- Symptomatic treatment is given; no antimicrobial drugs are administered
276
Q

Main biological features for Clostridium difficile

  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Positive
  • Endospores: Yes
  • Capsule:
  • Unusual features:
  • O2 requirements: Anaerobic
A
  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Positive
  • Endospores: Yes
  • Capsule:
  • Unusual features:
  • O2 requirements: Anaerobic
277
Q

Clinical manifestations for Clostridium difficile

A
  • Causes antibiotic-associated pseudomembranous colitis

* most common nosocomial cause of diarrhea

278
Q

Mechanism of disease for Clostridium difficile

A

Toxic-mediated:

  • Antibiotics suppress drug-sensitive members of the normal flora, allowing to multiply and produce exotoxins A and B
  • Clindamycin was the first antibiotic to be recognized as a cause of pseudomembranous colitis, but many antibiotics are known to cause this disease
  • cancer chemotherapy also predisposes to pseudomembranous colitis
279
Q

Transmission for Clostridium difficile

A
  • carried in the gastrointestinal tract in approximately 3% of the general population and up to 30% of hospitalized patients
  • Most people are not colonized
  • transmitted by the fecal-oral route
  • hands of hospital personnel are important intermediaries.
280
Q

Prevention for Clostridium difficile

A

There are no preventive vaccines or drugs. Antibiotics should be prescribed only when necessary.

281
Q

Treatment for Clostridium difficile

A
  • causative antibiotic should be withdrawn
  • Oral metron- idazole or vancomycin should be given and fluids replaced
  • life-threatening cases, surgical removal of the colon may be required or vancomycin should be used
  • treatment does not eradicate the carrier state and repeated episodes of colitis can occur
  • Fecal bacteria therapy possible therapeutic approach
282
Q

Main biological features for Pseudomonas

  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Positive
  • Endospores: Yes
  • Capsule:
  • Unusual features:
  • O2 requirements:
A
  • Cell shape: Rod
  • Arrangement:
  • Gram stain: Negative
  • Endospores:
  • Capsule:
  • Unusual features:
  • O2 requirements:
283
Q

Clinical manifestation of Pseudomonas

A

causes melioidosis, a rare dis- ease found primarily in Southeast Asia

284
Q

Mechanism of disease for Pseudomonas

A

characterized by high fever and bloody, purulent sputum.

285
Q

Transmission for Pseudomonas

A

found in soil and is transmitted most often when soil contaminates skin abrasions. Untreated cases can proceed to sepsis and death.

286
Q

Prevention for Pseudomonas

A

?

287
Q

Treatment for Pseudomonas

A

treatment of choice is ceftazidime, which is administered for several weeks.

288
Q

Main biological features for GI tract organism Campylobacter jenuni

A
  • Cell shape: Rod comma or S shaped
  • Arrangement:
  • Gram stain: Negative
  • Endospores:
  • Capsule:
  • Unusual features: microaerophilic, growing best in 5% oxygen rather than in the 20% present in the atmosphere.
  • O2 requirements:
289
Q

Clinical manifestations of GI tract campylobacter jenuni

A
  • Cause of enterocolitis, especially in children. Common antecedent to Guillain- Barre syndrome. Other Campylobacter species are rare causes of systemic infection, particularly bacteremia.
  • major cause of diarrhea in the United States
290
Q

Mechanism of disease for GI tract campylobacter jenuni

A
  • Domestic animals such as cattle, chickens, and dogs serve as a source of the organisms for humans.
    *
291
Q

Transmission for GI tract campylobacter jenuni

A
  • usually fecal-oral
  • Puppies with diarrhea are a common source for children.
  • Human-to-human transmission occurs but is less frequent than animal-to-human transmission.
    *
292
Q

Streptococcus pneumoniae

1) Major cause of?
2) hemolysis?
3) Capsule?
4) Transmission?
5) Treatment?
6) Prevention

A

1) pneumonia
2) Alpha hemolysis
3) Capsule is a virulence factor
4) Transmission: 5-20% of individuals harbor the bacteria (oropharynx)
5) Treatment: Penicillin,streptomycin
6) Prevention: Vaccine (capsule sugar) protection for 5 years

293
Q

Neisseria meningitides

1) hosts
2) Transmission
3) Pathogenesis
4) Treatment
5) Prevention

A

1) hosts: humans
2) Transmission: Saliva droplets, 5%
individuals are carriers
3) Pathogenesis: Capsule, LPS, enzymes
4) Treatment: Penicillin G
5) Prevention: Vaccine (capsule sugar)

294
Q

Bacillus anthracis 5 Main features

A

– Large gram + bacilli
– Toxin is coded in a Plasmid
– Capsule (D-glutamate) is coded in a Plasmid
– Non motile
– Causes disease in skin, lungs and gastrointestinal tract

295
Q

Bacillus anthracis Mechanism of Disease

A

– Production of 2 toxins causing edema (swelling) and cell death.
– If left untreated, infection will became systemic and result in death.

296
Q

Bacillus anthracis Treatment

A

Ciprofloxacin

-No cases of resistance have been reported.

297
Q

Clostridium (Gram positive Bacilli)

1) O2 requirement
2) Main features
3) Transmission
4) Mechanism of disease
5) Treatment
6) Prevention

A

1) O2 requirement: anaerobic bacteria
2) Main features: Causes Tetanus (lockjaw)
3) Transmission: Endospores live in the soil and get access to tissue via wound
4) Mechanism of disease: Toxin (tetanoplasmin) – acts on nervous system
5) Treatment: Tetanus antitoxin (antibodies to neutralize toxin) + vaccine + antibiotics
6) Prevention: Vaccine is available (inactivated toxin). Given to children and every 10 years (association with Diphtheria and Pertussis – DTaP)

298
Q

C. botulinum:

1) causes
2) Transmission
3) Disease mechanism
4) Treatment
5) Prevention

A

1) botulism
2) Spores are widespread in soil and contaminate
3) Toxin blocks nervous system – paralysis
4) Antitoxin (neutralizing antibodies) + Respiratory support
5) Food must be properly disinfected before canned or vacuum packed

299
Q

Clostridium perfringens

1) Gram
2) Found in
3) Diseases:
4) Transmission

A

1) positive bacilli
2) Found in the soil and microbiota of colon and vagina.
3) Diseases:
– Gasgangrene
– Food poisoning
4)Contamination of wounds and food.

300
Q

Clostridium perfringens:

1) Mechanism of disease
2) Manifestation
3) Prevention – No vaccine, cleanliness.

A

1) Mechanism of disease
– Woundcontamination–alphatoxin–membrane damage
– Food poisoning-enterotoxin
2) Manifestation
– Wound contamination–Fast evolving tissue damage, septicemia, death.
– Food poisoning–Diarrhea on set in 8-16 hrs, resolves 24hs.
3) Prevention – No vaccine, cleanliness.

301
Q

Clostridium difficile

1) Gram
2) Found in
3) Diseases
4) Transmission

A

1) Gram positive bacilli
2) Found in the soil and microbiota of colon (3%
general population, 30% hospitalized).
3) Diseases: Pseudomenbrane colon- Biofilm
4) Transmission: Fecaloralroute

302
Q

Clostridium difficile

1) Mechanism of disease
2) Manifestation
3) Prevention

A

1) Mechanism of disease
– Overgrowth and colonization (biofilm) form in carriers after a prolonged antibiotic therapy regimen. Production of Toxins.
2) Manifestation
– Chronic non blood diarrhea.
3) Prevention – Antibiotics only when necessary, cleanliness.

303
Q

Non endospore forming Gram positive bacilli, Corynebacterium diphtheriae

1) Main features
2) Transmission
3) Disease Mechanism
4) Treatment
5) Prevention

A

1) Main features
– Club shaped gram positive bacilli – no endospores
2) Transmission
– Humans are the only host
– Bacteria colonizes upper airway and is transmitted by airborne droplets.
3) Disease Mechanism
- Bacterial toxin damages host cells.
- Gray pseudomenbrane over tonsils and throat. Rare in US
- Heart and nervous system complications can occur
4) Treatment
– Anti-toxin antibodies + antimicrobials
5) Prevention
– Vaccine is available (DTaP). Recommended for children 2, 4,6 yo. Boosters at 1 and 6. Vaccine does not prevent colonzation.

304
Q

1) L. monocytogenes causes?

2) Main features

A

1) L. monocytogenes causes meningitis and sepsis in newborns, pregnant women and immunossupressed adults. Also causes outbreaks of febrile gastroenteritis.
2) Main features
– L. monocytogenes grows well at cold temperatures, enhancing growth over refrigeration.
– Bacteria is present in soil, plants and animals, and it is transmitted to humans by ingestion of unpasteurized milk, raw or undercooked meats and raw vegetables.

305
Q

Listeria monocytogenes mechanism of Disease

A

– Disease depends on the ability of the bacteria to invade and survive within cells.
– Suppression of immunity favors Listeria infection
– During pregnancy Listeria causes abortion.
– In immunocompromised adults Listeria causes meningitis and sepsis.

306
Q

Treatment for Listeria monocytogenes

A

Antibiotics

307
Q

Prevention for Listeria monocytogenes

A

There is no vaccine. Pregnant and immunocompromised patients may avoid contact with farm animals, raw vegetables and meat and unpasteurized milk.

308
Q

Enterobacteriaceae – large number of gram negative bacilli species living in the colon of humans and animals as part of the normal flora.
3 Main facts

A

– All ferment glucose
– Use N as final electron acceptor in respiration
– All are facultative anaerobes

309
Q

Gram Negative bacilli related to the enteric tract Mechanism of Disease

A

– Gram negative–Lipopolyssaccharide (LPS )and toxin production.
– Highly antibiotic resistant due to production of beta lactamases
– High level of conjugation and transference of plasmids that code resistance to antimicrobial drugs.

310
Q

Coliforms include species that inhabit the?

A

colon, especially E.coli.
– Because E. coli is the only bacteria that lives exclusively in the colon, it is used as an indicator of fecal contamination in water.
– More than 4 bacteria per dL of water indicates unacceptable fecal contamination.

311
Q

E coli causes?

A

Urinary infection and gram negative sepsis.

312
Q

Escherichia coli Main features

A

– Most abundant facultative anaerobe in colon and
feces.
– E coli ferments lactose
– Reservoirs include human and animals

313
Q

Escherichia coli Mechanism of disease

A

– Urinary infection
– contamination with patients’ own colonic flora
– Meningitis in newborns
– contamination during birth from mother’s flora.
– Traveler’s diarrhea
– ingestion of food contaminated with feces.
– Production of toxins and invasion of tissue are the main mechanisms of disease.

314
Q

Escherichia coli

1) Treatment
2) Prevention

A

1) antibiotics
2) No vaccine is available
– Reduce time of urinary catheters and intravenous lines (if possible)
– Cranberry juice–Tannins inhibit binding of the bacteria.
– Avoid drinking untreated water.

315
Q

Salmonella species cause?

A

enterocolitis, typhoid fever and septicemia

316
Q

Main features of salmonella

A

– Salmonella do not ferment lactose

– Can be divided in typhoidal species and non typhoidal species

317
Q

Salmonella Enterocolitis 2 main points

A

– Salmonella has to invade colon tissue to cause disease.

– 100,000 organisms in the inoculum are necessary to produce disease

318
Q

Salmonella Thyphoid fever main points

A

– Salmonella has to invade colon tissue, and then spreads to liver gallbladder and spleen.
– Spread of bacteria leads to bacteremia and results in fever.
– Gallbladder infection can turn host in reservoir that secrets bacteria in the feces.
– Disease resolves by the third weekend 3% of patients become carriers.

319
Q

Salmonella Septicemia

A

– Only 5 to 10% of salmonella infections result in septicemia.
– Happens in patients with underlying chronic disease such as Sickle cells anemia & Cancer

320
Q

Salmonella Transmission main points

A

– Salmonella transmission is associated with ingestion of food and water contaminated with human and animal feces.
– Sal. typhi, the cause of typhoid fever, is transmitted only by humans. Other species can came from animals
– Most common source of animal salmonella is poultry and eggs.

321
Q

Salmonella Treatment

A

– Infection is usually self-limited and resolves without treatment.
– Antibiotics do not shorten the disease or reduce the symptoms, and are indicated only for newborns and immunossupressed patients.
– Antibiotic resistance is common – Plasmids
– For invasive forms antibiotic may be used along with removal of the gallbladder.

322
Q

Salmonella Prevention

A

– Mainly Public Health and personal hygiene measures.

– 2 vaccines are available with limited efficiency (50-80% )

323
Q

Shigella main features

A

cause enterocolitis
– Gram negative bacilli–non lactose fermenting
– 100 shigella can cause disease
– Shigellosis is a human disease transmitted by fecal contamination
– Toxin (shiga toxin) causes bloody diahrrea.
– No antibiotics are indicated for mild cases.
– Personal and public health measures can prevent
disease.

324
Q

Vibrio cholerae causes?

A

cholera

325
Q

Vibrio cholerae Main features

A

– Curved gram negative bacilli
– Transmitted by fecal contamination
– Main animal source of V. cholerae is marine shellfish.
– Toxin produce clear diarrhea in large volumes, loss of water leads to cardiac and renal damage.
– Treatment consists of water replacement
– Prevention –
– public health and personal higyene
– Vaccine is available (not in US) with limited efficiency (50%)

326
Q

Pseudomonas aeruginosa

Klebsiella pneumoniae

A

.

327
Q

Three major groups of Mycobacteria

A

 M. tuberculosis – causes tuberculosis
 M. leprae – causes leprosy
 M. avium-intracellulare – tuberculosis like disease

328
Q

Mycobacteria Important features

A

– Aerobic ,acid fast rod
– Grows slowly
– Relatively resistant to acids, alkalis and dehydration
– Resistance to main drug is wide spread- isoniazid

329
Q

Haemophilus influenzae Important properties

A

– Leading cause of Meningitis in children before the vaccine.
– Upper Respiratory tract infection
– Small Gram negative rod, encapsulated

330
Q

Yersinia pestis is the cause of?

A

Yersinia pestis is the cause of plague, also known as the black death, the scourge of the Middle Ages

331
Q

Yersinia pestis main biological features

A

Cell shape: rod
Gram: negative
Capsule: yes
Characteristics: Most virulent bacteria known
Reservoir: prairie dogs are the main reservoir
Treatment: antibiotics
Prevention: controlling the spread of rats. patient with plague must be placed in strict isolation (quarantine) for 72 hours after antibiotic therapy is started.
Vaccine: yes

332
Q

Haemophilus influenzae Epidemiology and transmission

A

– Infects only humans

– Mechanism of disease rely on capsule and production of toxin.

333
Q

Haemophilus influenzae Clinical findings & Treatment

A

1) Clinical findings
– Meningitis, 90% mortality if left untreated
– Upper respiratory infection (otitis, sinusitis, pneumonia.
2) Treatment – antibiotics

334
Q

Haemophilus influenzae Prevention

A

Vaccine – reduces 90% incidence of meningitis

335
Q

Gram Negative Rods related to the Respiratory tract: Bordetella pertussis Important properties

A

– Causes Whooping cough (pertussis)

– Small Gram negative rod, encapsulated

336
Q

Bordetella pertussis Epidemiology and transmission

A

– Pathogen only for humans
– Transmitted by airborne droplets, highly contagious
– Mechanism of disease – adherence to airway epithelia and production of toxin.

337
Q

Bordetella pertussis Clinical findings

A

– Whooping cough is an acute tracheobronchitis – hacking coughs and mucus

338
Q

Bordetella pertussis Treatment & Prevention

A

1) Treatment- Antibiotic and supportive care (oxygen therapy and suction of mucus).
2) Prevention- Vaccine – acellular vaccine used in US
- 5 proteins including Pertussis toxin.
- Genetically modified – Toxin in the vaccine does not induce Gs ribosilation.
- Vaccine schedule- 2mo, 12mo, 15mo, pre-school, 10- 18yo, 19-64yo.

339
Q

Gram Negative Rods related to animal sources: Brucella Important properties

A

– Causes brucellosis (undulant fever)

– Small Gram negative rod, encapsulated

340
Q

Brucella Epidemiology and transmission

A

– Three species are pathogens for humans
* B. melitensis (goats and sheep)
* B. abortus (Cattle)
* B. suis (pigs)
– Transmission- contaminated milk products (unpasteurized milk products) or direct skin contact.

341
Q

Brucella

1) Clinical findings
2) Treatment – Antibiotics
3) Prevention

A

1) Clinical findings– Fever, chills, malaise
2) Treatment – Antibiotics
3) Prevention:`
– There is no human Vaccine
– Prevention involves pasteurization of milk and vaccination of animals.

342
Q

Helicobacter pylori

1) causes
2) Shape & gram
3) Pathogensis and epidemiology
4) Transmission
5) Treatment and prevention

A

1) causes gastritis and peptic ulcers.
2) Curved gram negative rods
3) * attaches to the mucus secreting cells of gastric mucosa leads to damage of mucosa
* loss of protective mucus leads to disease
* Natural habitat human stomach
* Often found in MALT lesion
4) * person to person
5) antibiotics + drug to reduce gastric acidity
- no vaccine

343
Q

Organism, type of pathogenesis, typical diseases, site of infection, main approach to therapy

1) Vibrio cholerae
2) Campylobacter jejuni
3) Helicobacter pylori

A

1) Vibrio cholerae- toxigenic, watery diahrrea, small intestine, fluid replacement
2) Campylobacter jejuni- inflammatory, bloody diahrreae, colon, antibiotics
3) Helicobacter pylori- inflammatory, gastritis & peptic ulcer, stomach duodenum, antibiotics

344
Q

Pse. aeruginosa a significant cause of?

A

urinary tract infection and sepsis in hospitalized patients, does not ferment glucose or reduce nitrates and is oxidase-positive. a strict aerobe and derives its energy from oxidation, not fermentation.

345
Q

Two organisms cause more than 80% of cases of bacterial meningitis in infants older than 2 months of age

A

Streptococcus - pneumoniae and N. meningitidis

346
Q

N. meningitidis ranks second to S. pneumoniae as a cause of meningitis but is the?

A

most common cause in persons between the ages of 2 and 18 years

Microbiology (35 decks)

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