CH 25 - Blood & Lymphatic Infections Flashcards
Bubo
(definition)
Enlarged, tender lymph node characteristic of plague & some sexually transmitted infection
Cytokine storm
(definition)
Uncontrolled release of pro-inflammatory cytokines that causes blood vessel leakiness & may lead to shock
Disseminated Intravascular Coagulation (DIC)
(definition)
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
Infective Endocarditis
(definition)
Inflammation of heart valves or lining of heart chambers resulting from infection
Lymphangitis
(definition)
Inflammation of lymphatic vessels
Paroxysm
(definition)
Sudden recurrence or worsening of symptoms as seen in cycle of chills, fever, & sweats of malaria
Petechiae
(definition)
Purple spots on skin & mucous membranes caused by blood leakage from small blood vessels
Sepsis
(definition)
Acute illness caused by inflammatory response that results when pathogens or their products circulate in the bloodstream
Septic shock (definition)
Range of effects that result from systemic inflammatory response to a bloodstream infection or circulating endotoxin
Effects include:
- Fever
- Drop in BP
- DIC
Septicemia
Illness that results from circulating agent in bloodstream
Bacteremia
Circulating of bacteria in bloodstream
Viremia
Circulating of viruses in bloodstream
Fungemia
Circulating of fungus cells in bloodstream
Toxemia
Circulating of bacterial toxins in blood
Endocarditis
Infections of heart valves or inner/blood-bathed surfaces of heart
Septicemia, bacteremia, & toxemia:
S/S
- 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
Exotoxins
Released from living microorganisms
Endotoxin
Released from G- bacteria
Septicemia, Bacteremia, & Toxemia:
Pathogens & virulence factors
Often opportunistic or nosocomial infections
- Capsule (resists phagocytosis)
- Capacity to capture iron needed for bacterial growth
- Endotoxin (produced by G- bacteria)
G- Septicemia:
Causative Agent
G- bacteria
- LPS endotoxin
More likely fatal cause of septicemia
G- Septicemia:
Symptoms
- Chills
- Fever
- Low BP
Shock common despite treatment
Mortality rate nearly 50%
G- Septicemia:
Blood cultures from pts usually reveal…
- 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
G- Septicemia:
Pathogenesis
- G- bacterial infection
- Endotoxin in bloodstream
- Macrophages activated
- Cytokines released (TNF-alpha & IL-1)
- Clotting activated (DIC, hemorrhage)
- Complement activated (lung tissue damage)
Tularemia (Rabbit Fever):
Causative Agent
F. tularensis
- High virulence (Category A agent of biological terrorism)
- G- rod
- Aerobic
- Non-motile
Tularemia (Rabbit Fever):
Pathogenesis
Causes ulcer where it enters skin
Spreads via lymphatic & blood vessels
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
Tularemia (Rabbit Fever):
Syndromes
(listed)
- Ulcerogladnular (70-85%)
- Glandular
- Typhoidal
- Pneumonic
- Oculoglandular
- Oropharyngeal
Tularemia (Rabbit Fever):
Symptoms
- Ulcer in side of entry
- Enlarged lymph nodes
- Fever
- Chills
- Achiness
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
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
Brucellosis (Undulant Fever)
Chronic infectious disease of domestic animals
Brucellosis (Undulant Fever):
Causative Agent
Brucella
- G- rod
4 varieties of genus Brucella cause disease in humans
- All fall under single species: Brucella melitensis
4 varieties of genus Brucella depending on preferred host
- B. abortus = cattle
- B. canis = dogs
- B. melitensis = goats
- B. suis = pigs
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
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
Brucellosis (Undulant Fever):
Pathogenesis
- Organism penetrates mucous membranes or break in skin
- Disseminated via lymphatic or blood vessels (generally to heart or kidney)
- 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
Brucellosis (Undulant Fever):
Treatment
Tetracycline combine with rifampin
- Usually given for 6 weeks (slow growing)
Plague (Black Death):
Causative Agent
Yersinia pestis
- G-
Transmission from infected flea bite
- Pneumonic plague transmitted person to person
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”)
Plague (Black Death):
Pathogenesis
- Masses of organism obstruct digestive tract of rats fleas
- Flea regurgitates infected material into bite wound - Most organisms destroyed by neutrophils
- Multiply within macrophages
- Produces capsule while in macrophages - Macrophages die & release organism
- Organ encapsulated & produces Yop proteins (& other mechanisms that enhance survival) - Inflammation in lymph nodes = swelling
- Lymph nodes become necrotic & spill organisms into bloodstream
Septic Plague
Endotoxin release results in shock & disseminated intravascular coagulation (DIC)
Pneumonic Plague
Results from infection of lungs
Plague (Black Death):
Virulence Factors
- Type III secretion system (T3SS)
- Yop
- Pla proteases
- Envelop (F-1) antigen
Plague (Black Death):
Yop
Group of 11 proteins
- Coded by plasmids
- Essential for pathogenesis
Secreted into host cells by T3SS
Plague (Black Death):
Pla proteases
Causes blood clots to dissolve
Destroys C3b & C5a components of complement
Plague (Black Death):
Envelope (F-1) antigen
Protein-polysaccharide complex
Anti-phagocytic
Plague (Black Death):
Prevention
Rodent control
- Proper garbage disposal
- Rat-proof buildings
- Guards on mooring ropes
- Extermination programs
Vaccines under development
Plague (Black Death):
Treatment
Antibiotics (control epidemics)
- Gentamycin
- Ciprofloxacin
- Doxycycline
Effective if given early
Infectious Mononucleosis
Viral infection that produces flu-like symptoms
Infected people have increased number of mononuclear leukocytes in blood
Infectious Mononucleosis:
Causative Agent
Epstein-Barr virus
- dsDNA
- Herpes virus family
1st isolated from Burkitt’s lymphoma
- Malignant tumor derived from B lymphocytes
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
Infectious Mononucleosis:
Pathogenesis
Virus infects cells that express receptor for complement C3D component (CR2/CD21)
- Epithelial cells of oro/nasopharynx & B cells
- Infection begins in throat & mouth
- Carried to lymph nodes
- Infect B cells
- Active B cells to proliferate & produce immunoglobulin
- T cells destroy infected B cells
Productive infection = virus kills cells
Nonproductive infection = virus is latent
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
Infectious Mononucleosis:
Prevention
Avoiding saliva of another person
NO vaccine
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
Yellow Fever:
Causative Agent
RNA arbovirus
- Enveloped
- ssRNA
- Flavivirus family
Transmitted to humans via bite of infected Aedes mosquitoes
- Multiplies within mosquitoes
Yellow Fever:
Pathogenesis
- Aedes mosquito bite
- Multiples & enters bloodstream (survives within macrophages)
- Carried to liver
- Damage (jaundice)
- Injury to small blood vessels (DIC)
Kidney failure = common consequence
- Loss of circulating blood & low BP
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
Yellow Fever:
Epidemiology
Reservoir = mosquitoes & primates
- Central/South American & Africa
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
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
Malaria:
Symptoms
- Fever
- Headache
- Pain in joints & muscles
Fever & chills on periodic basis
Malaria:
Life Cycle of Plasmodium spp.
- Mosquito injects sporozoites
- Liver - develop into merozoites
- Burst out of liver & infects RBCs - RBCs - develop into gametocytes
- Burst out of RBCs - Mosquitoes pick up gametocytes in blood
- Fertilization (zygote)
- Meiosis (oocyst)
- Sporozoites
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)
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
Malaria:
Prevention
Mosquito control
Malaria:
Treatment
Chloroquine
- Effective against erythrocyte stage
- Will NOT cure liver infection
Primaquine & tafenoquine
- Effective against exoerythrocyte stage & certain species gametocytes
