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[9e] MODULE 7 UNIT 1: OTHER MEDICALLY - IMPORTANT BACTERIA > LECTURE > Flashcards

LECTURE Flashcards

1
Q

is the only genus in the Mycobacteriaceae family.

A

Mycobacterium

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2
Q

All mycobacteria are called [?]

A

acid-fast organisms

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3
Q

is a term that is used to describe bacteria that resist decolorization with acidified alcohol once they have been stained

A

Acid-fast

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4
Q

Acid-fast retain the pink to red color with

A

carbol fuchsin

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5
Q

The acid-fastness property of mycobacteria, that distinguishes them from other bacteria, depends on the integrity of their [?] that contain large amounts of lipids (long-chain fatty acids C78–C90) called mycolic acids or [?]

A

unique cell walls

hydroxymethoxy acids

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6
Q

Mycobacterium generally are considered gram-positive. However, because of their [?], the bacterial cells of mycobacteria do not stain well with crystal violet, the primary stain used in the Gram’s stain.

A

thick waxy cell wall

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7
Q

Mycobacterium are observed as [?] surrounded by a clear halo.

A

poorly or nonstaining bacilli

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8
Q

They may appear as either [?], which represents nonuniform staining of the bacilli, or almost as a [?] against the counterstained background, thus they are described as

A

beaded
negative image
“gram neutral,” or “gram ghost”

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9
Q
  • Acid-fast bacilli (AFB), very thin, slightly curved or straight rods (0.2-0.6 x 1-10 µm)
  • Nonmotile
  • Non–spore forming
  • Aerobic
  • Grow more slowly than most other human pathogenic bacteria
A

Mycobacterium

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10
Q

spore forming Mycobacterium

A

Mycobacterium marinum

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11
Q

The mycobacteria are divided into 3 major groups of based on fundamental differences in [?] and [?]

A

epidemiology and association with disease

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12
Q

refers to the mycobacterial species that occur in humans and are capable of causing tuberculosis: M. tuberculosis (MTB), M. bovis, and M. africanum.

A

Mycobacterium tuberculosis complex (MTBC)

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13
Q

consists of mycobacterial species that do not belong to the MTBC, thus it is also known as Mycobacteria Other Than Tubercle Bacilli (MOTT).

A

Nontuberculous Mycobacteria (NTM)

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14
Q

It is a diverse group of organisms commonly found in the environment, and the group includes both saprophytes and opportunistic human pathogens.

A

Nontuberculous Mycobacteria (NTM)

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15
Q

causes leprosy (Hansen’s disease). It is distinct from other mycobacteria because it does not grow in artificial culture media.

A

Mycobacterium leprae

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16
Q
  • Koch’s bacillus

* Human Tubercle Bacillus

A

Mycobacterium tuberculosis

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17
Q
  • Thin, slightly curved bacilli that measure 0.3 to 0.6 × 1 to 4 µm
  • Strongly acid-fast (pink to red staining), with a distinct beaded appearance due to volutin granules known as Much’s granules
  • Either grow as discrete rods in Chinese letter (X, Y, V & L) configuration, or as aggregates of numerous bacilli that are arranged in long, parallel strands called serpentine cords; cording is associated with virulent strains of MTB (due to cord factor, the unique mycolic acid (trehalose-6’6-dimycolate), and is observed in smear preparations from broth cultures.
  • Nonmotile
  • Non-spore-forming
  • Strict aerobe
  • Slow grower, with a generation time of 15-20 hours
  • Produces niacin
  • Produces heat-sensitive catalase
A

Mycobacterium tuberculosis

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18
Q

Humans are the only reservoir which generally infects the lungs, as facultative intracellular parasites in alveolar macrophages. But, they can also affect other parts of the body.

A

Mycobacterium tuberculosis

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19
Q

Transmission is by inhalation of droplet nuclei from a person with active disease in the lungs. It is estimated that less than 10 bacilli may initiate a pulmonary infection in a susceptible individual.

A

Mycobacterium tuberculosis

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20
Q

are propelled into the air when infectious person coughs, sneezes, sings, talks, or spits, or during respiratory manipulations such as bronchoscopy. They are more than 5 µm in diameter, so they immediately settle out of air. When inhaled, they become lodged in the [?] (the nose and throat), where infection is unlikely to develop. However, the smaller droplet nuclei, which are the dried-out residuals of droplets, may reach the alveoli, where infection begins.

A

Droplets containing tubercle bacilli

upper respiratory tract

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21
Q

When tubercle bacilli are inhaled, they reach the alveoli where they are phagocytized by alveolar macrophages and multiply.

A

Tuberculosis (TB)

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22
Q

Whether or not a person develops TB is determined by:

A
  1. immune status of the host
  2. amount of exposure
  3. strain of MTB
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23
Q
  • number of tubercle bacilli inhaled
  • virulence
  • anti-mycobacterial cellular immune response
A
  • amount of exposure
  • strain of MTB
  • immune status of the host
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24
Q

This is also referred to as “active tuberculosis”. It is a chronic (long-term) inflammatory disease, which presents as pulmonary TB (PTB) that may progress into extrapulmonary TB (EPTB), leading into death of patients who do not receive treatment.

A

TB disease

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25
Q

The term “tuberculosis” most often refers to the

A

disease state with signs and symptoms

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26
Q

refers to a case of TB involving the lung parenchyma

A

pulmonary TB (PTB)

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27
Q

A person with PTB disease shows the following four cardinal signs and symptoms:

A

i. at least two weeks duration of cough
ii. unexplained fever
iii. unexplained weight loss
iv. night sweats.

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28
Q

Other symptoms include chest pains, sputum production (with or without hemoptysis, i.e., coughing out of blood), and fatigue.

A

TB

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29
Q

refers to a case of TB involving organs other than the lungs (e.g. larynx, pleura, lymph nodes, abdomen, genitourinary tract, skin, joints and bones, meninges). Signs and symptoms may vary depending on the organ involved. it may coexist with PTB.

A

extrapulmonary TB

EPTB

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30
Q

This is also referred to as “latent tuberculosis infection” (LTBI). This occurs when a person has the tubercle bacilli within the
body, but the bacteria are present in very small numbers.
and they are kept under control by the body’s immune
system.

A

TB infection

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31
Q

A person with [?] has no symptoms, and is not infectious. i.e., he cannot spread the tubercle bacilli on to other people. In addition, unlike TB disease, he will usually have a normal chest x-ray and a negative sputum test, but a positive skin (tuberculin) test.

A

“latent tuberculosis infection” (LTBI)

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32
Q

Majority (about 90%) of those infected with MTB have LTBI, but some are at risk to develop active disease — including

A

young children and immunocompromised patients such as (PLHIV)

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33
Q

which stage of TB disease develops when a host has first contact with tubercle bacilli, usually during childhood. It may be in any part of the lung but is most often in the mid-lung fields which is well aerated, or the base.

A

Primary Tuberculosis

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34
Q

Primary Tuberculosis

the tubercle bacilli multiply virtually unrestricted within the phagosome of the nonactivated alveolar macrophages, until the
macrophages burst. Other macrophages begin to extravasate from peripheral blood. These macrophages also phagocytize MTB, but they are also nonactivated and hence, cannot destroy MTB. Tubercle bacilli spread from the initial site via the lymphatics to the regional
lymph nodes.

A

1 to 3 weeks after initial infection

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35
Q

Primary Tuberculosis

Mycobacterial proteins trigger Type IV hypersensitivity, which is often called delayed type hypersensitivity
(DTH) as the reaction takes several days to develop. At
this stage, lymphocytes begin to infiltrate. The infected macrophages present processed TB antigens on their
surface in association with MHC Class II to the
lymphocytes, specifically T-cells. This results in T-cell
activation and the liberation of cytokines including
gamma interferon (IFN), which causes the recruitment
and activation of macrophages.

A

3 to 4 weeks after, the host’s immune system mounts a complex, cell-mediated immune (CMI ) response

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36
Q

Primary Tuberculosis

Initial exposure most often results in [?]— an
exudative lesion which consists of inflammatory reaction with edema fluid, polymorphonuclear leukocytes and
later mononuclear cells around the tubercle bacilli; this may be self-limiting (heal) or may develop into
granulomatous type.

A

pneumonitis

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37
Q

Primary Tuberculosis

The activated macrophages form a cluster around the
infected macrophages resulting in productive or
proliferative lesions characterized by ganulomas, known as

A

tubercles

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38
Q

These are grayish white tissue
nodules, measuring 1-2 cm in diameter, and when fully
developed, consist of three (3) zones:

A

i. Central area of giant cells
ii. Mid zone of pale epithelioid cells
iii. Peripheral zone of fibroblasts, lymphocytes,
and monocytes

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39
Q

is large and multinucleated
resulting from the fusion of the cytoplasm of
macrophages

A

Giant cell

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40
Q

The tubercle is characterized by [?] where the center of the tubercle breaks down into necrotic lesion with semi-solid or “cheesy” consistency (L. caseus - cheese). It may heal by fibrosis followed by
calcification, where normal lung tissue is replaced by
calcium deposits.

A

“caseation necrosis”

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41
Q

This healed lesion (Ghon focus), along with hilar lymphadenopathy, is referred to as the [?]. Depending on the size and severity, the it may never subside. Typically it is readily visible as radio-opaque patches upon chest X-ray.

A

Ghon complex or primary complex

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42
Q

MTB cannot multiply within tubercles because of the

A

low pH and anoxic environment

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43
Q

MTB persist within the tubercles for extended periods

A

dormant

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44
Q

it is necessary to control an MTB infection and also responsible for much of the pathology associated with tuberculosis. Tubercles cause blockade of blood flow which will contribute to further necrosis of the tissue

A

cell-mediated immune (CMI) response

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45
Q

is evident through the tuberculin reaction in skin tests

A

host’s CMI against the tubercle bacilli

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46
Q

will not aid in the control of a MTB infection because MTB is intracellular and if extracellular, it is resistant to complement killing due to the high lipid concentration in its cell wall

A

antibody-mediated immune (AMI) rsponse

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47
Q

stage of TB that occurs in adults due to the reactivation and replication of dormant tubercle bacilli from the primary lesion. The progression to disease occurs, weeks, months or years after the primary episode of infection.

A

Secondary (Reactivation) Tuberculosis

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48
Q

Secondary (Reactivation) Tuberculosis

these liquefy, rupture, discharge their contents and form air-filled tuberculous
cavities; this liquid is very conducive to MTB growth and hence the organism begins to rapidly multiply extracellularly. This also allows MTB to spill into other airways and rapidly spread to other parts of the lung. The lesions are usually
localized in the apices of the lungs,
where the oxygen tension (PO2) is
highest.

A

caseous centers of the tubercles

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49
Q

Secondary (Reactivation) Tuberculosis

is characterized by chronic tissue
lesions, the formation of tubercles,
caseation, and fibrosis. Regional lymph nodes are only slightly involved, and they do not caseate

A

Reactivation tuberculosis

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50
Q

This refers to the seeding of many organs outside the pulmonary tree with tubercle bacilli through the blood
stream. The most common sites of spread of MTB are the spleen, highly oxygenated parts of the host’s body such
as the liver, bone marrow (especially of long bones), kidney, as well as the adrenal gland and in some cases the genital tract, usually in that order of occurrence.

A

Extrapulmonary Tuberculosis (EPTB) or Dissemination Tuberculosis

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51
Q

Extrapulmonary Tuberculosis (EPTB) or Dissemination Tuberculosis

The bloodstream can also be invaded by erosion of a vein by a [?] or lymph node. If a caseating lesion discharges its contents into a bronchus, they are aspirated and distributed to other parts of the lungs or are swallowed and passed into the stomach and intestines

A

caseating tubercle

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52
Q

Extrapulmonary Tuberculosis (EPTB) or Dissemination Tuberculosis

is derived from the fact that metastasizing tubercles are about the same size as a millet seed, a grain commonly grown in Africa

A

miliary tuberculosis

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53
Q

results in necrosis and scarring of the
renal medulla and the pelvis, ureters, and bladder. This damage is accompanied by painful urination, fever, and the presence of blood and the TB bacillus in urine

A

Renal tuberculosis

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54
Q

in males damages the prostate
gland, epididymis, seminal vesicles, and testes; in females, the fallopian tubes, ovaries, and uterus. It often affects the reproductive function in both sexes

A

Genital tuberculosis

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55
Q

is a combo complication. The spine is a frequent site of infection, though the hip, knee, wrist, and elbow can also be involved.

A

Tuberculosis of the bone and joint

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56
Q

Advanced infiltration of the vertebral column produces degenerative changes that collapse the vertebrae , resulting in abnormal curvature of the thoracic region (humpback or kyphosis) or the lumbar region (swayback or lordosis). Neurological damages stemming form compression on nerves can cause extensive paralysis and sensory loss.

A

Pott’s disease

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57
Q

is the result of an active brain lesion seeding bacilli into the meninges. Over a period of several weeks, the infection of the cranial compartments can create mental deterioration,
permanent retardation, blindness, and deafness. Untreated tubercular meningitis is invariably fatal.

A

Tuberculous meningitis

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58
Q

Inhibits migration of WBCs to the site of infection and causes chronic granulomas

A

Cord factor (trehalose-6’6-dimycolate)

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59
Q

Prevents fusion of phagosome and lysosome allowing MTB to survive and multiply within macrophages

A

Sulfatides

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60
Q

High lipid concentration in cell wall accounts for impermeability and
resistance to antimicrobial agents, resistance to killing by acidic and alkaline
compounds in both the intracellular and extracellular environment, and resistance to osmotic lysis via complement deposition and attack by lysozyme

A

Mycolic acid

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61
Q

Because of MTB’s [?], the immune system may not readily recognize the bacteria or may not be triggered sufficiently to eliminate them

A

Slow generation time

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62
Q

The intracellular location of MTB is an
effective means of evading the immune system. In particular, antibodies and
complement are ineffective. Caseous materials block the penetration of drugs. This is attributed to the necessity for protracted (prolonged) therapy against TB, which usually lasts for 6-9 months

A

Intracellular growth and granuloma formation

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63
Q

Cows serve as the primary reservoirs; it is the etiologic agent of TB in cow; Bovine tubercle bacilli

A

Mycobacterium bovis

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64
Q

Rarely, humans are infected by the consumption of [?] from

tuberculous cows

A

unpasteurized milk

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65
Q

It causes gastrointestinal TB, a disease in humans closely resembling that caused by MTB and is treated similarly

A

Mycobacterium bovis

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66
Q

This route of transmission can lead to the development of extrapulmonary TB, exemplified in history by bone infections that led to hunched backs. Rarely, the organisms can enter through abraded skin

A

Mycobacterium bovis

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67
Q

It is an intermediate form between MTB and M. bovis

A

Mycobacterium africanum

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68
Q

Mode of transmission and pathogenesis are similar to M. tuberculosis

A

Mycobacterium africanum

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69
Q

Found in East and West tropical Africa

A

Mycobacterium africanum

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70
Q

Other MTBC species include

A 
M. caprae
M. microti
M. canettii
M. mungi
M. orygis
M. pinnipedii
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71
Q

Vaccine against MTB is called

A

BCG (Bacillus of Calmette and Guerin)

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72
Q

BCG is consists of a live attenuated strain derived from [?]. It is given at birth (or anytime after birth) as a single dose by
intradermal route. It is a component part of the National Immunization
Program in the Philippines.

A

Mycobacterium bovis

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73
Q

The BCG vaccine is not 100% effective. Studies suggest a [?] % effective
rate in children.

A

60-80%

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74
Q

The BCG vaccine does not prevent [?], only disease. BCG given at
earliest possible age protects the possibility of TB meningitis and other TB
infections in which infants are prone.

A

infection

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75
Q

The BCG vaccine cannot circumvent [?] in previously exposed individuals

A

disease reactivation

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76
Q

BCG Vaccination may complicate the way the tuberculin skin test is read
because it causes [?]. In places that do not vaccinate, the skin test may be used to monitor the effectiveness of antibiotic therapy.

A

false positives

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77
Q

Prompt initiation of effective TB treatment of people with TB disease is recommended to reduce MTB transmission.

A

Treatment

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78
Q

Treatment is given to individuals who are at risk of developing active TB disease to reduce that risk and transmission. Also referred to as LTBI treatment or preventive therapy.

A

TB Preventive treatment (TPT)

79
Q

Covering one’s mouth when coughing minimizes the spread of potentially infectious aerosols, including those laden with MTB. Surgical face masks should be used among patients presumed or confirmed to have infectious PTB until they are deemed non-infectious.

A

Respiratory separation

80
Q

[?] people with presumed or demonstrated infectious TB is recommended to reduce MTB transmission

A

Isolation

81
Q

have greatly reduced M. bovis infections.

A

Eradication of tuberculosis in cattle; pasteurization of milk

82
Q

A classification for Nontuberculous Mycobacteria (NTP) was introduced by [?] in 1959.

A

Ernest Runyon

83
Q

Four groups of NTM are classified based on 2 criteria

A
  1. Growth rate

2. Colonial pigmentation

84
Q
  • produce colonies in >7 days.
A

a. Slow growers (Runyon groups I, II, and III)

85
Q
  • produce colonies in <7 days.
A

b. Rapid growers (Runyon groups IV)

86
Q

based on the abillity/inability of NTM to synthesize

carotenoids (a group of yellow to red pigments) with or without light

A

Colonial pigmentation

87
Q

(Runyon group I)
(Runyon group II)
(Runyon groups III and IV)

A

a. Photochromogens
b. Scotochromogens
c. Nonphotochromogens

88
Q

a. Slow growers - produce colonies in >7 days

A

Runyon groups I, II, and III

89
Q

b. Rapid growers - produce colonies in <7 days

A

Runyon groups IV

90
Q

Assessment of Photoreactivity of Mycobacteria

  1. Inoculate the surfaces of three Löwenstein–Jensen slant media or three
    [?] agar plates with fluid from a dilute broth culture of the
    organism to be tested. Wrap two of the tubes or plates with aluminum
    foil; leave the third exposed to the ambient light in the incubator.
A

Middlebrook 7H11

91
Q

Assessment of Photoreactivity of Mycobacteria

  1. Incubate one of the wrapped tubes or plates at [?]; the other
    wrapped tubes or plates at 37°C.
A

25°C–30°C

92
Q

Assessment of Photoreactivity of Mycobacteria

  1. Several days after growth is noted in the light-exposed control tube or
    plate, examine the [?] or plates for growth.
A

wrapped tubes

93
Q

Assessment of Photoreactivity of Mycobacteria

  1. If early growth is detected in the wrapped tubes or plates, expose one of
    each pair to a strong light for approximately 5 hours. A [?]
    bulb or fluorescent equivalent is adequate. Loosen the cap of the culture
    tube during this period of light exposure.
A

100-W tungsten

94
Q

Assessment of Photoreactivity of Mycobacteria

  1. Following exposure to light, the tube or plate is returned to the incubator
    and inspected after [?] for the appearance of yellow pigment.
A

24–48 hours

95
Q 
NTM colonies that develop yellow
pigment on exposure to light after being
grown in the dark (nonpigmented in
dark) and take longer than 7 days to
appear on solid media
A

Runyon Group I

PHOTOCHROMOGENS

96
Q

NTM colonies that develop pigment in
the dark or light and take longer than 7
days to appear on solid media

A

Runyon Group II

SCOTOCHROMOGENS

97
Q

NTM colonies that are nonpigmented
regardless of whether they are grown in
the dark or light and take longer than 7
days to appear on solid media

A

Runyon Group III

NONPHOTOCHROMOGENS

98
Q

NTM colonies that grow on solid media

and take fewer than 7 days to appear

A

Runyon Group IV

RAPID GROWERS

99
Q

M. marinum
M. kansasii
M. simiae
M. asiaticum

A

Runyon Group I

PHOTOCHROMOGENS

100
Q

M. scrofulaceum
M. szulgai (35-37 oC)
M. gordonae
M. flavescens

A

Runyon Group II

SCOTOCHROMOGENS

101
Q 
M. avium complex
M. genavense
M. gastri
M. malmoense
M. haemophilum
M. shimoidei
M. ulcerans
M. xenopi
M. terrae-M. triviale complex
M. nonchromogenicum
A

Runyon Group III

NONPHOTOCHROMOGENS

102
Q

M. fortuitum
M. chelonae
M. abscessus
M. smegmatis

A

Runyon Group IV

RAPID GROWERS

103
Q

Widely present in fresh and salt water, and have been implicated in diseases of fish

A

Mycobacterium marinum

104
Q

Causes cutaneous infections in humans when traumatized skin comes into
contact with salt water or inadequately chlorinated freshwater containing the
organism

A

Mycobacterium marinum

105
Q

Lesion usually appears 2–3 weeks after inoculation and typically presents as single, tender red or blue-red subcutaneous nodule, or “swimming pool granuloma” or “fish tank granuloma”, usually occurring on the elbow, knee, toe, or finger and often becomes verrucous or ulcerated

A

Mycobacterium marinum

106
Q

Grows best at 30-32 oC; negative or no growth at 37 oC

A

Mycobacterium marinum

107
Q

Was first described as the “yellow bacillus”

A

Mycobacterium marinum

108
Q

Strains have been isolated from water, but the natural source of human
infection is not clear. Infections caused are not normally considered
contagious from person to person

A

Mycobacterium kansasii

109
Q

It can produce pulmonary and systemic disease indistinguishable from tuberculosis, especially in patients with impaired immune responses. Extrapulmonary infections, including lymphadenitis, skin and soft tissue
infections, and joint infection, have been reported occasionally. Disseminated
infection rarely occurs in immunocompetent individuals but has been reported in severely immunocompromised patients, particularly those with AIDS

A

Mycobacterium kansasii

110
Q

Optimum growth occurs 37oC; grows slowly at 24 oC; and, negative growth at
42 oC

A

Mycobacterium kansasii

111
Q

Original strains were isolated from lymph nodes of monkeys and some were
recovered from tap water

A

Mycobacterium simiae

112
Q

Infrequent cases of human infection have been reported and are often
associated with HIV-positive patients which manifests itself as pulmonary
disease, but lymphadenitis, skin lesions, and other presentations have been
reported

A

Mycobacterium simiae

113
Q

Occurs in the environment under moist conditions

A

Mycobacterium scrofulaceum

114
Q

Cause of cervical lymphadenitis (known as scrofula) especially in children.
Infection manifests itself in one or more enlarged lymph nodes, often adjacent
to the mandible and high in the neck, with little or no pain and are usually
treated by surgical incision and drainage

A

Mycobacterium scrofulaceum

115
Q

Has no temperature preference; grows at 25 oC, 32 oC, and 37 oC

A

Mycobacterium scrofulaceum

116
Q

Is rarely recovered from the environment, its isolation is almost always considered clinically significant

A

Mycobacterium szulgai

117
Q

The most common manifestation is pulmonary disease similar to TB.
Extrapulmonary infections, including lymphadenitis and bursitis, also have been reported.

A

Mycobacterium szulgai

118
Q

Is a photochromogen at 25 oC, but a scotochromogen at 35-37 oC

A

Mycobacterium szulgai

119
Q

“Tap water bacillus”, typically found in aqueous environments

A

Mycobacterium gordonae

120
Q

Is generally a nonpathogen and is possibly the mycobacterium that is
recovered in clinical laboratories with greatest frequency as a contaminant

A

Mycobacterium gordonae

121
Q

It rarely causes human infections which include meningitis secondary to
involvement of ventriculoatrial shunts, hepatoperitoneal disease, endocarditis
in a prosthetic aortic valve, cutaneous lesions of the hand, and possibly
patients with pulmonary involvement

A

Mycobacterium gordonae

122
Q

Refers to strains of M. avium and M. intracellulare

A

Mycobacterium avium complex (MAC)

123
Q

“Battery bacillus”

A

Mycobacterium avium complex (MAC)

124
Q

Transmission to man is via the gastrointestinal tract, but transmission via the respiratory tract is also possible.

A

Mycobacterium avium complex (MAC)

125
Q

Causes pulmonary infections and other clinical; manifestations in individuals
with underlying lung disease, old age, immunosuppression, and depleted T-cell
immunity such as those in advanced AIDS

A

Mycobacterium avium complex (MAC)

126
Q

Grows at 35-37 oC and 42 oC; no growth at 24 oC

A

Mycobacterium avium complex (MAC)

127
Q

Is endemic in areas of Australia (where it was first isolated), Zaire, Uganda,
Nigeria, Ghana, Cameroon, Malaysia, New Guinea, Guyana, and Mexico

A

Mycobacterium ulcerans

128
Q

Its natural reservoir and usual route of its transmission to humans remain
unknown

A

Mycobacterium ulcerans

129
Q

Implicated in skin infection that forms nodules and ulcerates (referred to as
Bairnsdale ulcer in Australia, and Buruli ulcer in Uganda)n younger than 15 year

A

Mycobacterium ulcerans

130
Q

Grows best at 30-32 oC; negative or no growth at 37 oC

A

Mycobacterium ulcerans

131
Q

Was first isolated from a toad of the genus Xenopus

A

Mycobacterium xenopi

132
Q

Birds are a possible natural reservoir.

A

Mycobacterium xenopi

133
Q

Has been cultured from hot and cold water taps, hospital hot water generators
and storage tanks, and other environmental sources

A

Mycobacterium xenopi

134
Q 
Infections range from pulmonary disease of varying chronicity, focal
extrapulmonary infections (osteomyelitis, arthritis, lymphadenitis), and
disseminated disease in persons with AIDS
A

Mycobacterium xenopi

135
Q

Optimum growth occurs at 42 oC; positive growth at 35-37 oC; and negative growth at 25 oC

A

Mycobacterium xenopi

136
Q

Produces a “bird’s nest” appearance with sticklike projections on Middlebrook
7H10 medium

A

Mycobacterium xenopi

137
Q

Unique in its growth requirement for hemoglobin or hemin

A

Mycobacterium haemophilum

138
Q

Disease most commonly is manifested by multiple cutaneous nodules, ulcers, or
painful swellings, typically involving the extremities, which occasionally become
abscesses

A

Mycobacterium haemophilum

139
Q

Although uncommon, infections are usually seen in persons who have an
underlying immunodeficiency such as lymphoma, exogenous immunosuppression after organ transplantation, or AIDS, but lymphadenitis in otherwise healthy children has also been reported

A

Mycobacterium haemophilum

140
Q

Common in the environment and has been isolated from water, soil, and dust

A

Mycobacterium fortuitum

141
Q

It has been implicated frequently in infections of the skin and soft tissues,
including localized infections and abscesses at the site of puncture wounds

A

Mycobacterium fortuitum

142
Q

Infections associated with long-term use of intravenous and peritoneal
catheters, injection sites, and surgical wounds

A

Mycobacterium fortuitum

143
Q

Is found in the environment and is associated with many of the same
opportunistic infections as those associated with M. fortuitum

A

Mycobacterium chelonae

144
Q

This rapidly growing species most likely isolated from disseminated cutaneous
infections in immunocompromised patients including a variety of infections of
the skin, lungs, bone, central nervous system, and prosthetic heart valves

A

Mycobacterium chelonae

145
Q

Is now more specifically referred to as Mycobacterium abscessus subspecies
abscessus

A

Mycobacterium abscessus

146
Q

Tap water is an essential reservoir for this rapid grower

A

Mycobacterium abscessus

147
Q

It is commonly isolated in association with chronic lung disease, otitis media
following tympanostomy tube insertion, and disseminated cutaneous
infections

A

Mycobacterium abscessus

148
Q

It is associated with approximately 80% of the cases of pulmonary disease
caused by rapidly growing mycobacteria have also been seen in patients with
cystic fibrosis

A

Mycobacterium abscessus

149
Q

A commonly considered as a saprophyte has been implicated in rare cases of
pulmonary, skin, soft tissue, and bone infections

A

Mycobacterium smegmatis

150
Q

Hansen’s bacillus

A

Mycobacterium leprae

151
Q
  • Aerobic, acid-fast bacilli
  • Obligately intracellular
  • Has not been be cultured in vitro; but, can been grown in footpads of mice and in armadillos
  • Optimal growth at less than body temperature
A

Mycobacterium leprae

152
Q

Humans are the sole reservoir; In infected individuals, it is inhabiting skin (sparing warm areas such as armpit, groin and perineum), and the superficial nerves. It is intracellular typically within skin histiocytes and endothelial cells and the Schwann cells of the peripheral nerves

A

Mycobacterium leprae

153
Q

Genetically identical species have also been isolated form [?] that develop a granulomatous disease similar to leprosy

A

armadillos

154
Q

Spread from person-to-person requires prolonged contact with infected person. The most common mode of transmission is by inhalation of infectious aerosols from nasal secretions, and less commonly by skin contact with skin lesions.

A

Mycobacterium leprae

155
Q

It is a chronic, progressive disease of the skin and the nerves with a usual incubation period varying from 2 to 5 years, with extremes of 23 months to 40 years.

A

Leprosy or Hansen’s disease

156
Q

Leprosy. From Greek lepros, meaning

[?]. Translated from a Hebrew word that refers to “uncleanliness”

A

“scaly” or “rough”

157
Q

Leprosy

Macrophages successfully destroy the bacilli, and there are no manifestations of disease in healthy persons. However, in small percentage of cases, a weakened or slow macrophage and T-cell
response leads to [?] of the pathogen.

A

intracellular survival

158
Q

In untreated cases of Leprosy, the bacilli grow slowly in the skin macrophages and
Schwann cells of peripheral nerves, and the disease progresses to one of several
outcomes. The neurological involvement in leprosy results in [?] leading to deformities and disability.

A

sensory-motor deficits

159
Q

Its most severe effect is early damage to the nerves that control the muscles of the hands and feet which result to [ ? or ?]. Sensory nerve damage can also lead to trauma and loss of fingers and toes.

A

drop foot and claw hands

160
Q

Deformation of the hands in leprosy.

The clawing and muscle wasting are
chiefly due to nerve damage hat interfere
with the [?] activity. Individuals in a later phase of the disease
can loose their fingers or their hands.

A

musculoskeletal

161
Q
  • The WHO expert committee on leprosy has defined a case of leprosy as
    an individual who has one of the following cardinal signs:
    = a definite loss of sensation in
    a pale (hypopigmented) or reddish skin patch
  • a thickened or enlarged
    peripheral nerve with a loss of sensation and/or weakness in the
    muscles supplied by the nerve
  • the presence of acid-fast bacilli in an
A

i. Cutaneous lesion and anesthesia:
ii. Peripheral nerve involvement:
iii. Slit Skin Smear (SSS)

162
Q

Leprosy is defined by the [?] manifestations of the disease, which are due to the variability in the type and strength of the
body’s immune response thus making diagnosis difficult

A

‘spectral’

163
Q

This classifies leprosy as
an immune-mediated spectral disease. The five-group system reflects
the host response or level of cellular immunity which results in the wide
variation in disease manifestation and prognosis.

A

Ridley-Jopling Classification for Leprosy (1966)

164
Q

There are two (2) polar types of leprosy:; one at the end of the spectrum and one at the other; CLINICALLY STABLE

A 
Tuberculoid leprosy (TT)
Lepromatous leprosy (LL)
165
Q

Immunologically, strong CMI correlates with the [?]

Weak CMI correlates with the [?]

A
  • TT type

- LL type

166
Q

Leprosy is a continuum of disease, which usually starts out with an indeterminate stage called

A

“borderline”

167
Q

moving up the spectrum - towards [?]

  • upgrading, and the prognosis is good
  • TT lesion can even self-heal
  • nerve damage-related disability can occur
A

TT

168
Q

moving down the spectrum - towards [?]

  • downgrading
  • prognosis is poor
  • LL can be fatal
A

LL

169
Q

Infection of the skin and mucus membranes of the nose, lips, chin, and brows produces a moderate facial deformation, typical of lepromas.

A

lepromatous leprosy

170
Q

lesions appear as shallow lesions

(a)Infection in dark-skinned
persons manifests as
hypopigmented patches or
macules.
(b)In light-skinned individuals,
it appears as reddish
patches or papules.
A

Tuberculous leprosy

171
Q

CUTANEOUS LESIONS

  • Erythematous or hypopigmented plaques with flat centers and raised demarcated borders
  • <5 lesions, usually solitary, <10 cm diameter
  • Dry, scaly and infiltrated
  • Hairless
  • Completely anesthetic (no sensation)
A

TUBERCULOID LEPROSY

172
Q

CUTANEOUS LESIONS

  • Macules, plaques, and nodular lesions (called lepromas). Diffuse dermal infiltration causes earlobe enlargement, nasal root widening (“saddle nose”), skin thrown into folds (“leonine facies”), fusiform swelling of fingers
  • Numerous lesions showing tendency to symmetry in distribution.
  • Shiny
  • Almost normal initially Madarosis (loss of eyebrow)
  • Patchy sensory loss
A

LEPROMATOUS LEPROSY

173
Q

NERVE INVOLVEMENT

  • Asymmetrical, single nerve enlargement
  • Nerve to patch may be palpable
A

TUBERCULOID LEPROSY

174
Q

NERVE INVOLVEMENT

  • Symmetrical involvement of nerve trunks with glove and stocking anesthesia
  • Nerves may feel normal on palpation or may be thickened
A

LEPROMATOUS LEPROSY

175
Q

CELL-MEDIATED IMMUNITY

-Strong

A

TUBERCULOID LEPROSY

176
Q

CELL-MEDIATED IMMUNITY

-Week

A

LEPROMATOUS LEPROSY

177
Q

NUMBER OF ORGANISMS IN TISSUES

-Low

A

TUBERCULOID LEPROSY

178
Q

NUMBER OF ORGANISMS IN TISSUES

-High

A

LEPROMATOUS LEPROSY

179
Q

INFECTIVITY

-Low

A

TUBERCULOID LEPROSY

180
Q

INFECTIVITY

-High

A

LEPROMATOUS LEPROSY

181
Q
  • Isolation of leprosy patients
  • Chemoprophylaxis and constant surveillance of high risk populations to discover early cases, particularly among those in close contact (household members and/or relatives) with leprotics.
  • Therapeutic trials may also be indicated for patients whose signs and symptoms are suggestive of leprosy but who do not have a definitive diagnosis.
A

Leprosy

182
Q

is primarily controlled by prompt antimicrobial therapy which is most effective when performed before permanent damage to nerves and other tissues has occurred.

A

M. leprae infection

183
Q

There [?] named Nocardia spp., and more than half have reportedly been isolated from humans.

A

> 100

184
Q

The most commonly encountered species are

A

Nocardia brasiliensis, N. cyriacigeorgica, N. farcinica, N. abscessus complex, and N. nova

185
Q
  • They are long, thin, beaded (irregularly spaced),

aerobic, gram-positive bacilli

A

Nocardia species

186
Q
  • The cells remain together after division to form
    elongated chains of bacteria with occasional
    “tree-like” branches.
A

Nocardia species

187
Q
  • They are partially (or weakly) acid fast — they are
    able to retain the primary stain only when a weak
    acid is used as the decolorizer during the acid-fast
    staining process. This characteristic is also known
    as modified acid-fast positive.
A

Nocardia species

188
Q
  • The nocardiae are found in soil and organic
    material worldwide and cause disease in many
    animals and in fish.
A

Nocardia species

189
Q
  • Infections result either by inhalation of the
    organism from soil or dust or following trauma and
    contact with contaminated soil.
A

Nocardia species

190
Q

in most cases is an opportunistic infection associated with risk factors, most of which impair the cell-mediated immune responses, including corticosteroid treatment, immunosuppression, AIDS, and alcoholism

A

Nocardiosis

191
Q

The most common form of infection with Nocardia species

A

Pulmonary nocardiosis

192
Q

Pulmonary nocardiosis

The initial lesion in the lung is often a [?] that advances to necrosis. The abscesses that form can extend into the tissue and coalesce with each other. Sputum is thick and purulent. Dissemination to other organs, especially the brain, may occur, and may involve virtually every organ

A

pneumonitis

193
Q

[?] is the most frequent cause of Cutaneous nocardiosis, which is
usually seen in the hands and feet as a result of minor trauma, such as from a thorn or wood sliver

A

N. brasiliensis

194
Q

Cutaneous nocardiosis begins as a localized subcutaneous abscess that is invasive and may cause destruction of the tissues and underlying bone. These lesions are termed

A

actinomycotic mycetomas

[9e] MODULE 7 UNIT 1: OTHER MEDICALLY - IMPORTANT BACTERIA (2 decks)

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