Download Blood and Lymphatic Infections

Blood and Lymphatic
Infections
Chapter 28
Tularemia (Rabbit Fever)
Symptoms
Characterized by
development of skin
ulcerations and
enlargement of regional
lymph nodes
Other symptoms include
Fever
Chills
Achiness
Tularemia (Rabbit Fever)
Causative agent - Francisella tularensis (aerobic, Gram- rod)
Pathogenesis
Causes ulcer at entry sight
Lymphatic vessels carry organism to regional lymph nodes, which
may rupture
Spread to other body sites via lymphatics and blood vessels
Pneumonia occurs in 10% -15% of lung infections
Mortality rate as high as 30%
Multiplies within phagocytes
Cell mediated immunity responsible for ridding infection
90% of infected individuals survive in the absence of treatment
Tularemia (Rabbit Fever)
Epidemiology
Occurs among wild animals in Northern Hemisphere
In eastern U.S. most infections occur in winter
Result from skinning hunted rabbits
In western U.S. infections increase in summer
Due to bites from fleas and ticks
Other reservoirs for infection include
Muskrats, beavers, squirrels, and deer
Animals generally free of illness
Tularemia (Rabbit Fever)
Prevention and Treatment
Uses of rubber gloves and goggles when working
with animal carcasses
Insect repellents and protective clothing
Inspect routinely for ticks after exposure
Vaccine available for workers at higher risk of
exposure
Treated with gentamicin
Brucellosis (Undulant Fever)
Symptoms
Onset usually gradual and symptoms vague
Symptoms include
Aches and pains
Enlarged lymph nodes
Weight loss
Without treatment most cases recover within 2 months
15% will be symptomatic for 3 months or longer
Brucellosis
(Undulant
Fever)
Causative agent
Four varieties of genus Brucella cause disease
in humans (Gram- rod)
All fall into a single species Brucella
melitensis
Traditionally each variety given own
species name depending on preferred
host
»
B. abortus  cattle
»
B. canis  dogs
»
B. melitensis  goats
»
B. suis  pigs
Brucellosis (Undulant Fever)
Pathogenesis
Organism penetrates mucous membranes or break in skin
Disseminated via lymphatic or blood vessels
Generally to heart and kidneys
Spleen enlarges in response to infection
Organisms resistant to phagocytic killing
Can grow within phagocytes
These organisms inaccessible to antibodies and some antibiotics
Mortality generally due to endocarditis
Rate is approximately 2%
Osteomyelitis is often serious side effect
Brucellosis (Undulant Fever)
Epidemiology
Chronic infection of domestic animals
Generally involving the mammary gland and uterus
Causes contaminated milk and abortions
Abortion not a feature of human disease
Occurs in workers in meat packing industry
Major problem in animals used for food
Brucellosis (Undulant Fever)
Prevention and Treatment
Pasteurization most important control measure
Inspection of domestic animals
Protective eyewear and gloves when working with
animals or animal carcass
Attenuated vaccine controls disease in domestic
animals
Tetracycline combined with rifampin used for treatment
Treatment usually given for 6 weeks
Plague (Black Death)
Symptoms
Develop abruptly 1 – 6 days post infection
Transmission via bite from infected flea
Disease characterized by large tender lymph nodes
called buboes
Other symptoms include
High fever
Shock
Delirium
Patchy bleeding under the skin
May also have cough and bloody sputum
Only in lungs infected
Pneumonic plague
Plague (Black Death)
Causative agent - Yersinia pestis
Facultative intracellular bacteria
Resemble safety pin in stained preparation
Has three plasmids
Smallest is Pla
Causes protective clots to dissolve via activation of
plasminogen activator
Middle plasmid codes Yops (Yersinia outer-membrane
proteins) and regulators of Yops proteins
Yops permits entry of organism into macrophages where
they replicate and interfere with innate immunity
Last is F1
Becomes anitphagocytic capsule
Used in plague vaccine
Not very good and notorious for adverse reactions
Pathogenesis Plague
(Black Death)
Masses of organism obstruct digestive tract
of rat fleas
Flea regurgitates infected material into bite
wound
Pla is essential to spread from site of entry
Organisms multiply within macrophages
Produce F1 capsule while in macrophages
Macrophages die and release organism
Organism encapsulated and produces Yops
and other mechanisms that enhance survival
Inflammation in nodes results in
characteristic swelling
Nodes become necrotic and spill organisms
Septicemic plague
Mortality rate of untreated reaches between
50% and 80%
Plague (Black Death)
Epidemiology
Endemic on rodent populations in all continents except
Australia
Prairie dogs, rock squirrels and their fleas are main
reservoir
Hundreds of fleas can transmit plague and can remain
infectious for a year
Can spread person to person by household fleas
Organism can remain viable for weeks in dried sputum and
flea feces
Plague (Black Death)
Prevention and Treatment
Prevention directed by rat control
Proper garbage disposal
Rat-proof buildings
Guards on mooring ropes
Extermination programs
Killed vaccine gives short-term partial protection
Treatment via tetracycline for some exposed individuals to
control epidemics
Gentimicin, ciprofloxacin and doxycycline effective on
disease if given early
Infectious Mononucleosis
Symptoms
Appear after long incubation
Usually 30 to 60 days post infection
Symptoms include fever, sore throat covered
with pus, fatigue, enlarged lymph nodes and
spleen
Most cases fever and sore throat disappear
within 2 weeks, lymph node enlargement
within 3
Infectious Mononucleosis
Causative agent
Caused by Epstein-Barr virus
Double stranded DNA virus
Belongs to herpesvirus family
Pathogenesis
Infection begins in cells of throat and mouth and
become latent in another cell type
Virus carried to lymph nodes after replication in
epithelial cells of mouth, saliva producing glands and
throat
Infects B lymphocytes
Infection can be productive or nonproductive
Productive – kills cells
Nonproductive – virus is latent
Virus activates B cells to produce multiple clones
Clones produce immunoglobulin
Pathogenesis of Epstein-Barr Virus
Infectious Mononucleosis
Epidemiology
Distributed worldwide
Infects individuals in crowded, economically
disadvantaged areas
Infects at early age without producing symptoms producing
immunity
More affluent populations missed exposure and lack immunity
Occurs almost exclusively in adolescents and adults
who lack antibody
Virus present in saliva for up to 18 months
Mouth-to-mouth kissing important mode of transmission
No animal reservoir
Infectious Mononucleosis
Prevention and Treatment
Avoiding saliva of another person
No vaccine
Acyclovir inhibits productive infection
Has no activity on latent viruses
Yellow Fever
Symptoms
Disease can range from mild to severe
Most common form may be only fever and slight
headache lasting a day or two
Severe disease characterized by high fever, nausea,
nose bleeds and bleeding into the skin, black vomit
from GI bleeding and jaundice
Mortality rate of severe disease can reach 50%
Reason for the variation in symptoms is unknown
Yellow Fever
Causative agent
Enveloped, single stranded RNA arbovirus
Belongs to flavivirus family
Virus multiplies in mosquitoes
Mosquitoes transmit virus to humans
Pathogenesis
Introduce via bite of Aedes mosquitoes
Multiplies and enters blood stream
Carried to liver
Jaundice results in liver damage
Injury to small blood vessels produces petechiae
Kidney failure is a common consequence of disease
Yellow Fever
Epidemiology
Reservoir mainly infected mosquitoes and primates in
tropical regions of Central and South America and
Africa
Periodically spread to urban areas via mosquito bite
Prevention and Treatment
Control achieved by spraying and elimination of
breeding sites
Control almost impossible in jungle regions
Attenuated vaccine available for high risk groups
No antiviral treatment
Malaria
Symptoms
“flu-like”
Includes fever, headache and pain in the joints and
muscles
Generally begin 2 weeks post infection
Transmission via bite of infected mosquito
Symptom pattern changes after 2 to 3 weeks
Fall into three categories
Cold phase – abruptly feels cold and develops shaking
Hot phase – follows cold phase
Temperature rises steeply reaching 104°F
Wet phase – follows hot phase
Temperature falls and drenching sweat occurs
Malaria
Malaria
Causative agent
Human malaria caused by
four species of genus
Plasmodium
•
P. vivax, P. falciparum, P.
malatiae, P. ovale
Infectious form of parasite
injected via mosquito
Carried by bloodstream to
liver
Infects cells of liver
Thousands of offspring
released to produce infection
in erythrocytes
Pathogenesis
Malaria
Characteristic feature
Recurrent bouts of fever followed by times of wellness
Caused by erythrocytic cycle of growth and release of offspring
Each species has different incubation periods, degrees
of severity and preferred host age and range
Spleen enlarges to cope with large amount of foreign
material and abnormal RBC
Common cause of splenic rupture
Parasites cause anemia by destroying red RBC and
converting iron from hemoglobin to an unusable form
Stimulates immune system
Overworked immune system fails and immunodeficiency
develops
Malaria
Epidemiology
Once common in both temperate and tropical areas
Now dominantly disease of warm climate
Eliminated from continental U.S. in late 1940s
Mosquitoes of genus Anopheles are biological vectors
Infected mosquitoes and humans constitute reservoir
Transmission via mosquitoes, blood transfusion and
sharing of syringes
Malaria
Prevention and Treatment
Treatment is complicated
Due to different stages of mosquito life cycle
Chloroquine
Effective against erythrocyte stage
Will not cure liver infection
Primaquine and tafenoquine
Generally effective against exoerythrocyte stage
and certain species gametocytes