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
The term "tuberculosis" most often refers to the
disease state with signs and symptoms
26
refers to a case of TB involving the lung parenchyma
pulmonary TB (PTB)
27
A person with PTB disease shows the following four cardinal signs and symptoms:
i. at least two weeks duration of cough ii. unexplained fever iii. unexplained weight loss iv. night sweats.
28
Other symptoms include chest pains, sputum production (with or without hemoptysis, i.e., coughing out of blood), and fatigue.
TB
29
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.
extrapulmonary TB | EPTB
30
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.
TB infection
31
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.
"latent tuberculosis infection" (LTBI)
32
Majority (about 90%) of those infected with MTB have LTBI, but some are at risk to develop active disease --- including
young children and immunocompromised patients such as (PLHIV)
33
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.
Primary Tuberculosis
34
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.
1 to 3 weeks after initial infection
35
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.
3 to 4 weeks after, the host’s immune system mounts a complex, cell-mediated immune (CMI ) response
36
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.
pneumonitis
37
Primary Tuberculosis The activated macrophages form a cluster around the infected macrophages resulting in productive or proliferative lesions characterized by ganulomas, known as
tubercles
38
These are grayish white tissue nodules, measuring 1-2 cm in diameter, and when fully developed, consist of three (3) zones:
i. Central area of giant cells ii. Mid zone of pale epithelioid cells iii. Peripheral zone of fibroblasts, lymphocytes, and monocytes
39
is large and multinucleated resulting from the fusion of the cytoplasm of macrophages
Giant cell
40
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.
"caseation necrosis"
41
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.
Ghon complex or primary complex
42
MTB cannot multiply within tubercles because of the
low pH and anoxic environment
43
MTB persist within the tubercles for extended periods
dormant
44
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
cell-mediated immune (CMI) response
45
is evident through the tuberculin reaction in skin tests
host’s CMI against the tubercle bacilli
46
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
antibody-mediated immune (AMI) rsponse
47
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.
Secondary (Reactivation) Tuberculosis
48
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.
caseous centers of the tubercles
49
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
Reactivation tuberculosis
50
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.
Extrapulmonary Tuberculosis (EPTB) or Dissemination Tuberculosis
51
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
caseating tubercle
52
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
miliary tuberculosis
53
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
Renal tuberculosis
54
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
Genital tuberculosis
55
is a combo complication. The spine is a frequent site of infection, though the hip, knee, wrist, and elbow can also be involved.
Tuberculosis of the bone and joint
56
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.
Pott’s disease
57
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.
Tuberculous meningitis
58
Inhibits migration of WBCs to the site of infection and causes chronic granulomas
Cord factor (trehalose-6’6-dimycolate)
59
Prevents fusion of phagosome and lysosome allowing MTB to survive and multiply within macrophages
Sulfatides
60
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
Mycolic acid
61
Because of MTB's [?], the immune system may not readily recognize the bacteria or may not be triggered sufficiently to eliminate them
Slow generation time
62
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
Intracellular growth and granuloma formation
63
Cows serve as the primary reservoirs; it is the etiologic agent of TB in cow; Bovine tubercle bacilli
Mycobacterium bovis
64
Rarely, humans are infected by the consumption of [?] from | tuberculous cows
unpasteurized milk
65
It causes gastrointestinal TB, a disease in humans closely resembling that caused by MTB and is treated similarly
Mycobacterium bovis
66
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
Mycobacterium bovis
67
It is an intermediate form between MTB and M. bovis
Mycobacterium africanum
68
Mode of transmission and pathogenesis are similar to M. tuberculosis
Mycobacterium africanum
69
Found in East and West tropical Africa
Mycobacterium africanum
70
Other MTBC species include
``` M. caprae M. microti M. canettii M. mungi M. orygis M. pinnipedii ```
71
Vaccine against MTB is called
BCG (Bacillus of Calmette and Guerin)
72
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.
Mycobacterium bovis
73
The BCG vaccine is not 100% effective. Studies suggest a [?] % effective rate in children.
60-80%
74
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.
infection
75
The BCG vaccine cannot circumvent [?] in previously exposed individuals
disease reactivation
76
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.
false positives
77
Prompt initiation of effective TB treatment of people with TB disease is recommended to reduce MTB transmission.
Treatment
78
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.
TB Preventive treatment (TPT)
79
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.
Respiratory separation
80
[?] people with presumed or demonstrated infectious TB is recommended to reduce MTB transmission
Isolation
81
have greatly reduced M. bovis infections.
Eradication of tuberculosis in cattle; pasteurization of milk
82
A classification for Nontuberculous Mycobacteria (NTP) was introduced by [?] in 1959.
Ernest Runyon
83
Four groups of NTM are classified based on 2 criteria
1. Growth rate | 2. Colonial pigmentation
84
- produce colonies in >7 days.
a. Slow growers (Runyon groups I, II, and III)
85
- produce colonies in <7 days.
b. Rapid growers (Runyon groups IV)
86
based on the abillity/inability of NTM to synthesize | carotenoids (a group of yellow to red pigments) with or without light
Colonial pigmentation
87
(Runyon group I) (Runyon group II) (Runyon groups III and IV)
a. Photochromogens b. Scotochromogens c. Nonphotochromogens
88
a. Slow growers - produce colonies in >7 days
Runyon groups I, II, and III
89
b. Rapid growers - produce colonies in <7 days
Runyon groups IV
90
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.
Middlebrook 7H11
91
Assessment of Photoreactivity of Mycobacteria 2. Incubate one of the wrapped tubes or plates at [?]; the other wrapped tubes or plates at 37°C.
25°C–30°C
92
Assessment of Photoreactivity of Mycobacteria 3. Several days after growth is noted in the light-exposed control tube or plate, examine the [?] or plates for growth.
wrapped tubes
93
Assessment of Photoreactivity of Mycobacteria 4. 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.
100-W tungsten
94
Assessment of Photoreactivity of Mycobacteria 5. Following exposure to light, the tube or plate is returned to the incubator and inspected after [?] for the appearance of yellow pigment.
24–48 hours
95
``` 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 ```
Runyon Group I | PHOTOCHROMOGENS
96
NTM colonies that develop pigment in the dark or light and take longer than 7 days to appear on solid media
Runyon Group II | SCOTOCHROMOGENS
97
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
Runyon Group III | NONPHOTOCHROMOGENS
98
NTM colonies that grow on solid media | and take fewer than 7 days to appear
Runyon Group IV | RAPID GROWERS
99
M. marinum M. kansasii M. simiae M. asiaticum
Runyon Group I | PHOTOCHROMOGENS
100
M. scrofulaceum M. szulgai (35-37 oC) M. gordonae M. flavescens
Runyon Group II | SCOTOCHROMOGENS
101
``` M. avium complex M. genavense M. gastri M. malmoense M. haemophilum M. shimoidei M. ulcerans M. xenopi M. terrae-M. triviale complex M. nonchromogenicum ```
Runyon Group III | NONPHOTOCHROMOGENS
102
M. fortuitum M. chelonae M. abscessus M. smegmatis
Runyon Group IV | RAPID GROWERS
103
Widely present in fresh and salt water, and have been implicated in diseases of fish
Mycobacterium marinum
104
Causes cutaneous infections in humans when traumatized skin comes into contact with salt water or inadequately chlorinated freshwater containing the organism
Mycobacterium marinum
105
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
Mycobacterium marinum
106
Grows best at 30-32 oC; negative or no growth at 37 oC
Mycobacterium marinum
107
Was first described as the “yellow bacillus”
Mycobacterium marinum
108
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
Mycobacterium kansasii
109
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
Mycobacterium kansasii
110
Optimum growth occurs 37oC; grows slowly at 24 oC; and, negative growth at 42 oC
Mycobacterium kansasii
111
Original strains were isolated from lymph nodes of monkeys and some were recovered from tap water
Mycobacterium simiae
112
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
Mycobacterium simiae
113
Occurs in the environment under moist conditions
Mycobacterium scrofulaceum
114
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
Mycobacterium scrofulaceum
115
Has no temperature preference; grows at 25 oC, 32 oC, and 37 oC
Mycobacterium scrofulaceum
116
Is rarely recovered from the environment, its isolation is almost always considered clinically significant
Mycobacterium szulgai
117
The most common manifestation is pulmonary disease similar to TB. Extrapulmonary infections, including lymphadenitis and bursitis, also have been reported.
Mycobacterium szulgai
118
Is a photochromogen at 25 oC, but a scotochromogen at 35-37 oC
Mycobacterium szulgai
119
“Tap water bacillus”, typically found in aqueous environments
Mycobacterium gordonae
120
Is generally a nonpathogen and is possibly the mycobacterium that is recovered in clinical laboratories with greatest frequency as a contaminant
Mycobacterium gordonae
121
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
Mycobacterium gordonae
122
Refers to strains of M. avium and M. intracellulare
Mycobacterium avium complex (MAC)
123
"Battery bacillus"
Mycobacterium avium complex (MAC)
124
Transmission to man is via the gastrointestinal tract, but transmission via the respiratory tract is also possible.
Mycobacterium avium complex (MAC)
125
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
Mycobacterium avium complex (MAC)
126
Grows at 35-37 oC and 42 oC; no growth at 24 oC
Mycobacterium avium complex (MAC)
127
Is endemic in areas of Australia (where it was first isolated), Zaire, Uganda, Nigeria, Ghana, Cameroon, Malaysia, New Guinea, Guyana, and Mexico
Mycobacterium ulcerans
128
Its natural reservoir and usual route of its transmission to humans remain unknown
Mycobacterium ulcerans
129
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
Mycobacterium ulcerans
130
Grows best at 30-32 oC; negative or no growth at 37 oC
Mycobacterium ulcerans
131
Was first isolated from a toad of the genus Xenopus
Mycobacterium xenopi
132
Birds are a possible natural reservoir.
Mycobacterium xenopi
133
Has been cultured from hot and cold water taps, hospital hot water generators and storage tanks, and other environmental sources
Mycobacterium xenopi
134
``` Infections range from pulmonary disease of varying chronicity, focal extrapulmonary infections (osteomyelitis, arthritis, lymphadenitis), and disseminated disease in persons with AIDS ```
Mycobacterium xenopi
135
Optimum growth occurs at 42 oC; positive growth at 35-37 oC; and negative growth at 25 oC
Mycobacterium xenopi
136
Produces a “bird’s nest” appearance with sticklike projections on Middlebrook 7H10 medium
Mycobacterium xenopi
137
Unique in its growth requirement for hemoglobin or hemin
Mycobacterium haemophilum
138
Disease most commonly is manifested by multiple cutaneous nodules, ulcers, or painful swellings, typically involving the extremities, which occasionally become abscesses
Mycobacterium haemophilum
139
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
Mycobacterium haemophilum
140
Common in the environment and has been isolated from water, soil, and dust
Mycobacterium fortuitum
141
It has been implicated frequently in infections of the skin and soft tissues, including localized infections and abscesses at the site of puncture wounds
Mycobacterium fortuitum
142
Infections associated with long-term use of intravenous and peritoneal catheters, injection sites, and surgical wounds
Mycobacterium fortuitum
143
Is found in the environment and is associated with many of the same opportunistic infections as those associated with M. fortuitum
Mycobacterium chelonae
144
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
Mycobacterium chelonae
145
Is now more specifically referred to as Mycobacterium abscessus subspecies abscessus
Mycobacterium abscessus
146
Tap water is an essential reservoir for this rapid grower
Mycobacterium abscessus
147
It is commonly isolated in association with chronic lung disease, otitis media following tympanostomy tube insertion, and disseminated cutaneous infections
Mycobacterium abscessus
148
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
Mycobacterium abscessus
149
A commonly considered as a saprophyte has been implicated in rare cases of pulmonary, skin, soft tissue, and bone infections
Mycobacterium smegmatis
150
Hansen’s bacillus
Mycobacterium leprae
151
* 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
Mycobacterium leprae
152
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
Mycobacterium leprae
153
Genetically identical species have also been isolated form [?] that develop a granulomatous disease similar to leprosy
armadillos
154
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.
Mycobacterium leprae
155
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.
Leprosy or Hansen’s disease
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Leprosy. From Greek lepros, meaning | [?]. Translated from a Hebrew word that refers to “uncleanliness”
“scaly” or “rough”
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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.
intracellular survival
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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.
sensory-motor deficits
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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.
drop foot and claw hands
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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.
musculoskeletal
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- 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
i. Cutaneous lesion and anesthesia: ii. Peripheral nerve involvement: iii. Slit Skin Smear (SSS)
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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
‘spectral’
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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.
Ridley-Jopling Classification for Leprosy (1966)
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There are two (2) polar types of leprosy:; one at the end of the spectrum and one at the other; CLINICALLY STABLE
``` Tuberculoid leprosy (TT) Lepromatous leprosy (LL) ```
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Immunologically, strong CMI correlates with the [?] Weak CMI correlates with the [?]
- TT type | - LL type
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Leprosy is a continuum of disease, which usually starts out with an indeterminate stage called
"borderline"
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moving up the spectrum - towards [?] - upgrading, and the prognosis is good - TT lesion can even self-heal - nerve damage-related disability can occur
TT
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moving down the spectrum - towards [?] - downgrading - prognosis is poor - LL can be fatal
LL
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Infection of the skin and mucus membranes of the nose, lips, chin, and brows produces a moderate facial deformation, typical of lepromas.
lepromatous leprosy
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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. ```
Tuberculous leprosy
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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)
TUBERCULOID LEPROSY
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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
LEPROMATOUS LEPROSY
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NERVE INVOLVEMENT - Asymmetrical, single nerve enlargement - Nerve to patch may be palpable
TUBERCULOID LEPROSY
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NERVE INVOLVEMENT - Symmetrical involvement of nerve trunks with glove and stocking anesthesia - Nerves may feel normal on palpation or may be thickened
LEPROMATOUS LEPROSY
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CELL-MEDIATED IMMUNITY -Strong
TUBERCULOID LEPROSY
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CELL-MEDIATED IMMUNITY -Week
LEPROMATOUS LEPROSY
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NUMBER OF ORGANISMS IN TISSUES -Low
TUBERCULOID LEPROSY
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NUMBER OF ORGANISMS IN TISSUES -High
LEPROMATOUS LEPROSY
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INFECTIVITY -Low
TUBERCULOID LEPROSY
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INFECTIVITY -High
LEPROMATOUS LEPROSY
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- 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.
Leprosy
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is primarily controlled by prompt antimicrobial therapy which is most effective when performed before permanent damage to nerves and other tissues has occurred.
M. leprae infection
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There [?] named Nocardia spp., and more than half have reportedly been isolated from humans.
>100
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The most commonly encountered species are
Nocardia brasiliensis, N. cyriacigeorgica, N. farcinica, N. abscessus complex, and N. nova
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- They are long, thin, beaded (irregularly spaced), | aerobic, gram-positive bacilli
Nocardia species
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- The cells remain together after division to form elongated chains of bacteria with occasional “tree-like” branches.
Nocardia species
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- 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.
Nocardia species
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- The nocardiae are found in soil and organic material worldwide and cause disease in many animals and in fish.
Nocardia species
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- Infections result either by inhalation of the organism from soil or dust or following trauma and contact with contaminated soil.
Nocardia species
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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
Nocardiosis
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The most common form of infection with Nocardia species
Pulmonary nocardiosis
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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
pneumonitis
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[?] 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
N. brasiliensis
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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
actinomycotic mycetomas