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microbio km > microbio lecture 22 chapter 25 > Flashcards

microbio lecture 22 chapter 25 Flashcards

1
Q

Alexandre Emile John Yersin (1863 to 1943)

A
  • physician, bored w/ research
  • established med school in Vietnam to study diseases affecting people (plague, unknown transmission)
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2
Q

in 1894, Alexandre Yersin went to Hong Kong to study an outbreak

A

Discovered in lymph nodes of plague victims a bacillus, which was eventually named Yersinia pestis for him and pestis for the pestilence, or plague.

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3
Q

Yersinia pestis was used to make

A

a vaccine; later antiserum against the organism
cured a patient with plague (convalescent serum therapy)

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4
Q

Cardiovascular system circulates

A

blood and lymph

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5
Q

cardiovascular system supplies

A

nutrients and O2 to cells, removes waste

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6
Q

the CV system also

A

heats, cools body to maintain optimum temperature

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7
Q

infections can be serious, since infectious agents can become

A

systemic - carried throughout the body

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8
Q

When a substance is circulating, conditions are named after

A

infectious agent: bacteremia, viremia, and fungemia

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9
Q

systemic does not imply a _______ state and may not _______ ________—for
example, a person can become briefly bacteremic after brushing their teeth

A

disease; involve symptoms

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10
Q

immune system normally removes

A

microbes that enter bloodstream

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11
Q

cardiovascular system

A

heart, blood vessels, blood

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12
Q

lymphatic system

A

Lymph, lymph vessels, lymph nodes, and lymphoid organs including tonsils, appendix, spleen

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13
Q

in the lymphatic system, Phagocytic cells remove

A

infectious agents, foreign material

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14
Q

both cardiovascular and lymphatic systems

A

are normally sterile

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15
Q

lymphangitis

A

Infection of limb may result in visible red streak from infection site to lymph node

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16
Q

Blood, and lymph both carry _________, and ________ _________
(antibodies, complement, lysozyme, interferon)

A

leukocytes; antimicrobial proteins

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17
Q

clotting may prevent

A

spread of infection

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18
Q

Bacteria that cause vascular infections usually carried into
bloodstream by

A

the flow of lymph from the area of infection in tissues

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19
Q

some bacteria multiply in blood, then

A

colonize and form biofilms on structures such as heart valves

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20
Q

some bacteria multiply in

A

cells of mononuclear phagocyte system

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21
Q

infective endocarditis (IE)

A

Infection of inner surface of heart, often a heart valve

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22
Q

infective endocarditis (IE) predisposing factors

A

use of indwelling catheters, heart
defects, or injected drug abuse

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23
Q

some types of IE progress slowly, formerly called

A

subacute bacterial endocarditis (SBE)

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24
Q

infective endocarditis signs and symptoms

A
  • Noticeable fatigue, slight fever
  • Typically become ill gradually and slowly lose energy over weeks or months
  • Small hemorrhagic lesions form in the conjunctiva, skin, or under nails
  • Strokes can be a life-threatening complication
    (Fever, loss of energy over a period of weeks or months; sometimes, a stroke)
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25
Q

infective endocarditis incubation period

A

poorly defined, usually weeks

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26
Q

infective endocarditis causative agents

A

Staphylococcus aureus or S. epidermidis; enterococci; streptococci including oral viridans streptococci

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27
Q

infective endocarditis pathogenesis

A

Normal microbiota or organisms from an infected body site enter bloodstream; turbulent blood flow causes the formation of a thin clot that traps circulating organisms; a biofilm forms, protecting the organisms from phagocytes; pieces of clot break off, blocking blood vessels, leading
to tissue death

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28
Q

infective endocarditis epidemiology

A

People at risk are mainly those with heart abnormalities, including artificial valves or damage from rheumatic fever; may develop after dental procedures or other situations that cause bacteremia; injected drug abuse

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29
Q

infective endocarditis treatment and prevention

A

Treatment: a combination of antibiotics. Prevention: in certain cases, administration of an antibiotic immediately before anticipated bacteremia, such as before dental work.

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30
Q

Sepsis and septic shock

A

A deadly immunologic disorder precipitated typically by bacteremia

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31
Q

sepsis is a ______ disease without ___________, often _____________`

A

progressive; intervention; uncontrollable

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32
Q

Sepsis

A

infection-induced systemic inflammatory response; involves
pro-inflammatory cytokines

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33
Q

severe sepsis

A

results in violent shaking, chills, fever; Often rapid
breathing, anxiety, confusion; blood pressure dropping, but typically controllable

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34
Q

septic shock

A

dramatic irreversible drop in blood pressure due to
uncontrolled inflammatory response of sepsis; very often fatal; leading cause of death in hospital setting

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35
Q

in septic shock, ___________ drops

A

urine output

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36
Q

in septic shock, ___________ increases

A

respiration and pulse

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37
Q

in septic shock,arms and legs become ___________

A

cool, dusky

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38
Q

causative agents of sepsis

A
  • systemic infection by an microorganism
    -gram negative with endotoxin can cause most fatal cases
  • normal microbiota of large intestine commonly cause (e.coli and other facultative anaerobes/enterobacteria, anaerobes like Bacteroides)
  • environmental bacteria like Pseudomonas aeruginosa
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39
Q

sepsis/septic shock pathogenesis

A
  • Almost always starts from infection in sites such as the lung, urinary tract, meninges, surgical wounds
  • Infection fostered by a compromised immune response
  • Progresses in stages, excessive inflammatory response
  • Pattern recognition receptors (PRRs) on macrophages, neutrophils detect
    microbe-associated molecular patterns (MAMPs: endotoxin, other
    bacterial products); release pro-inflammatory cytokines
  • Cytokine storm results
  • Further amplified by activated complement pathway
  • Additional phagocytes recruited, produce more PRRs;
    increased sensitivity to MAMPs further amplifies
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40
Q

what are predominant cytokines responsible for sepsis

A

IL-6, Il-8, IL-10, IL-18 and TNF-α

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41
Q

sepsis response to MAMPS and damage-associated molecular patterns (DAMPs)

A
  • Inhibition of systems that normally control inflammation
  • Suppression of adaptive immune response
  • Activation of blood clotting mechanisms
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42
Q

Widespread clotting called disseminated intravascular coagulation (DIC); may lead to multi-organ failure

A
  • Blood depleted of clotting proteins, platelets; hemorrhage
  • Phagocytes release tissue-damaging lysosomal enzymes; may
    seriously damage lungs
  • Decreased muscular tone of heart and vessel walls
  • Low blood pressure due to fluid leakage from vessels
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43
Q

sepsis/septic shock treatment and prevention

A
  • Antimicrobial medications to clear causative organisms
    ( But bacteriocidal antibiotics often lyse cells, increase release of endotoxin from Gram-negative organisms )
  • Treatment for shock, tissue hypoxia; fluid replacement and support for organ dysfunction
  • Sepsis prevented by quick identification, treatment of localized
    infections
  • Treatment of predisposing conditions
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44
Q

CDC stats about sepsis

A
  • Each year, at least 1.7 million adults in America develop sepsis.
  • Nearly 270,000 Americans die as a result of sepsis.
  • 1 in 3 patients who dies in a hospital has sepsis
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45
Q

sepsis signs and symptoms

A

Chills, fever, shaking, rapid breathing and pulse, confusion, and anxiety; if shock develops, drop in urine output, bruising, bleeding, and organ failure

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46
Q

sepsis incubation period

A

variable

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47
Q

sepsis causative agents

A

Usually bacteria (both Gram-positive and Gram-negative) but other microbes as well; common bacterial causes of fatal cases include E. coli, Enterobacter species, and P. aeruginosa.

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48
Q

sepsis pathogenesis

A

Sepsis starts from infection in the body tissues; macrophages and neutrophils release pro-inflammatory cytokines in response to bacterial products; complement is activated; dysregulated inflammatory response results, leading to disseminated intravascular coagulation (DIC) and organ failure.

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49
Q

sepsis epidemiology

A

mainly a healthcare-associated disease, especially nosocomial

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50
Q

sepsis treatment prevention

A

Treatment: multiple antibiotics as well as fluid and supportive therapy. Prevention: prompt identification and treatment of localized infections.

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51
Q

plague spread slowly and inevitably from

A

village to village by infected rats and humans

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52
Q

plague Killed about _________% of Europe’s population between 1346 and 1350 due to _______, ________

A

30; crowded conditions, uncontrolled rat populations

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53
Q

bubonic plague signs/symptoms

A

Following bite by infected flea, symptoms appear
within 2 to 6 days
* Enlarged and tender lymph nodes: buboes; bubonic plague
* High fever, shock, delirium, patchy bleeding under skin

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54
Q

pneumonic plague signs/ symptoms

A

Following inhalation of respiratory droplets from
infected patient or animal, pneumonic plague may develop within 1 to 3 days
* Headache, fever, cough, pneumonia

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55
Q

if plague spread by blood stream, _______ _______ may develop

A

septicemic plague

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56
Q

endotoxin released in plague causes _________; DIC causes _________ into skin and organs

A

shock; bleeding

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57
Q

plague causative agent

A

Yersinia pestis

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58
Q

Yersinia pestis description

A

Enterobacteriaceae, a facultative anaerobe, Gram-negative rod

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59
Q

Yersinia pestis attributes

A
  • Non-motile, grows best at 28 degrees Celsius
  • Certain dyes stain ends more intensely; safety pin appearance
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60
Q

Plague epidemiology

A
  • Zoonotic disease endemic in rodent populations worldwide except
    Australia
  • In U.S., mostly occurs in western states
  • (Wild rodents such as prairie dogs and their fleas are the main reservoirs / Rats, rabbits, dogs, cats can also be hosts)
  • Hundreds of species of fleas are able to transmit plague; remain infectious for a year or more
  • Once an individual is fully involved with bubonic plague and the lungs become involved (pneumonic plague), respiratory droplets from pneumonic can
    spread; this form of illness is very dangerous, reaching critical stage quickly
  • Category A bioterrorism threat
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61
Q

Plague pathogenesis

A
  • Forms biofilms in the digestive tract of infected fleas, blocks tract
  • Fleas starve, increasing the likelihood of feeding
  • Causes bacteria to be regurgitated into bite wound
  • Can transmit via feces when person scratches flea bite
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62
Q

(plague pathogenesis) Multiple virulence factors allow avoidance of host defenses

A

Protease released, resisting macrophages, inflammatory reactions

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63
Q

protease (PIa) clears

A

lymphatics and capillaries of clots, inactivates certain complement system components allowing organisms to spread

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64
Q

when taken up by macrophages in regional lymph nodes,

A

resist killing effects of macrophages and multiply

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65
Q

acute inflammatory reaction develops in

A

lymph nodes-> they become extremely painful

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66
Q

infected macrophage die and

A

release bacteria ready to withstand host defenses

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67
Q

Y. pestis produces ______ to avoid phagocytosis;

A

capsule

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68
Q

siderophores in Y.pestis

A

trap iron

69
Q

Yersinia outer proteins (YOPS) are delivered into host cells by

A

type III secretion system; multiple effects

70
Q

Yersinia outer proteins (YOPS) are delivered into host cells by

A

type III secretion system; multiple effects

71
Q

in plague pathogenesis, lymph nodes become

A

necrotic: numerous bacteria spread into bloodstream

72
Q

in plague, endotoxin causes

A

septicemic plague; septic shock

73
Q

_________% of plague infect lungs, leading to pneumonic plague –>

A

10-20, respiratory droplets can transmit a fully virulent pathogen

74
Q

Pla (protease) coded by __________ : action _______________

A

pPCP1 plasmid; Activates plasminogen; destroys C3b, C5a,
and clotss

75
Q

Yops (proteins) coded by __________ : action _______________

A

pCD1 plasmid; Interfere with phagocytosis and the immune
response

76
Q

V antigen coded by __________ : action _______________

A

pCD1 plasmid; Controls type III secretion system that
delivers Yops (proteins)

77
Q

F1 coded by __________ : action _______________

A

pMT1 plasmid; Forms antiphagocytic capsule at 37 degrees
Celsius

78
Q

OsaA (adhesin) coded by __________ : action _______________

A

Chromosome; Role in attachment to host cells

79
Q

Complement resistance coded by __________ : action _______________

A

Chromosome; Protects against lysis by activated
complement

80
Q

Iron acquisition coded by __________ : action _______________

A

Chromosome; Traps iron-containing substances; stores iron
compounds intracellularly

81
Q

Plague: Treatment and prevention

A
  • Antimicrobial medications, especially if given within 24 hours of the onset of symptoms
  • Rat control measures (garbage disposal, rat-proofing buildings, rat
    extermination programs) are significantly important
  • Extermination must be combined with insecticide use to prevent
    escape of infected fleas from dead rats
  • No current vaccine, but efforts are underway to develop one
  • Doxycycline is given as preventive to exposed individuals
82
Q

bubonic plague case-fatality if untreated

A

50-80%

83
Q

pneumonic plague case-fatality if untreated

A

100%

84
Q

plague signs and symptoms

A

High fever, large lymph nodes called buboes,
skin hemorrhages; sometimes bloody sputum

85
Q

plague incubation period

A

usually 1 to 6 days

86
Q

plague causative agents

A

Yersinia pestis, a Gram-negative rod; a member
of the Enterobacteriaceae with multiple
virulence factors

87
Q

plague pathogenesis

A

Enters the body with bite of infected flea or
inhalation; bacteria taken up by macrophages.
Intracellular environment causes the bacterial
cells to produce multiple virulence factors that
allow attachment to host cells, and provide
defense against the immune system

88
Q

plague epidemiology

A

Endemic in rodents and their fleas, particularly
in the western United States. Bubonic plague is
transmitted by fleas; pneumonic plague can be
transmitted person to person in respiratory
droplets. Pneumonic plague is the most
dangerous because Y. pestis is fully virulent at
the time of transmission

89
Q

plague treatment and prevention

A

Treatment: prompt diagnosis and antibacterial
treatment necessary to prevent high mortality.
Prevention: currently no vaccine available; new
vaccines are under development. Avoiding
contact with wild rodents and their burrows.
Insecticides and rat control.

90
Q

plague pathogenesis detailed process

A

Y.pestis from bite of flea/skin scratching with flea feces –> bacteria carried to regional lymph nodes –> phagocytes ingest bacteria but intracellular conditions activate capsules and other genes for virulence –> fully virulent bacteria break out phagocytes and infect lymph nodes causing buboes in bubonic plague –> bacteria may be carried in bloodstream (septicemic plague) –> lungs become infected and cause v. contagious and lethal pneumonic plague –> bacteria exit with coughing

91
Q

Lyme disease

A
  • Named after a cluster of cases in Lyme, Connecticut in the
    1970’s, but was widespread before then
  • Approximately 30,000 new cases each year; most common
    vector-borne disease in U.S.
92
Q

Lyme disease signs and symptoms

A
  • Three stages; one or more may be asymptomatic
93
Q

first stage of lyme disease

A

early localized infection: erythema migrans
(bull’s-eye rash), follows few days, weeks after tick
bite
* Nearby lymph nodes enlarge
* Flu-like symptoms: chills, fever,
headache, joint/muscle pains,
fatigue

94
Q

second stage of lyme disease

A

Early disseminated infection: 2 to 8 weeks later, nervous system
affected, electrical conduction in heart impaired
* Dizzy spells, fainting, paralysis of face, severe headache, stiff neck, pain
when moving eyes, difficulty concentrating, emotional instability,
fatigue, numbness or pain in legs or arms

95
Q

third stage of lyme disease

A

Late persistent infection: approximately 6 months after skin rash,
joint pain, swelling appear; slowly disappear over years
* Chronic nervous system impairments may occur
* Pain, paralysis, depression

96
Q

lyme disease causative agent

A

Borrelia burgdorferi

97
Q

Borrelia burgdorferi characteristics

A

Large, Gram-negative, microaerophilic spirochete with multiple copies of
linear chromosome
* Plasmids with genes usually found on chromosomes

98
Q

lyme disease pathogenesis

A
  • Spirochetes introduced into skin by bite of infected tick
  • Multiply, migrate outward in circular fashion; LPS causes inflammatory reaction in skin
  • Enter bloodstream, flu-like symptoms
  • Immune response likely responsible for signs and symptoms of second and third stages
  • Possible autoimmune response
99
Q

lyme disease epidemiology

A
  • Zoonosis; humans are accidental host
  • Widespread in U.S.; several species of ticks are vectors
  • Most important in eastern states is the black-legged (deer) tick, Ixodes
    scapularis
  • 80% of these ticks may be infected
  • Often bite without being detected
100
Q

lyme disease epidemiology cont’

A
  • Ticks mature during 2-year cycle
  • Nymph mainly responsible for transmitting B. burgdorferi
  • Preferred host is mouse, which spreads bacteria to other ticks
  • Deer are preferred host of adult ticks; mating occurs on deer
  • Deer spread disease widely
  • Peak incidence from May to December when nymphs are active
101
Q

lyme disease treatment and prevention

A
  • Antibiotics effective in patients during early stages
  • In late disease, antibiotics are less effective
  • Likely because spirochetes not actively multiplying
  • Prolonged treatment with intravenous ampicillin or ceftriaxone has cured
    many cases
  • Preventative measures include avoiding exposure to ticks, wearing protective clothing, repellants
  • No vaccine
102
Q

lyme disease signs and symptoms

A

Early localized infection: enlarging rash
that resembles a bull’s eye develops at the
site of the bite; lymph node enlargement
near bite, flu-like symptoms. Early
disseminated infection: heart and nervous
system involvement. Late persistent
infection: chronic arthritis and nervous
system impairment.

103
Q

lyme disease incubation period

A

several days to several weeks

104
Q

lyme disease causative agents

A

Borrelia burgdorferi, a spirochete

105
Q

lyme disease pathogenesis

A

Spirochetes injected into the skin by an
infected tick multiply and spread radially;
spirochetes enter the bloodstream and are
carried throughout the body; immune
reaction to bacterial antigens causes tissue
damage

106
Q

lyme disease epidemiology

A

Spread by the bite of ticks, Ixodes species,
usually found in association with animals
such as white-footed mice and white-tailed
deer living in wooded areas.

107
Q

lyme disease treatment and prevention

A

Treatment: early treatment with
appropriate antibiotics; prolonged antibiotic
therapy in chronic cases. Prevention:
avoiding ticks, protective clothing, and tick
repellents. No vaccine.

108
Q

lyme disease process of infection

A

tick bite infected with borrella burgdorferi into skin –> bacteria multiply and spread radially in skin (expanding red rash erythema migrans that clears centrally) –> bacteria enters bloodstream and can cause fever, acute injury to heart + nervous system –> chronic symptoms develop (arthritis, paralysis due to persisting bacteria + immune response)

109
Q

Brucellosis (“undulant fever” “Malta Fever”, “Mediterranean
“Fever, or “Bang’s disease”) is a

A

highly contagious zoonosis caused by the ingestion of unpasteurized milk, cheese, or undercooked meat from infected animals, or close contact with animal
secretions.

110
Q

brucellosis signs and symptoms/ Symptoms start gradually, are vague

A
  • Mild fever, sweating, weakness, aches and pains, enlarged lymph nodes,
    depression, weight loss
  • Recurrence of fevers over weeks or months
  • Recovery within 2 months without treatment; some develop chronic illness
111
Q

brucellosis causative agent

A

typically, Brucella melitensis the most virulent and
invasive species (sometimes B. abortus).

112
Q

B. melitensis is most commonly associated with

A

goats and sheep.

113
Q

B. melitensis

A

Small, aerobic, non-motile Gram-negative rods with complex nutritional requirements

114
Q

four species can infect humans (brucellosis)

A

B. abortus, B. canis, B. melitensis, and B. suis,
with melitensis being the most common; all species cause disease in other animals (cattle, pigs, dogs, goats).

115
Q

Brucellosis pathogenesis

A
  • Penetrate mucous membranes or wounds, weak initial immune response
  • Grow within phagocytes, avoid antibodies
  • Infected macrophages carry to other parts of body
  • Low mortality rate; death generally from endocarditis or meningitis; osteomyelitis (bone infection) is complication
116
Q

brucellosis epidemiology

A
  • Typically chronic zoonotic infection of domestic animals
  • Contaminates milk of animal species; causes abortions in cattle
  • Causes millions of dollars in agricultural losses globally
  • Occupational exposure; consumption of unpasteurized milk products;
    hunting, eating meat from infected animals
  • Category B bioterrorism threat
117
Q

brucellosis treatment and prevention

A
  • Doxycycline with rifampin or streptomycin for 6 weeks
  • Some chronic cases may require 6 months or more
  • Pasteurization of dairy products; inspection of domestic animals for
    evidence of disease
  • Protective gear (goggles or face shield, gloves) for veterinarians, butchers,
    slaughterhouse workers
  • Attenuated vaccine controls disease in domestic animals
118
Q

Brucellosis general infection

A

B. melitensis enters mucous membranes (ingestion/inhalation/skin abrasions) –> bacteria taken by phagocytes (resist digestion and grow w/in cells) –> bacteria enter lymphatics and bloodstream carried through body –> infection is established in body tissues (heart valves, meninges, bones) –> osteomyelitis is rare but serious complication (deaths due to endocarditis/meningitis)

119
Q

malaria

A

Ancient disease; malaria means “bad air”
* In 1902, Ronald Ross received Nobel Prize for demonstrating life cycle of protozoan cause of malaria

120
Q

in 1955, who began program for global elimination

A
  • Insecticide use; diagnosing and treating infected patients
  • 52 nations participated; by 1960, 10 eradicated malaria
  • Mosquito vectors developed resistance; program failed
121
Q

in 2019, over 228 million cases with over

A

400,000 deaths

122
Q

malaria signs and symptoms

A
  • Flu-like, with fever, headache, and pain in joints, muscles
  • Usually begin about 2 weeks after mosquito bite, but may be later
  • After 2 to 3 weeks, symptoms fall into three phases
123
Q

malaria symptoms phases

A

cold phase, hot phase, wet phase

124
Q

cold phase / stage

A

shaking chills that last up to an hour
(sensation of cold, shivering; 15 – 60 min)

125
Q

hot phase / stage

A

temperature rises sharply to 40 degrees Celsius or more
(fever, headaches, vomiting; seizures in young
children; 2-6 hours)

126
Q

wet phase / sweating stage

A

temperature falls, drenching sweat
(sweats, return to normal temperature,
tiredness; 2-4 hours)

127
Q

paroxysm

A

cycle of three phases malaria

128
Q

Except for fatigue, patient feels well until 24 or 48 hours later, when

A

next paroxysm occurs

129
Q

classic malaria attack lasts

A

6-10 hours

130
Q

attacks occur every _____ day with (P. falciparum, P. vivax,
and P. ovale) and every ______ day with the (P. malariae).

A

second; third

131
Q

malaria causative agent

A
  • Protozoa of genus Plasmodium; transmitted by infected female Anopheles mosquitoes
  • Five species cause malaria with different severity and treatment: P. vivax, P. falciparum, P. malariae, P. ovale, P. knowlesi
132
Q

complex life cycle of Plasmodium

A

(exoerythrocytic stage) and red blood cell
stage (erythrocytic stage)

133
Q

infectious form of Plasmodium is

A

sporozoite

134
Q

sporozoite carried by

A

bloodstream to liver, infects hepatocytes

135
Q

parasites enlarge, divide asexually, produce

A

merozoites

136
Q

merozoites

A

infect red blood cells (RBC)

137
Q

some species of Plasmoides can form

A

hypnozoites

138
Q

hypnozoites

A

live in hepatocytes for years before reproducing to form merozoites

139
Q

Merozoites develop into larger

A

motile trophozoites (feeding stage) and then schizont (reproducing stage)

140
Q

Schizont divides asexually to yield

A

merozoites; when RBC ruptures, they enter new RBCs and multiply, repeat cycle

141
Q

Some that enter RBCs develop into

A

gametocytes (specialized sexual forms), which are transmittable form

142
Q

Gametocytes ingested by mosquito; drop in temperature causes them to

A

become gametes, fertilize, form zygotes

143
Q

Zygotes form _______ that divide asexually

A

oocysts

144
Q

Sporozoites released from ______ travel to salivary glands and saliva; injected into ___ _____ ____

A

oocysts; new human host

145
Q

protozoan disease pathway

A

Infected mosquito injects P. vivax sporozoites
into a capillary as it feeds. –> Sporozoites are carried to the liver, where they multiply in liver cells to form merozoites.
The liver cells burst, releasing merozoites into
liver blood channels. –> The merozoites infect and differentiate in red blood cells (RBCs), becoming a ring form, then a trophozoite, then a schizont. The infected
RBC breaks open, releasing merozoites. Some
merozoites infect new RBCs, repeating this
cycle. Others infect new RBCs and then
differentiate in them, forming male or female
gametocytes. –> Another feeding mosquito ingests RBCs with gametocytes. –> The gametocytes are released as the RBCs are digested. –> The gametocytes become gametes, and fertilization occurs, forming a zygote. –> The zygote becomes motile and penetrates
the gut wall. –> In the gut wall, the zygote forms an oocyst
and multiplies asexually. –> The oocyst releases sporozoites that infect the mosquito’s salivary glands.

146
Q

malaria pathogenesis

A
  • Recurrent paroxysms result from cycle of growth and release of merozoites from RBCs
  • Infections in the millions of RBCs becomes synchronous
  • Anemia due to burst RBCs and loss of recyclable iron
  • Immune system strongly stimulated, may fail
  • Spleen enlarges to cope with high levels of foreign material and abnormal red blood cells; may rupture
  • P. falciparum infections often severe
  • It can infect all RBCs; other species infect either young or old RBCs
147
Q

malaria pathogenesis cont’

A

pfEMP1 (P. falciparum erythrocyte membrane protein) inserts in RBC membranes

148
Q

pfEMP1 causes

A

RBCS to stick to capillaries

149
Q

when RBS sticks to capillaries

A
  • Vessels blocked, tissues deprived of O2
  • Cerebral malaria: blockage of blood flow to the brain
  • Can block blood flow to developing fetus
  • Infected cells not cleared by spleen
150
Q

Antigenic variation in genes for pfEMP1 allow parasite to

A

evade adaptive immunity

151
Q

People generally develop some immunity from repeated infections; crosses the placenta and partially protects newborn

A

Greatest risk of death is to children over 6 months

152
Q

P. vivax and P. ovale often relapse because they form ______ that live in liver in dormant state

A

hypnozoites

153
Q

hypnozoites

A

Months or years later, can begin growth, start new erythrocytic cycles of infection

154
Q

malaria epidemiology

A

Once common in temperate and tropical areas of the world
* Eliminated from the continental U.S. in late 1940s
* Mostly a disease of warm climates; half of world’s population lives in endemic areas

155
Q

anopheles mosquitos act as

A

vectors, only females feed on blood and transmit disease

156
Q

what can transmit malaria?

A

Blood transfusions, sharing of needles among intravenous drug users

157
Q

some people of_______ _______ __________ are genetically resistant, RBCs lack receptors (Duffy antigen) for the parasite

A

black African heritage

158
Q

Individuals with certain genetically determined blood diseases (for example, sickle cell anemia) are

A

partially protected

159
Q

Malaria Treatment and prevention

A

chloroquine phosphate & Artemisinin-based combination therapies (ACTs)

160
Q

Chloroquine phosphate

A

Chloroquine is the preferred treatment for any parasite that is sensitive to the drug. But in many parts of the world, parasites are resistant to chloroquine, and the drug is no longer an effective treatment.

161
Q

Artemisinin-based combination therapies (ACTs).

A

ACT is a combination of two or more drugs that work against the malaria parasite in different ways. This is usually the preferred treatment for chloroquine-resistant malaria. Examples include artemether-lumefantrine (Coartem) and artesunate-mefloquine.

162
Q

prevention has become a

A

global focus

163
Q

In 1998, initiative called Roll Back Malaria started
* Goal was to ______________
* Efforts have led to _____ decrease
* Indoor spraying with DDT, insecticide-impregnated bed nets, elimination of ____ _____ _____

A

reduce deaths by 75% by 2015
60%
mosquito breeding areas

164
Q

malaria signs and symptoms

A

Recurrent cycles of intense chills and fever alternating with feeling healthy

165
Q

malaria incubation period

A

Varies with species; 6 to 37 days

166
Q

malaria causative agents

A

Five species of protozoa of the genus Plasmodium.

167
Q

malaria pathogenesis

A

Protozoan enters hepatocytes and multiplies in them; cells burst and release protozoa causing fever; organisms infect red blood cells, differentiating in them; spleen enlarges in response to removing large amount of foreign material and
many abnormal blood cells from the circulation; with P. falciparum infection, red blood cells stick together and to walls of capillaries, blocking vessels and
depriving tissue of O2.

168
Q

malaria epidemiology

A

Transmitted from person to person by the bite of infected Anopheles mosquito.

169
Q

malaria treatment and prevention

A

Treatment: usually Artemisinin-based combination therapies; other medicines if sensitivity known. Prevention: the same medications used for treatment; eradication of mosquito vectors; mosquito netting impregnated with insecticide; vaccines under development.

microbio km (6 decks)

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