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Microbiology > CH 25 - Blood & Lymphatic Infections > Flashcards

CH 25 - Blood & Lymphatic Infections Flashcards

1
Q

Bubo
(definition)

A

Enlarged, tender lymph node characteristic of plague & some sexually transmitted infection

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2
Q

Cytokine storm
(definition)

A

Uncontrolled release of pro-inflammatory cytokines that causes blood vessel leakiness & may lead to shock

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3
Q

Disseminated Intravascular Coagulation (DIC)
(definition)

A

Condition in which clots form in small blood vessels throughout body

Causes organ failure due to lack of O2 & bleeding due to shortage of clotting proteins

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4
Q

Infective Endocarditis
(definition)

A

Inflammation of heart valves or lining of heart chambers resulting from infection

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5
Q

Lymphangitis
(definition)

A

Inflammation of lymphatic vessels

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6
Q

Paroxysm
(definition)

A

Sudden recurrence or worsening of symptoms as seen in cycle of chills, fever, & sweats of malaria

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7
Q

Petechiae
(definition)

A

Purple spots on skin & mucous membranes caused by blood leakage from small blood vessels

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8
Q

Sepsis
(definition)

A

Acute illness caused by inflammatory response that results when pathogens or their products circulate in the bloodstream

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9
Q

Septic shock (definition)

A

Range of effects that result from systemic inflammatory response to a bloodstream infection or circulating endotoxin

Effects include:
- Fever
- Drop in BP
- DIC

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10
Q

Septicemia

A

Illness that results from circulating agent in bloodstream

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11
Q

Bacteremia

A

Circulating of bacteria in bloodstream

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12
Q

Viremia

A

Circulating of viruses in bloodstream

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13
Q

Fungemia

A

Circulating of fungus cells in bloodstream

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14
Q

Toxemia

A

Circulating of bacterial toxins in blood

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15
Q

Endocarditis

A

Infections of heart valves or inner/blood-bathed surfaces of heart

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16
Q

Septicemia, bacteremia, & toxemia:
S/S

A
  • Fever
  • Chills
  • Nausea
  • Vomiting
  • Diarrhea
  • Malaise
  • Septic shock (can develop rapidly)
  • Petechiae (small hemorrhagic lesions)
  • Osteomyelitis ( can occur when bacteria invade bones)

Toxemia symptoms vary depending on endotoxin vs exotoxin

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17
Q

Exotoxins

A

Released from living microorganisms

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18
Q

Endotoxin

A

Released from G- bacteria

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19
Q

Septicemia, Bacteremia, & Toxemia:
Pathogens & virulence factors

A

Often opportunistic or nosocomial infections

  • Capsule (resists phagocytosis)
  • Capacity to capture iron needed for bacterial growth
  • Endotoxin (produced by G- bacteria)
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20
Q

G- Septicemia:
Causative Agent

A

G- bacteria
- LPS endotoxin

More likely fatal cause of septicemia

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21
Q

G- Septicemia:
Symptoms

A
  • Chills
  • Fever
  • Low BP

Shock common despite treatment
Mortality rate nearly 50%

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22
Q

G- Septicemia:
Blood cultures from pts usually reveal…

A
  1. E. coli
    - G- facultative anaerobe
  2. P. aeruginosa
    - G- aerobe
    - Generally found in natural environment
  3. Bacteroides species
    - G- anaerobe
    - Part of normal intestine & upper respiratory flora
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23
Q

G- Septicemia:
Pathogenesis

A
  1. G- bacterial infection
  2. Endotoxin in bloodstream
    - Macrophages activated
    - Cytokines released (TNF-alpha & IL-1)
    - Clotting activated (DIC, hemorrhage)
    - Complement activated (lung tissue damage)
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24
Q

Tularemia (Rabbit Fever):
Causative Agent

A

F. tularensis
- High virulence (Category A agent of biological terrorism)
- G- rod
- Aerobic
- Non-motile

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25
Q

Tularemia (Rabbit Fever):
Pathogenesis

A

Causes ulcer where it enters skin

Spreads via lymphatic & blood vessels

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26
Q

Tularemia (Rabbit Fever):
Pneumonia

A

Occurs when bacteria infect lung from bloodstream or by inhalation

Occurs in 10-15% of lung infections
- Mortality rate as high as 30%

Can survive & replicate in macrophages

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27
Q

Tularemia (Rabbit Fever):
Syndromes
(listed)

A
  1. Ulcerogladnular (70-85%)
  2. Glandular
  3. Typhoidal
  4. Pneumonic
  5. Oculoglandular
  6. Oropharyngeal
28
Q

Tularemia (Rabbit Fever):
Symptoms

A
  • Ulcer in side of entry
  • Enlarged lymph nodes
  • Fever
  • Chills
  • Achiness
29
Q

Tularemia (Rabbit Fever):
Epidemiology

A

Eastern US infections
- Winter months
- Skinning rabbits

Western US infections
- Summertime
-Bites of ticks & deer flies

European epidemics
- Inhalation tularemia
- Dust arising from mowing lawns or rodent infested buildings

30
Q

Tularemia (Rabbit Fever):
Prevention & Treatment

A

Cell-mediated immunity responsible for eliminating infection

Inspect routinely for ticks after exposure

Live/attenuated vaccine
- Available for workers at higher risk of exposure

Streptomycin (drug of choice)
- Also treated with gentamicin

31
Q

Brucellosis (Undulant Fever)

A

Chronic infectious disease of domestic animals

32
Q

Brucellosis (Undulant Fever):
Causative Agent

A

Brucella
- G- rod

4 varieties of genus Brucella cause disease in humans
- All fall under single species: Brucella melitensis

33
Q

4 varieties of genus Brucella depending on preferred host

A
  1. B. abortus = cattle
  2. B. canis = dogs
  3. B. melitensis = goats
  4. B. suis = pigs
34
Q

Brucellosis (Undulant Fever):
Symptoms

A

Gradual onset

Vague symptoms
- Aches
- Pains
- Enlarged lymph nodes
- Weight loss
- Fever

Recurrence in some cases of fevers over weeks/months (“undulant fever”)

Most cases recover within 2 months without treatment
- 15% symptomatic for 3 months or longer

35
Q

Brucellosis (Undulant Fever):
Epidemiology

A

Chronic infection of domestic animals
- Involving mammary gland & uterus (organs rich in sugar)
- Causes contaminated milk & abortions (no abortion in humans)

Occurs in workers in meat packing industry

Major problem in animals used for food

36
Q

Brucellosis (Undulant Fever):
Pathogenesis

A
  1. Organism penetrates mucous membranes or break in skin
  2. Disseminated via lymphatic or blood vessels (generally to heart or kidney)
  3. Spleen enlarges in response to infection
    - Can grow within phagocytes
    - Inaccessible to Abs or antibiotics

Mortality due to endocarditis (~2%)

Most frequent serious complication = bone infection

37
Q

Brucellosis (Undulant Fever):
Treatment

A

Tetracycline combine with rifampin
- Usually given for 6 weeks (slow growing)

38
Q

Plague (Black Death):
Causative Agent

A

Yersinia pestis
- G-

Transmission from infected flea bite
- Pneumonic plague transmitted person to person

39
Q

Plague (Black Death):
Symptoms

A

Develop abruptly 1-6 days post infection

  • Large/tender lymph nodes (buboes = “bubonic”)
  • High fever
  • Shock
  • Delirium
  • Patchy bleeding under skin (intramuscular coagulations; “black death”)
40
Q

Plague (Black Death):
Pathogenesis

A
  1. Masses of organism obstruct digestive tract of rats fleas
    - Flea regurgitates infected material into bite wound
  2. Most organisms destroyed by neutrophils
  3. Multiply within macrophages
    - Produces capsule while in macrophages
  4. Macrophages die & release organism
    - Organ encapsulated & produces Yop proteins (& other mechanisms that enhance survival)
  5. Inflammation in lymph nodes = swelling
    - Lymph nodes become necrotic & spill organisms into bloodstream
41
Q

Septic Plague

A

Endotoxin release results in shock & disseminated intravascular coagulation (DIC)

42
Q

Pneumonic Plague

A

Results from infection of lungs

43
Q

Plague (Black Death):
Virulence Factors

A
  1. Type III secretion system (T3SS)
  2. Yop
  3. Pla proteases
  4. Envelop (F-1) antigen
44
Q

Plague (Black Death):
Yop

A

Group of 11 proteins
- Coded by plasmids
- Essential for pathogenesis

Secreted into host cells by T3SS

45
Q

Plague (Black Death):
Pla proteases

A

Causes blood clots to dissolve

Destroys C3b & C5a components of complement

46
Q

Plague (Black Death):
Envelope (F-1) antigen

A

Protein-polysaccharide complex

Anti-phagocytic

47
Q

Plague (Black Death):
Prevention

A

Rodent control

  • Proper garbage disposal
  • Rat-proof buildings
  • Guards on mooring ropes
  • Extermination programs

Vaccines under development

48
Q

Plague (Black Death):
Treatment

A

Antibiotics (control epidemics)

  • Gentamycin
  • Ciprofloxacin
  • Doxycycline

Effective if given early

49
Q

Infectious Mononucleosis

A

Viral infection that produces flu-like symptoms

Infected people have increased number of mononuclear leukocytes in blood

50
Q

Infectious Mononucleosis:
Causative Agent

A

Epstein-Barr virus
- dsDNA
- Herpes virus family

1st isolated from Burkitt’s lymphoma
- Malignant tumor derived from B lymphocytes

51
Q

Infectious Mononucleosis:
Symptoms

A

Appear after long incubation
- 30-60 days post infection

  • Fever
  • Sore throat (covered with pus)
  • Fatigue
  • Enlarged lymph nodes & spleen

In most cases:
- Fever & sore throat disappear within 2 weeks
- Lymph node enlargement disappears within 3 weeks

52
Q

Infectious Mononucleosis:
Pathogenesis

A

Virus infects cells that express receptor for complement C3D component (CR2/CD21)
- Epithelial cells of oro/nasopharynx & B cells

  1. Infection begins in throat & mouth
  2. Carried to lymph nodes
  3. Infect B cells
  4. Active B cells to proliferate & produce immunoglobulin
  5. T cells destroy infected B cells

Productive infection = virus kills cells
Nonproductive infection = virus is latent

53
Q

Infectious Mononucleosis:
Epidemiology

A

Infects at early age without producing symptoms (leads to immunity)
- More affluent populations missed exposure & lack immunity

Occurs almost exclusively in adolescents & adults who lack Ab

Present in saliva for up to 18 months
- Mouth to mouth kissing = important mode of transmission

NO animal reservoir

54
Q

Infectious Mononucleosis:
Prevention

A

Avoiding saliva of another person

NO vaccine

55
Q

Infectious Mononucleosis:
Treatment

A

Acyclovir
- Inhibits productive infection
- NO activity on latent virus

Latent virus linked to:
- Cancers (Hodgkin’s & Burkitt’s lymphoma)
- Possible MS, Parkinson’s, & others

56
Q

Yellow Fever:
Causative Agent

A

RNA arbovirus
- Enveloped
- ssRNA
- Flavivirus family

Transmitted to humans via bite of infected Aedes mosquitoes
- Multiplies within mosquitoes

57
Q

Yellow Fever:
Pathogenesis

A
  1. Aedes mosquito bite
  2. Multiples & enters bloodstream (survives within macrophages)
  3. Carried to liver
    - Damage (jaundice)
    - Injury to small blood vessels (DIC)

Kidney failure = common consequence
- Loss of circulating blood & low BP

58
Q

Yellow Fever:
Symptoms

A

Range from mild to severe
- Reason for variation unknown

Fever & headache lasting 1-2 days (most common)

Severe disease:
- High fever
- Nose bleeds
- Bleeding into skin
- “Black” vomit (GI bleeding)
- Jaundice

59
Q

Yellow Fever:
Epidemiology

A

Reservoir = mosquitoes & primates
- Central/South American & Africa

60
Q

Yellow Fever:
Prevention & Treatment

A

Spraying & eliminating breeding sites of Aedes egypti
- Almost impossible in jungle regions

Attenuated vaccine (high risk groups)

NO proven antiviral treatment

61
Q

Malaria:
Causative Agent

A

4 species of genus Plasmodium (human malaria:
1. P. vivax
2. P. falciparum
3. P. malariae
4. P. ovale

Infectious form of parasite injected via Anopheles mosquito

Most common serious infectious disease worldwide

62
Q

Malaria:
Symptoms

A
  • Fever
  • Headache
  • Pain in joints & muscles

Fever & chills on periodic basis

63
Q

Malaria:
Life Cycle of Plasmodium spp.

A
  1. Mosquito injects sporozoites
  2. Liver - develop into merozoites
    - Burst out of liver & infects RBCs
  3. RBCs - develop into gametocytes
    - Burst out of RBCs
  4. Mosquitoes pick up gametocytes in blood
    - Fertilization (zygote)
    - Meiosis (oocyst)
    - Sporozoites
64
Q

Malaria:
Pathogenesis

A

Most common cause of splenic rupture

P. falciparum = most severe infection
- Infects RBCs of all ages

P. vivax & ovale develop treatment-resistant forms
- Can begin multiplying into exoerythrocytic cycle months after treatment

Develop into merozoites in liver & infect RBCs
- Erythrocytic cycle (growth & release of merozoites)

65
Q

Malaria:
Epidemiology

A

Dominant disease of warm climate

Eliminated from US in late 1940s

Biological vectors = Anopheles mosquitoes
- Mosquitoes & humans = reservoir

Transmitted via:
1. Mosquitoes
2. Blood transfusion
3. Sharing syringes

66
Q

Malaria:
Prevention

A

Mosquito control

67
Q

Malaria:
Treatment

A

Chloroquine
- Effective against erythrocyte stage
- Will NOT cure liver infection

Primaquine & tafenoquine
- Effective against exoerythrocyte stage & certain species gametocytes

Microbiology (15 decks)

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