Ch 25: Circulatory and Lymphatic System infections Flashcards

1
Q

Organs in the circulatory and lymphatic system

A

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
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2
Q

Primary lympoid tissue

A

bone marrow which contains hematopoietic stem cells

thymus where T cells mature

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3
Q

Secondary lymphoid tissue

A

splees wherre filtration of the lymph fluid takes place

macrophage and DC for antigen presentation

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4
Q

lymph nodes

A

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

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5
Q

Circulatory system is nomally sterile

A

no normal flora, circulating microoganisms can occur

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6
Q

bacteremia

A

circulating bacteria in the bloodstream

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7
Q

septicemia

A

reproducing bacteria in the bloodstream

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8
Q

viremia

A

viruses circulating in the bloodstream

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9
Q

septic shock

A

low blood pressure, loss of blood volume, organ failure, death

release of IL-1 and TNF due to infection

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10
Q

Toxic shock syndrome

A

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

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11
Q

Treatment of toxic shock syndrome

A

treatment of circulating bacteria

clindamycin, vancomycin, daptomycin

removal of infected tissue - debridement

vasopressors to increase blood pressure

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12
Q

Puerperal sepsis

A

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

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13
Q

Infectious arthritis

A

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
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14
Q

Osteomyelitis

culprits

A

inflammation of bone tissue by bacteria

staphylococcus aureus
mycobacterium tuberculosis
pseudomonas aeruginosa
strep spp.

childer most commonly infected through the blood stream

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15
Q

symptoms and treatment of osteomyelitis

A

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

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16
Q

Gas Gangrene

A

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

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17
Q

Tularemia

A

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

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18
Q

Tularemia dissemination

A

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

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19
Q

Tularemia subspecies

A

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

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20
Q

Brucellosis

A

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

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21
Q

Brucellosis Transmission

A

contact with contaminated animals, tools
airborne

consumption of contaminated meat or milk/ milk products (major route)

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22
Q

Brucellosis symptoms

A

undulating fever, sweating, headache, malaise, fatigue, join pain and depression

23
Q

Brucellosis treatment

A

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

24
Q

Cat-scratch disease

A

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

25
Q

Transmission of cat-scratch fever

A

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

26
Q

B. henselae migration to the lymph nodes

A

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

27
Q

Trench fever

A

caused by bartonella quintana, transmitted by the human louse

human reservoir but has been found in cats, dogs, and fleas and ticks

28
Q

Carrions diseaase

A

caused by bartonella bacilliformis

characterized by acute hemolytic bacteriemia

human reservoir

29
Q

Other bartonella species

A

HAVE BEEN FOUND ISOLATED FROM squirrels, mice, fox, cattle and sea otters

other bartonella species (there are 22) have been implicated in human diseases

30
Q

Bubonic plauge

A

yersinia pestis

Gram negative, non-motile bacillus, faculatatively anerobic, negative to most biochemical tests, slow grower`

31
Q

Mammalian hosts of y pesits

A

mormots, gerbils, ground squirrels and prarie dogs

blat rats, and norwegian rats

32
Q

Y pestis transmision by fleas

A

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

33
Q

Vector transmission of bubonic plauge

A

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)

34
Q

Transmission cycles of Y. pestis

A

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

35
Q

Y pestis symptoms

A

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)

36
Q

Y pestis

DIC= disseminated intravascular coagulation

A

DIC leads to blockafe of capillaries and small blood vessels, necrosis of tissue
=> blackening of toes and fingers

Septic shock, organ failure, respirator distress

37
Q

mortality rates of plauge

A

50% IN BUBONIC

100 in septicemic

100% in 2 days with pneumonic

(all above without antibiotic treatment)

38
Q

Pneumonic plague

A

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

39
Q

Typhus

A

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

40
Q

Lyme diseas (emergin disease?)

A

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

41
Q

Primary stage of lyme disease

A

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

42
Q

Lyme disease Secondary stage

A

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

43
Q

Lyme disease tertiary stage

A

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

44
Q

Rare neurolofical complications of lyme disease tertiary stage

chroncally progressive meningoencephalitis

A

chroncally progressive meningoencephalitis which is irreversible CNS damage

45
Q

Rare neurolofical complications of lyme disease tertiary stage

cerbral vasculitis

A

cerbral vasculitis whihc is a destructive inflammation of the blood vessel accomplnied by a lyphocytic infiltrate

46
Q

Rare neurolofical complications of lyme disease tertiary stage

subacute encephalopathy

A

subacute encephalopathy whihc causes memory loss, lack of concentrationa and personality changes

47
Q

Post-Lyme disorder

A

patients with well diagnosed lyme disease who, after receiving adequate antibiotic therapy suffer:

nonspecific fatigue

sleep disorders

headaches

memory disorders

joint and muscle pain

48
Q

post lymantibiotic refractory lyme arthritis

A

arthritis persists after 1 or more antibiotic treatments

49
Q

treament of lyme disease

A

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

50
Q

Vectors of Lyme disease

A

ticks of the genus ixodes are usual vectors

ixodes scapularis (blacklegged tick) is the most common N american vector

51
Q

Vector biology of lyme disease

egg to larva

A

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

52
Q

Vector biology of lyme disease

mymphs to adult

A

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

53
Q

lyme disease in europe

A

borrelia afzelii and borrelia garinii in eurpoe

bullseye rash first noted in Sweden in 1909, Borrelia observed in 1948