CH 25 - Blood & Lymphatic Infections Flashcards
(67 cards)
1
Q
Bubo
(definition)
A
Enlarged, tender lymph node characteristic of plague & some sexually transmitted infection
2
Q
Cytokine storm
(definition)
A
Uncontrolled release of pro-inflammatory cytokines that causes blood vessel leakiness & may lead to shock
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
4
Q
Infective Endocarditis
(definition)
A
Inflammation of heart valves or lining of heart chambers resulting from infection
5
Q
Lymphangitis
(definition)
A
Inflammation of lymphatic vessels
6
Q
Paroxysm
(definition)
A
Sudden recurrence or worsening of symptoms as seen in cycle of chills, fever, & sweats of malaria
7
Q
Petechiae
(definition)
A
Purple spots on skin & mucous membranes caused by blood leakage from small blood vessels
8
Q
Sepsis
(definition)
A
Acute illness caused by inflammatory response that results when pathogens or their products circulate in the bloodstream
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
10
Q
Septicemia
A
Illness that results from circulating agent in bloodstream
11
Q
Bacteremia
A
Circulating of bacteria in bloodstream
12
Q
Viremia
A
Circulating of viruses in bloodstream
13
Q
Fungemia
A
Circulating of fungus cells in bloodstream
14
Q
Toxemia
A
Circulating of bacterial toxins in blood
15
Q
Endocarditis
A
Infections of heart valves or inner/blood-bathed surfaces of heart
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
17
Q
Exotoxins
A
Released from living microorganisms
18
Q
Endotoxin
A
Released from G- bacteria
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)
20
Q
G- Septicemia:
Causative Agent
A
G- bacteria
- LPS endotoxin
More likely fatal cause of septicemia
21
Q
G- Septicemia:
Symptoms
A
- Chills
- Fever
- Low BP
Shock common despite treatment
Mortality rate nearly 50%
22
Q
G- Septicemia:
Blood cultures from pts usually reveal…
A
- E. coli
- G- facultative anaerobe - P. aeruginosa
- G- aerobe
- Generally found in natural environment - Bacteroides species
- G- anaerobe
- Part of normal intestine & upper respiratory flora
23
Q
G- Septicemia:
Pathogenesis
A
- G- bacterial infection
- Endotoxin in bloodstream
- Macrophages activated
- Cytokines released (TNF-alpha & IL-1)
- Clotting activated (DIC, hemorrhage)
- Complement activated (lung tissue damage)
24
Q
Tularemia (Rabbit Fever):
Causative Agent
A
F. tularensis
- High virulence (Category A agent of biological terrorism)
- G- rod
- Aerobic
- Non-motile
25
Tularemia (Rabbit Fever):
Pathogenesis
Causes ulcer where it enters skin
Spreads via lymphatic & blood vessels
26
Tularemia (Rabbit Fever):
Pneumonia
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
27
Tularemia (Rabbit Fever):
Syndromes
(listed)
1. Ulcerogladnular (70-85%)
2. Glandular
3. Typhoidal
4. Pneumonic
5. Oculoglandular
6. Oropharyngeal
28
Tularemia (Rabbit Fever):
Symptoms
- Ulcer in side of entry
- Enlarged lymph nodes
- Fever
- Chills
- Achiness
29
Tularemia (Rabbit Fever):
Epidemiology
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
Tularemia (Rabbit Fever):
Prevention & Treatment
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
Brucellosis (Undulant Fever)
Chronic infectious disease of domestic animals
32
Brucellosis (Undulant Fever):
Causative Agent
Brucella
- G- rod
4 varieties of genus Brucella cause disease in humans
- All fall under single species: Brucella melitensis
33
4 varieties of genus Brucella depending on preferred host
1. B. abortus = cattle
2. B. canis = dogs
3. B. melitensis = goats
4. B. suis = pigs
34
Brucellosis (Undulant Fever):
Symptoms
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
Brucellosis (Undulant Fever):
Epidemiology
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
Brucellosis (Undulant Fever):
Pathogenesis
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
Brucellosis (Undulant Fever):
Treatment
Tetracycline combine with rifampin
- Usually given for 6 weeks (slow growing)
38
Plague (Black Death):
Causative Agent
Yersinia pestis
- G-
Transmission from infected flea bite
- Pneumonic plague transmitted person to person
39
Plague (Black Death):
Symptoms
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
Plague (Black Death):
Pathogenesis
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
Septic Plague
Endotoxin release results in shock & disseminated intravascular coagulation (DIC)
42
Pneumonic Plague
Results from infection of lungs
43
Plague (Black Death):
Virulence Factors
1. Type III secretion system (T3SS)
2. Yop
3. Pla proteases
4. Envelop (F-1) antigen
44
Plague (Black Death):
Yop
Group of 11 proteins
- Coded by plasmids
- Essential for pathogenesis
Secreted into host cells by T3SS
45
Plague (Black Death):
Pla proteases
Causes blood clots to dissolve
Destroys C3b & C5a components of complement
46
Plague (Black Death):
Envelope (F-1) antigen
Protein-polysaccharide complex
Anti-phagocytic
47
Plague (Black Death):
Prevention
Rodent control
- Proper garbage disposal
- Rat-proof buildings
- Guards on mooring ropes
- Extermination programs
Vaccines under development
48
Plague (Black Death):
Treatment
Antibiotics (control epidemics)
- Gentamycin
- Ciprofloxacin
- Doxycycline
Effective if given early
49
Infectious Mononucleosis
Viral infection that produces flu-like symptoms
Infected people have increased number of mononuclear leukocytes in blood
50
Infectious Mononucleosis:
Causative Agent
Epstein-Barr virus
- dsDNA
- Herpes virus family
1st isolated from Burkitt's lymphoma
- Malignant tumor derived from B lymphocytes
51
Infectious Mononucleosis:
Symptoms
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
Infectious Mononucleosis:
Pathogenesis
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
Infectious Mononucleosis:
Epidemiology
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
Infectious Mononucleosis:
Prevention
Avoiding saliva of another person
NO vaccine
55
Infectious Mononucleosis:
Treatment
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
Yellow Fever:
Causative Agent
RNA arbovirus
- Enveloped
- ssRNA
- Flavivirus family
Transmitted to humans via bite of infected Aedes mosquitoes
- Multiplies within mosquitoes
57
Yellow Fever:
Pathogenesis
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
Yellow Fever:
Symptoms
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
Yellow Fever:
Epidemiology
Reservoir = mosquitoes & primates
- Central/South American & Africa
60
Yellow Fever:
Prevention & Treatment
Spraying & eliminating breeding sites of Aedes egypti
- Almost impossible in jungle regions
Attenuated vaccine (high risk groups)
NO proven antiviral treatment
61
Malaria:
Causative Agent
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
Malaria:
Symptoms
- Fever
- Headache
- Pain in joints & muscles
Fever & chills on periodic basis
63
Malaria:
Life Cycle of Plasmodium spp.
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
Malaria:
Pathogenesis
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
Malaria:
Epidemiology
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
Malaria:
Prevention
Mosquito control
67
Malaria:
Treatment
Chloroquine
- Effective against erythrocyte stage
- Will NOT cure liver infection
Primaquine & tafenoquine
- Effective against exoerythrocyte stage & certain species gametocytes
