Ch 25: Circulatory and Lymphatic System infections Flashcards
Organs in the circulatory and lymphatic system
capillaries, capillaries, capillaries
Includes the circulatory system (blood) and lymphatic system (return of fluid from the tissues)
heart arteries, capillaries, veins lymphatic vessels spleen kidney figures 25.2, 25.3, 25.4
Primary lympoid tissue
bone marrow which contains hematopoietic stem cells
thymus where T cells mature
Secondary lymphoid tissue
splees wherre filtration of the lymph fluid takes place
macrophage and DC for antigen presentation
lymph nodes
contain germinal centres for B cells and Ab produciton
also many macrophage and DC for antigen presentation
Lymph fluid enters through afferent lymphatic vessels
leaves through efferent lymph vessels
Circulatory system is nomally sterile
no normal flora, circulating microoganisms can occur
bacteremia
circulating bacteria in the bloodstream
septicemia
reproducing bacteria in the bloodstream
viremia
viruses circulating in the bloodstream
septic shock
low blood pressure, loss of blood volume, organ failure, death
release of IL-1 and TNF due to infection
Toxic shock syndrome
Staphylococcus aureus
similar condition due to streptococcus pyogenes
production fo a toxin which acts as a superantigen
=> activation of about 20% of T cells and excess production of cytokines
sudden onset, high fever, vomiting, diarrgea, myalgia, sudden blood pressure drop, later peeling of skin
Treatment of toxic shock syndrome
treatment of circulating bacteria
clindamycin, vancomycin, daptomycin
removal of infected tissue - debridement
vasopressors to increase blood pressure
Puerperal sepsis
puerperal fever, childbed fever
nosocomial infection after childbirth, UTI or surgical wound
mostly streptococcus pyogenes
=> also other strep species, staph aureus, gram negative enterics such as E. coli, klebsiella pneumoniae, proteus species
anaerobes such as bacteriodes
antibiotic treatment
Infectious arthritis
also called septic arthritis
inflammation of the joint capsules and fluid due to bacterial pathogen ( less frequently fungi or viruses)
usually due to bacteria in the circulatory system
- hematogenous spread (bacteria spread though the circulatory system)
- treatment by prolonged antibiotic therapy (hard to get rid of, 20-30+ days)
- mortality 5-20%, 40% with permanent join damage
Osteomyelitis
culprits
inflammation of bone tissue by bacteria
staphylococcus aureus
mycobacterium tuberculosis
pseudomonas aeruginosa
strep spp.
childer most commonly infected through the blood stream
symptoms and treatment of osteomyelitis
fever, localized pain, swelling, soft tissue ulcers
spreads to joints and to bloodstream
broad spectrum antibiotics including vancomycin
=> implanted antibiotic beads
removal of infected bone
hyperbaric oxygen
Gas Gangrene
Due to anerobic condition in the tissue, lack of blood flow
clostridium perfringens, can be other anaerobes
expanding zone of necrotic tissues
pain, bad smell, gas bubbles, yellow discharge, tissue liquidification
usully need surgery or amputation
hyperbaric oxygen and antibiotics
50% fatality rate
Tularemia
caused by Francisella tularensis
=> zoonotic diseaase, reservoir are mammals like rabbits, muskrats and voles
spread through contact or vector
=> dog ticks (dermacentro variablis) and wood ticks (D> andersoni)
skin lesions (enter and leaave through cuts), fever and chills, swollen lymph nodes
3 day incubation
Tularemia dissemination
bacteria enters into lymphatic system though breaks in skin
ID50 = less than 50 cells needed to cause an infection (anything under 1000-100 in very contagious)
transport to regional lymph nodes
ingestion by macrophage
escape from lysosome and replication in macrophage cytoplasm
dissemination through circulatory system
formation of granulomas
Tularemia subspecies
also a pulmonary form from inhaling aerosols
there are two subspecies A and B
A is found only in North america and has a fatality rate of about 5%
=> 30-60% in repiratory cases
B is found in europe and asia and is `relatively benign
Brucellosis
Brucella abortus, B. canis, B. suis, B. melitensis
Gram-negative coccobacillus 0.6um long, 0.5 um wide
Facultatively intracellular
Aerobic but grow best in 5% CO2
Zoonotic infection, natural hosts dogs, cattle, reindeer, caribou, sheep and goat, pigs, deser wood rats
about 100 cases/ year in the us
Brucellosis Transmission
contact with contaminated animals, tools
airborne
consumption of contaminated meat or milk/ milk products (major route)
Brucellosis symptoms
undulating fever, sweating, headache, malaise, fatigue, join pain and depression
Brucellosis treatment
Doxycyline and streptomycin for 6-8 weeks
=> doxycyclin and rifampin
about 15% of treated patient will relapse.
Herd animal vaccination and eradication programs have reducted or elimated brucellosis in North America
Wild animal reservoir bison and caribou
Cat-scratch disease
also called cat scratch fever
bartonella henselae
Gram-negative pleomorphic bacilus 0.3-0.6um wide and 1-1.7 um long. no capsule, fastidious, aerobic but groaw best with 5% Co2
grows on blood agar but takes 5-45 days for colonies to grow
Transmission of cat-scratch fever
transmission by catt bite or scratch
=> up to 40% of domestic cats are infected
=> spread between them by fleas
Local pus filled nodule 1-3 weeks after infection
B. henselae can infect rbc and disseminate
also infect endothelial cells
B. henselae migration to the lymph nodes
may infect macrophages and other immune cells (no granuloma)
fever, chills, fatigue, swollen and painful lymph nodes
in immunocompromised patients may proceed to bacillary angiomatosis which are tumors in organs due to proliferation of blood vessels
Trench fever
caused by bartonella quintana, transmitted by the human louse
human reservoir but has been found in cats, dogs, and fleas and ticks
Carrions diseaase
caused by bartonella bacilliformis
characterized by acute hemolytic bacteriemia
human reservoir
Other bartonella species
HAVE BEEN FOUND ISOLATED FROM squirrels, mice, fox, cattle and sea otters
other bartonella species (there are 22) have been implicated in human diseases
Bubonic plauge
yersinia pestis
Gram negative, non-motile bacillus, faculatatively anerobic, negative to most biochemical tests, slow grower`
Mammalian hosts of y pesits
mormots, gerbils, ground squirrels and prarie dogs
blat rats, and norwegian rats
Y pestis transmision by fleas
fleas bite infected host, bacteria multiply and block the proventriculus, fleas starve and bite, blood mixed with blockage and is regurgitated into the bite wound
Vector transmission of bubonic plauge
epidemics of plauge spread thorugh natural hosts, fleas leave natural host and find new host
often a different host including people
spread to people by flea bite (vector transmission, bubonic plauge)
bacteria spread to circulatory system (septcemic plauge) and to lungs
Aerosol transmission (pneumonic plauge)
Transmission cycles of Y. pestis
Sylvatic cycle in natural hosts in non-urban areas, transmission through fleas
Urban cycle between rats through fleas
transmission from either source to humans with human to human transmission through fleas and aerosols
Y pestis symptoms
2-6 day incubation
abrupt fever and chills, headache, inflammation of regional lypmh nodes, painful, leads to swelling, hemorrhaging
Swollen lymph nodes particularly in the groin and armpits- buboes
if modes into septicemic plague then DIC (disseminated intravascular coafulation occurs)
Y pestis
DIC= disseminated intravascular coagulation
DIC leads to blockafe of capillaries and small blood vessels, necrosis of tissue
=> blackening of toes and fingers
Septic shock, organ failure, respirator distress
mortality rates of plauge
50% IN BUBONIC
100 in septicemic
100% in 2 days with pneumonic
(all above without antibiotic treatment)
Pneumonic plague
1-3 day incubation
chill followed by fever, productive cough (bloody or watery), pneumonia, shortness of breath, ulceration, caviation of lungs
antibiotic treatment
=> streptomycin (still sensitive)
=> doxycline/ ciprofloxacin (levofloxacin)
=> chloramphenicol
Typhus
epidemic typhus caused by Rickettsia prowazekii and transmitted by human louse Pediculus humanus
associated with war and civic disruptions
mortality rates of up to 40%
Gram negative, very pleomorphic cells
obligately intracellular, cannot synthesize amino acids, no glycolysis
Lyme diseas (emergin disease?)
LYME BORRELIOSIS
=> Borrelia burgdoferi
the most common tick-born disease in north america and europe
named after an outbreak of apparently rheumatoid arthritis in children around the town of old lyme, connecticut in 1975
most cases were characterised by an annular skin rash preceding the arthritis by a month
subsequent investigation of ticks from the area revealed a spirochete which was immunologically cross-reactive with the affected childrens’s serum
Primary stage of lyme disease
distinctive sign is erythema migrans (EM) the bulls eye rash at the site of the tick bite
=> 10% do not have RM
arthralfia, myalgia, fever, severe fatigue and regional lymphadenopathy are also common
bacteria may spread quickly through the blood (hematogenous dissemination) and secondary EMs appear in the skin
Lyme disease Secondary stage
neurological abnormalities
meningoradiculitis (bannwarth syndrome), inflammation of the meninges and spinal nerve roots
pain and paresis, facial palsy
meningitis
borrelial carditis (8% of patients) distruvance of heart beat
dizziness, palpitations
Lyme disease tertiary stage
asymmetric olifoarticlar arthirits (60% of patients)
one-sided arthritis of the major joints, usually the knees and elbows
episodes last days to weeks,may resolve or reoccur
Rare neurolofical complications of lyme disease tertiary stage
chroncally progressive meningoencephalitis
chroncally progressive meningoencephalitis which is irreversible CNS damage
Rare neurolofical complications of lyme disease tertiary stage
cerbral vasculitis
cerbral vasculitis whihc is a destructive inflammation of the blood vessel accomplnied by a lyphocytic infiltrate
Rare neurolofical complications of lyme disease tertiary stage
subacute encephalopathy
subacute encephalopathy whihc causes memory loss, lack of concentrationa and personality changes
Post-Lyme disorder
patients with well diagnosed lyme disease who, after receiving adequate antibiotic therapy suffer:
nonspecific fatigue
sleep disorders
headaches
memory disorders
joint and muscle pain
post lymantibiotic refractory lyme arthritis
arthritis persists after 1 or more antibiotic treatments
treament of lyme disease
oral doxycline except for children and pregnant woman then amoxicillin
14-28 days
for lyme neurological disease and severe cardiac complications parenteral ceftriaxone, cefotaxime or penicillin G
Vectors of Lyme disease
ticks of the genus ixodes are usual vectors
ixodes scapularis (blacklegged tick) is the most common N american vector
Vector biology of lyme disease
egg to larva
ticks have 4 life stages
egg, larva, mypmh, adult
generally eggs are not infected, the larvae acquire B. burgorferi after feeding on an infected host
for the larvae hosts are small mammals such as the white-footed mouse peromyscus leucopus
Vector biology of lyme disease
mymphs to adult
nymphs move from host to host
life stage which most commonly transmits the disease to humans
adult ticks move to larger hosts such as deer take a final blood meal and lay eggs
adults can transmit B. burgorferi to their hosts
do not usually pass on the bacterium to the eggs
lyme disease in europe
borrelia afzelii and borrelia garinii in eurpoe
bullseye rash first noted in Sweden in 1909, Borrelia observed in 1948
