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[9f] MODULE 7 UNIT 2 > LECTURE > Flashcards

LECTURE Flashcards

1
Q

are a group of gram-negative bacteria which possess characteristics that make them peculiar when compared to other members of the Kingdom Eubacteria.

A

spirochetes

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2
Q

Possession of a specialized locomotory apparatus, the endoflagellum or axial filaments which facilitate a movement likened to a boring cork screw

A

spirochetes

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3
Q

Reproduction by transverse binary fission

A

spirochetes

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4
Q

is a member of the phylum Spirochaetes

A

spirochetes (or spirochaetes)

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5
Q

All of its human pathogens are classified in the order (?)

A

Spirochaetales

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6
Q

three (3) genera of spirochetes:

A

Treponema, Borrelia, and Leptospira.

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7
Q

Long, slender, helically coiled, spiral, or corkscrewshaped gram-negative bacilli

A

spirochetes (or spirochaetes)

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8
Q

Has an outer sheath of glycosaminoglycan coating.

A

spirochetes (or spirochaetes)

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9
Q

Motile via the (?) which are flagella-like organelles in the periplasmic space encased by the outer membrane, begin at each end of the organism and spirally wrap around it, extending to and overlapping at the midpoint; attached to the cell wall by insertion disks located at the end of cells.

A

axial filaments (endoflagella)

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10
Q

Slender with numerous tight coils; 0.1-0.18 um iwide x 6-20 um long; has 8-20 evenly spaced coils.

A

Treponema

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11
Q

Thicker with fewer and looser coils; 0.3 µm wide x 3.0 µm long has 3-10 loose, irregular coils.

A

Borrelia

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12
Q

2 Family Spirochaetaceae

A

Treponema

Borrelia

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13
Q

Axial filaments of Treponema

A

6-10

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14
Q

Axial filaments of Borrelia

A

30-40

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15
Q

Insertion Disk/s of Treponema

A

1

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16
Q

Insertion Disk/s of Borrelia

A

2

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17
Q

Family Leptospiraceae

A

Leptospira

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18
Q

Slender, tightly coiled; ends bent to form question mark-like hooks; 0.1–0.2 µm wide x 5-15 µm long

A

Leptospira

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19
Q

Axial filaments of Leptospira

A

2

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20
Q

Insertion Disks of Leptospira

A

3-5

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21
Q

are found in the oral cavity, intestinal tract, and perigenital regions of humans and animals.

A

Treponema species

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22
Q

The pathogens are strict parasites with complex growth requirements that necessitate growing them in live cells.

A

Treponema species

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23
Q

Two species of the genus Treponema are responsible for disease in humans

A

T. pallidum and T. carateum.

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24
Q

Treponema pallidum is divided into three subspecies :

A

pallidum, pertenue, endemicum

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25
Q

Treponema pallidum subspecies pallidum: HABITAT

A

Humans are the only natural host of T. pallidum subspecies pallidum

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26
Q

Transmission occurs by the following routes:
i.Direct contact with active lesions, commonly through sexual contact
ii.Vertical transmission across the placenta may result when a woman with latent infection becomes pregnant, or when a pregnant woman becomes infected.
iii.Other routes of transmission includes:
‣Nonsexual contact with an active lesion
‣Transfusion of fresh blood products (< 48 hours of storage) from an infected person,
‣Accidental needle stick, or when infectious specimens are handled in the laboratory

A

Treponema pallidum subspecies pallidum: TRANSMISSION

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27
Q

Treponema pallidum subspecies pallidum is estimated that (?) are required for infection.

A

<60 treponemes

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28
Q

4 Diseases of Treponema pallidum

A

Venereal Syphilis, The Great Pox, French disease, Italian disease

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29
Q

is known as “the great imitator” because the varied and complex clinical manifestations of this illness can mimic many other diseases.

A

Syphilis

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30
Q

Once inoculated, the (?) penetrates an intact mucous membrane or gains access to tissue through abraded skin. It multiplies at the inoculation site, and then enters the lymphatic and circulatory system and spreads throughout the body.

A

treponeme

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31
Q

The slow generation time of this bacterium (?) as well as the delayed immune response of the host accounts for the slow, but progressive nature of the disease.

A

(30 hours)

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32
Q

The usual incubation period varies from

A

2 to 10 months averaging to 3 months.

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33
Q

The course of syphilis can be divided into predictable stages:

A

(1) Primary stage
(2) Secondary stage
(3) Tertiary stage (also, Late Syphilis)

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34
Q

This period usually occurs at an average of 3 weeks after exposure to the organism and is marked by the appearance of the primary syphilitic lesion referred to as chancre.

A

Primary stage of syphilis

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35
Q

The chancre which contains live treponemes, is a painless, non-suppurative lesion that is ulcerated with raised, firm edges and a smooth, hard base (“hard chancre”). It develops at site of inoculation

A

Primary stage of syphilis

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36
Q

commonly, the internal and external genitalia, the lips, oral cavity, nipples, fingers and the perianal region. It typically occurs singly but multiple chancres have been seen in some patients. Lymph nodes near the affected area are usually enlarged. Since it is painless, the chancre usually go unnoticed in some cases.

A

Primary stage of syphilis

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37
Q

The chancre spontaneously heal without scarring in approximately 2 to 8 weeks. However, healing is deceptive since the bacteria have already started disseminating to other organs by way of local lymph nodes and the bloodstream.

A

Primary stage of syphilis

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38
Q

This period usually occurs at an average of 3 weeks after exposure to the organism and is marked by the appearance of the primary syphilitic lesion referred to as (?)

A

chancre

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39
Q

Begins about 3 weeks to 6 months (average of 6 weeks) after the chancre heals.

A

Secondary stage of syphilis

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40
Q

This stage is characterized by widespread dissemination of spirochetes in the host’s body, mucocutaneous as well as organ involvement, and specific symptoms that include fever, sore throat, generalized lymphadenopathy, headache, lesions of the mucous membranes, and development of a red or brown rash that breaks out on all skin surfaces including the trunk, arms, and even palms and soles.

A

Secondary stage of syphilis

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41
Q

The spread of spirochetes into the organs result to major complications that develop in the bones, hair follicles, joints, liver, eyes, brain, and kidneys.

A

Secondary stage of syphilis

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42
Q

This stage usually last for 2 to 8 weeks and in some, can relapse.

A

Secondary stage of syphilis

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43
Q

After this stage, approximately 1/3 of untreated patients exhibit biological cure, with negative serological tests. Another third remain latent for life but have reactive sera. The remaining third ultimately develop tertiary or late syphilis.

A

Secondary stage of syphilis

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44
Q

The lesions may enlarge and coalesce to produce pale plaques referred to as

A

condyloma lata

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45
Q

During this period, the bacteria are no longer present, and clinical manifestations of the disease are absent but anti-treponeme antibodies can be readily detected.

A

Latent Syphilis

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46
Q

After resolution of secondary syphilis, (?)% of infected persons enter a period of latency which highly varies and can last for 20 years of longer.

A

30%

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47
Q

The period of latency is divided into:

A

(1) Early Latent Syphilis

(2) Late Latent Syphilis

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48
Q

occurs within 1 year of infection and characterized by occasional relapses

A

Early Latent Syphilis

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49
Q

occurs greater than 1 year of infection, relapses are uncommon.

A

Late Latent Syphilis

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50
Q

Only a fraction of patients progress into this period several years up to decades following initial infection.

A

(3) Tertiary stage (also, Late Syphilis)

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51
Q

Infected persons rarely progress to this period because of widespread use of antibiotics to treat infections.

A

3) Tertiary stage (also, Late Syphilis)

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52
Q

During this period, the combined action of the infection and the body’s response to it produce severe pathologic complications.

A

(3) Tertiary stage (also, Late Syphilis)

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53
Q

marked by development of granulomatous lesions (called gummas) in the skin, bones, and the liver which can occasionally lead to death.

A

Benign tertiary syphilis

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54
Q

development of granulomatous lesions in the skin

A

gummas

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55
Q

may involve any part of the nervous system but typically affects the blood vessels in the brain, cranial nerves, and dorsal roots of the spinal cord. The reactions can be diverse and include severe headaches, convulsions, behavioral changes, atrophy of the optic nerve which leads to blindness. Atrophy of the spinal cord leads to muscle wasting and loss of coordination.

A

Neurosyphilis

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56
Q

results from damage to small arteries in the aortic wall, cardiovascular lesions, aneurysms, and aortic valve insufficiency.

A

Cardiovascular syphilis

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57
Q

A ring-shaped erosive gumma appears on the arm of a patient. Other gummas can be internal.

A

Tertiary syphilitic lesion

58
Q

This results when treponemes from a pregnant woman’s circulation passes through the placenta and are carried through the tissues of the growing fetus.

A

Congenital syphilis

59
Q

Although it is more common in the (?), an infection that leads to congenital syphilis may occur in any of the three trimester.

A

2nd and 3rd trimester

60
Q

The treponeme inhibits fetal growth and disrupts development that leads to consequences ranging from mild to extremes such as

A

spontaneous miscarriage or stillbirth.

61
Q

results when mothers are in the stage of early syphilis during pregnancy. It encompasses the period from birth to 2 years of age and is usually first detected 3 to 8 weeks after birth. It resembles secondary syphilis in adults and is characterized by mucocutaneous lesions, osteochondritis, anemia, hepatosplenomegaly, and CNS involvement.

A

Early-onset congenital syphilis

62
Q

results following pregnancies when mothers have chronic, untreated infections. It occurs after age 2 years but generally are not apparent until the second decade of life. Symptoms corresponds to tertiary syphilis in adults, and include interstitial keratitis, bone and tooth deformities, deafness, neurosyphilis, and other tertiary manifestations.

A

Late-onset congenital syphilis

63
Q

A common characteristic of late congenital syphilis is

A

notched, barrel-shaped, incisors (Hutchinson’s teeth).

64
Q

T. pallidum subspecies pallidum has hyaluronidase that breaks down the hyaluronic acid in the ground substance of tissue and presumably the invasiveness of the organism.

A

Invasiveness

65
Q

T. pallidum subsp. pallidum has the ability to cross intact mucous membranes and the placenta, disseminate throughout the body, and infect almost any organ system.

A

Invasiveness

66
Q

T. pallidum subsp. pallidum coats itself with host proteins, hence delaying the antibody-mediated immune response of the host. The effectiveness of humoral response is reduced as the treponemes are already extravascular once antibodies are produced.

A

Evasion of host immune response

67
Q

The cell surface proteins of T. pallidum subspecies pallidum undergoes antigenic variation which contributes to its ability to evade host immune response and establish persistent infection.

A

Evasion of host immune response

68
Q

PREVENTION AND CONTROL of Treponema pallidum

A

Control measures depend on:

  1. Prompt and adequate treatment of all discovered cases.
  2. Follow up on sources of infection and their contacts so they can be treated.
  3. Educating people about sexually transmitted diseases (STDs), including providing information about the proper use of barrier contraceptives.
  4. Serologic screening of high-risk populations should be performed, and to avoid congenital syphilis, pregnant women should undergo serologic testing during early and late pregnancy.
69
Q

is the etiologic agent of yaws, a disease endemic to warm, humid, tropical regions of Africa, Asia, and South America.

A

Treponema pallidum subspecies pertenue

70
Q

is a West Indian name for chronic disease known by the regional names bouba, frambesia tropica, and patek.

A

Yaws

71
Q

Yaws readily spread from person-to-person by direct contact with skin lesions or fomites.

A

Treponema pallidum subspecies pertenue

72
Q

The earliest sign is a large, abscessed papule called the “(?)” which is usually on the legs or lower trunk.

A

mother yaw

73
Q

can result to deforming lesions on the face and extremities.

A

Later stages of yaws

74
Q

contribute to the acquisition of yaws.

A

Crowded living conditions and poor hygiene

75
Q

Causes bejel, also known as endemic syphilis and nonvenereal childhood syphilis which occurs in the Middle East and in the arid, hot areas of the world.

A

Treponema pallidum subspecies endemicum

76
Q

How Treponema pallidum subspecies endemicum transmitted?

A

by direct contact or shared household utensils (e.g., eating or drinking vessels) and other fomites and facilitated by minor abrasions or cracks in the skin or mucous membranes (e.g., lips).

77
Q

is a chronic, inflammatory childhood disease which begins as small, moist patches in the oral cavity and spreads to the skin folds of the body and to the palms.

A

Bejel

78
Q

It is found in isolated populations inhabiting the tropical forest and valley regions of Mexico, and South and Central America.

A

Treponema carrateum

79
Q

Treponema carrateum is the etiologic agent of (?)

A

pinta

80
Q

is a chronic skin infection which begins with a dry, scaly papule, which resemble that of psoriasis or leprosy. Overtime, pigmented secondary macules and blanched tertiary lesions appear. Although it is not life-threatening, it often creates scars on the afflicted area.

A

Pinta

81
Q

The genus (?) comprises several species of spirochetes that are morphologically similar but have different pathogenic properties and host ranges.

A

Borrelia

82
Q

All pathogenic Borrelia are

A

arthropod-borne (i.e. ticks and/or lice).

83
Q

is a louse-borne borrelia which has a world wide distribution although it once became more common in South America, Europe, Africa, and Asia.

A

Borrelia recurrentis

84
Q

body louse

A

Pediculus humanus

85
Q

How Borrelia recurrentis transmitted?

A

via the body louse, Pediculus humanus, which carries the borreliae in its body cavity. Transmission occurs when the infected lice are crushed and scratched into skin.

86
Q

are the only known reservoir of this louse-borne borrelia

A

Humans

87
Q

occur whenever conditions favorable for survival and spread of the louse vector, P. humanus, are present such as when famine, war, or natural disasters are coupled with poor hygiene, crowding, and inadequate medical attention.

A

Epidemic Relapsing Fever (or Louse-borne Relapsing Fever)

88
Q

After an incubation period of 2 to 15 days following the inoculation of the borrelae, presence of high numbers of spirochetes (?) in the blood (spirochetemia), triggers sudden high temperature, chills, severe headache, muscle pains, and weakness. This febrile period lasts about 3 to 7 days and ends abruptly only to recur several days to weeks later, following a less severe but similar course.

A

> 500,000 spirochetes/mL

89
Q

Later features of the disease include nausea, vomitting, muscle aches, and abdominal pain. In many cases, extensive damage to the liver, spleen, heart, kidneys, and cranial nerves occur. Half of the patients hemorrhage profusely into organs, and some develop a rash on the shoulders, trunk and legs.

A

Epidemic Relapsing Fever (or Louse-borne Relapsing Fever)

90
Q

The term “(?)” indicates fever follows a fluctuating course that is explained by changes in the spirochete and attempts of the host immune system to control it. Hence, in the course of the disease, the febrile periods worsen during the spirochetemia and wane as the immune response clears the bacteria from the circulation.

A

relapsing fever

91
Q

Borrelia species evades the immune system and avoids destruction by ?

A

by changing their surface antigens during growth (i.e. multiplication).

92
Q

During this time, antigenically (?) are produced, hence, initial antibodies produced against the spirochetes possessing the “original” antigenic determinants are rendered useless.

A

altered spirochetes

93
Q

Eventually, the immune systems forms (?), but it is soon faced with another antigenic form.

A

new antibodies

94
Q

A single strain has been known to generate

A

24 distinct serotypes

95
Q

can occur once immunity against the variety of antigens produced by the organism develops.

A

Complete recovery

96
Q

Louse-borne relapsing fever can be prevented by how?

A

by good personal and public hygiene, especially improvements in measures to avoid overcrowding and in delousing.

97
Q

Borrelia hermsii: HABITAT AND TRANSMISSION

A

B. hermsii is widely distributed throughout the world. It is transmitted by a large variety of soft ticks of the genus Ornithodoros. Transfer from the vector to a vertebrate host takes place via infected saliva during tick attachment.

98
Q

The occurrence, clinical manifestations, and pathologic mechanisms are similar with Borrelia recurrentis.

A

Endemic relapsing fever (Tick-borne Relapsing Fever)

99
Q

Tick-borne relapsing fever is best prevented by how?

A

by practices that limit exposure to ticks includes wearing protective clothing, rodent control, and the use of repellents.

100
Q

has been documented in North and West America, Asia, and in Europe.

A

Borreliella (formerly Borrelia) burgdorferi

101
Q

Mice and deer constitute the main animal reservoirs, but other rodents and birds may also be infected.

A

Borreliella (formerly Borrelia) burgdorferi

102
Q

B. burgdorferi is primarily transmitted by how?

A

by bites of hard ticks of the genus Ixodes, species of which may vary as determined by their geographical distribution.

103
Q

were identified as highest risk groups.

A

Hikers, backpackers and people living in newly developed communities near woodland and forests

104
Q

is complex, and nonfatal and it often evolves into a slowly progressive syndrome. - It can generally be divided into three stages.

A

Lyme disease

105
Q

a classic rash that is normally found at the site of larval tick bite as.

A

erythema migrans (EM)

106
Q

It begins as a red macule and expands and resembles that of a target or bullseye, with raised erythematous ring that gradually spreads outward and a pale central region. This rash is commonly accompanied by a flulike illness with fever, headache, chills, stiff neck, and dizziness

A

Lyme disease

107
Q

In unaddressed cases, the disease advances to the (?), which is disseminated and produces widely variable symptoms that include secondary skin lesions, migratory joint and bone pain, neurologic and cardiac disease, splenomegaly, and severe malaise and fatigue.

A

second stage

108
Q

consists of late manifestations, or late persistent infections which begins months to years later and occur mainly in the cardiac, musculoskeletal, and neurologic systems. Arthritis is the most common symptom, occurring weeks to years later.

A

Stage 3

109
Q

Mediate adhesion of B. burgdorferi to fibronectin and other extracellular elements of the host cells.

A

B. burgdorferi surface proteins

110
Q

Facilitate persistence of the spirochete by (?) thereby preventing complement deposition on host cells and promoting suppression of host immune response including inhibition of mononuclear and natural killer cell function, lymphocyte proliferation, and cytokine production.

A

binding the host’s serum factor H

111
Q

Bind with plasminogen and urokinase-type plasminogen activator. This binding convert plasminogen to (?), a potent protease and could facilitate tissue invasion.

A

plasmin

112
Q

Prevention is based on (?). Protective clothing must be worn and repellents should be used in areas where the risk of tick exposure is possible.

A

avoidance of exposure to ticks

113
Q

should be removed immediately because pathogen transmission is associated with the length of attachment.

A

Attached ticks

114
Q

Environmental control of ticks by application of (?) can reduce the number of tick larvae for a season.

A

insecticides

115
Q

has a world wide distribution. Rats, mice, wild rodents, dogs, swine, and cattle are the principal sources.

A

Leptospira interrogans

116
Q

The organisms in bodies of water contaminated with animal urine enter through breaks in the skin (cuts and abrasions) and mucous membranes (mouth, nose, conjunctivae).

A

Leptospira interrogans

117
Q

Persons working with animals or in rat-infested surroundings or those most likely to come in contact with water contaminated by (?) run the greatest risk of infection. Those with recreational exposure (e.g., camping near or swimming in infected waterways) are also at particular risk.

A

rats (eg, miners, sewer workers, farmers, and fishermen)

118
Q

It is essentially a zoonosis and human infection is only accidental.

A

Leptospirosis or Weil Disease

119
Q

The clinical disease is divided into two phases:

A
  1. First (bacteremic or leptospiremic) phase

2. Second (immune) phase

120
Q

After entry into the circulation, the organisms disseminate widely, including into the CNS and eye.

A

First (bacteremic or leptospiremic) phase

121
Q

The incubation period ranges from (?)

A

from 3 to 30 days but usually averages to 10 to 12 days.

122
Q

Appearance of nonspecific, infuenza-like symptoms is sudden and include high fever, chills, headache, conjunctivitis, severe myalgia, malaise, and vomiting.

A

First (bacteremic or leptospiremic) phase

123
Q

The spirochetes are found (?)

A

In the blood and CSF at this period.

124
Q

The spirochetes disappear in the blood largely due to the action of phagocytes, complement, and IgM antibodies, hence the term immune phase.

A

Second (immune) phase

125
Q

This period is marked by milder fever, headache due to meningitis

A

Second (immune) phase

126
Q

a cluster of symptoms characterized by kidney invasion, hepatic disease, jaundice, anemia and neurological disturbances.

A

Weil syndrome

127
Q

Meningitis occurring during the immune phase of leptospirosis has been termed as “(?)” owing to negative culture results of CSF samples from patients.

A

septic meningitis

128
Q

At this phase of the disease, diagnosis is mainly aided by how?

A

serological tests.

129
Q

Leptospira interrogans

Control measures include:

A
  • Rodent elimination and drainage of contaminated waters.
  • Preventing exposure to potentially contaminated water and reducing contamination by rodent control by wearing protective clothing (e.g., boots and gloves) in situations involving possible occupational exposure.
  • Short-term prophylaxis consisting of weekly doxycycline therapy may be appropriate in high-risk groups with expected occupational exposure.
130
Q

Preventing exposure to potentially contaminated water and reducing contamination by rodent control by (?) in situations involving possible occupational exposure.

A

by wearing protective clothing (e.g., boots and gloves)

131
Q

Short-term prophylaxis consisting of weekly (?) may be appropriate in high-risk groups with expected occupational exposure.

A

doxycycline therapy

132
Q

It is a gram-negative, tightly coiled bacterium (2–5 µm long by 0.5 µm wide), with bipolar tufts of flagella, more closely related to Neisseria species than to members of the family Spirochaetaceae.

A

Spirillum minus

133
Q

This bacterium is part of the respiratory flora of rats and is transmitted by how?

A

by a bite

134
Q

Spirillum minus more closely related to (?) than to members of the family Spirochaetaceae.

A

Neisseria species

135
Q

Infection in humans results in a relapsing fever called (?), most cases of which have been described in Japan, although cases have occurred worldwide.

A

sodoku

136
Q

Dissemination from the original bite occurs soon after inoculation through a (?)

A

rat bite

137
Q

The bite wound initially heals, but (?) weeks later, an indurated lesion, which may ulcerate, appears at the bite site.

A

1–4 weeks

138
Q

recur, separated by afebrile periods of 3–7 days.

A

Febrile periods

139
Q

can be accompanied by myalgia, headache, and vomiting.

A

Fever

140
Q

Half of patients have a (?) that may form large plaques.

A

macular rash

141
Q

Resolution usually occurs in (?) weeks, but relapses and complications such as endocarditis, meningitis, myocarditis, and nephritis can also occur

A

3–8 weeks

[9f] MODULE 7 UNIT 2 (2 decks)

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