Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

microbiology > Bacteremia, Septicemia and Brucellosis > Flashcards

Bacteremia, Septicemia and Brucellosis Flashcards

1
Q

def of Bacteremia

A

presence of bacteria in the blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

illustrate the possible cause of bacteremia

A
  • part of pathogenesis like what occurs in meningitis and typhoid fever
  • due to severe infection and invasion of blood stream
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  1. Bacteremia may be……..where small quantities of bacteria are in the blood
  2. or it can be…………, where the bacteria persist and multiply in the bloodstream causing ………
A
  1. transient
    • sustained
    • Septicemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what’s septicemia?

A

An acute illness that is associated with the persistence and multiplication of pathogenic microorganisms or their toxins in the blood. It triggers Sepsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

list Causative organisms of septicemia

A
  1. Gram-positive cocci:
    - Staphylococci responsible for more
    than 50% of cases ,
    - Streptococcus pyogenes
    - Streptococcus pneumoniae.
  2. Gram-negative cocci:
    Neisseria meningitides
  3. Gram-positive bacilli:
    Clostridium causing gas gangrene,
    bacillus anthracis
  4. Gram-negative bacilli:
    - Escherichia coli,
    - Salmonella spp.,
    - Pseudomonas aeruginosa,
    - Klebsiella species,
    - Yersinia pestis
    - Bacteroides
  5. Fungi:
    - Candida spp
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

discuss the pathogenesis of septicemia

A
  1. Direct inoculation of bacteria into the blood during medical procedures e.g. Prolonged peripheral and central inserted intravascular devices
  2. Translocation from GIT or respiratory flora due to mucosal barrier injury
    (e.g., patients with severe neutropenia)
  3. Surgical wounds, infected teeth and urinary tract infections
  4. spleen malfunctions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

list Clinical manifestations of Septicemia

A
  • Fever, chills, nausea, vomiting, diarrhea, malaise, shortness of breath,
    change in mental status, confusion and anxiety
  • drop-in blood pressure (shock) and
    dysfunction of at least one organ =septic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what’s sepsis ?

A

Sepsis
* life-threatening organ dysfunction caused by a dysregulated host response to infection.
* Sepsis can progress to septic shock (if not managed early and properly)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

illustrate Gram-negative Sepsis or endotoxic shock

A
  • Caused by gram-negative bacteria as the cell walls of many Gram-negative bacteria contain endotoxins that are released upon lysis of the cell.
  • They are the lipid A of the somatic
    lipopolysaccharides (LPS) of Gram negative bacteria cell wall
  • Often liberated when the bacteria lyse
  • The pathophysiologic effects of LPS are similar regardless of their bacterial origin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

illustrate Mechanism of action of endotoxin ?

A
  • In the bloodstream, they interact with
    receptors on macrophages, neutrophils, and other cells of RES.
  • Proinflammatory cytokines, such as IL-1, IL-6, IL-8, TNFα, and other cytokines, are released
  • Complement and coagulation cascades are activated, leading to manifestations of septic shock
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

illustrate Gram-Positive Sepsis

A
  • One of the most common causes of sepsis which develops as a severe form of toxemia.
  • Both staphylococci and streptococci produce potent exotoxins (e.g. Toxic shock syndrome toxin-1 of Staph
    aureus and pyrogenic toxin A of Streptococcus pyogenes) that cause toxic shock syndrome.
  • These exotoxins act as superantigens that activate large number of T cells with release of massive amountof cytokines that mediate shock and tissue injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

illustrate Laboratory Diagnosis of septicemia

A

Isolation of causative organism from blood using blood culture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

illustrate treatment of septicemia

A
  1. Antibiotics and IV fluids should start immediately (Before the Lab. results are
    released)
  2. Toxic shock syndrome therapy should include an antibiotic inhibitor of
    protein synthesis (e.g., clindamycin) to inhibit toxin synthesis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

*Bacteremia and Septicemia Caused by Zoonosis ……………..

A

1.Brucellosis
2.Tularemia
3.Plague

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q
  • Vector borne bacterial disease ………..
A
  1. Relapsing fever
  2. Lyme disease
  3. Rickettsial Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

intermittent fever caused by ………….

A
  1. Relapsing fever
  2. Brucellosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

skin rash caused by ………….

A

1.Lyme disease
2. Rickettsial Infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

lymphadenopathy caused by ………….

A
  1. Tularemia
  2. Plague
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

illustrate causative organism of Brucellosis

A
  1. B. abortus (from cattle)
  2. B. suis (from pigs)
  3. B. Canis (from dogs)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

illustrate MOT of brucellosis

A
  • true zoonotic disease (No human to
    human infection).
    1. Ingestion: of raw milk and unpasteurized milk products like fresh cheese
    2. Contact of skin abrasions and mucosal surfaces with tissues or organs, especially placenta, of infected animals
    3. Inhalation of contaminated aerosols or dried remnants of infected animal tissues or secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

illustrate pathogenesis of brucellosis in animals

A
  • It affects organs rich in the sugar erythritol that enhances the growth of Brucellae.
  • The organism localizes in breast, uterus, epididymis, and cause mastitis
    infertility, abortion
  • Brucellae are shed in large numbers in the animal’s urine, milk, placental fluid
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

illustrate virulence factor of brucellosis in pathogenic mechanism of animals

A
  1. endotoxins
  2. intracellular survival
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

illustrate pathogenesis of brucellosis in humans

A
  • main target :RES
  • Brucella is a facultative intracellular organism:
    1- multiply within phagocytic cells (monocytes and tissue macrophages); thereby evading the immune response.
  • It affect the reticule endothelial system
    2. Cell mediated immunity :
  • CMI is the principal component in defense against brucellae
  • resulting in formation of granulomas that may develop into abscesses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

illustrate Clinical Manifestations of brucellosis = Undulant fever=
Malta fever

A

1- Acute brucellosis:
- The organism reaches the blood stream via lymphatic or thoracic duct
causes Bacteremia. &septicemia
- characterized by: Fever: typically undulating (rising-and-falling) or FUO
and constitutional symptoms
- Constitutional symptoms :
* anorexia, malaise, fatigue , sweating.
* Enlarged lymph nodes, hepatomegaly and splenomegaly may be present.

  1. Chronic brucellosis:
    * May follow an acute attack or develop insidiously. From blood the organism reaches many parenchymatous organs as spleen, the central nervous system and bone marrow forming granulomatous nodules
25
Q

brucellosis = …………..=………….

A

brucellosis = Undulant fever=
Malta fever

26
Q
  • The incubation period of Malta fever is……………
A

1-6 weeks

27
Q

what’s the Treatment of Malta fever?

A

tetracycline + rifampin

28
Q

illustrate the laboratory diagnosis of undulant fever

A
  1. serology (indirect diagnosis):
    - most commonly used
    - in chronic brucellosis
    - organisms can’t be isolated
    - Standard serum Agglutination test (SAT) : is done by using
    standardized smooth brucella LPS antigen suspension and serially diluted patient serum, A rising titer or a titer above 1/80 indicates active infection
    - detect specific antibodies against Brucella antigens
  2. direct diagnosis:
  • Specimen:
  • Acute brucellosis: Blood.
  • Chronic brucellosis: serum
  • rapid diagnosis: PCR
  • isolation:
    I- culture condition:
    obligate aerobe &OT 37c
    B. abortus : 5-10 % CO2
    II- culture media :blood culture (Castaneda), incubation up to 3 weeks, subculture on brucella agar (5days), honey droplet colonies
  • identification :
    film stained with Gram -ve coccobacilli
    BR: oxidase+ve (B.canis variable)
    , urease +ve
29
Q

prozone phenomenon
* If the serum agglutination test result is ………….in patients with strong clinical evidence of Brucella infection
* “prozone phenomenon”
, tests must be made for the presence of…………………
These can be detected by adding antihuman globulin to the antigen serum mixture

A
  1. negative
  2. “blocking” antibodies
30
Q

illustratePrevention of malta fever

A
  • Pasteurization of milk
  • Health education of occupational hazards & use of appropriate personal protective equipment
  • Active immunization of animals with live-attenuated vaccine
31
Q

def of SPIROCHAETES

A
  • Heterogeneous group of spiral motile bacteria
  • 3 genera:
    (1) Treponema
    (2) Borrelia
    (3) Leptospira
32
Q

relapsing fever occurs in 2 forms :
1. ………….
2. ………….

A
  1. Epidemic
  2. Endemic
33
Q

illustrate epidemic relapsing fever

A
  • Caused by: Borrelia recurrentis
  • Borrelia are Obligate human
    pathogens.
  • It Is transmitted from
    person to person by Human body louse By rubbing crushed lice into bite wounds
34
Q

illustrate endemic relapsing fever

A
  • Caused by Borrelia duttonii & hermesii
  • Rodents are their Natural hosts
  • It Is transmitted By Contamination of the bite wound by the excreta of the tick or by the bite itself
35
Q

illustrate Pathogenesis and clinical picture of relapsing fever

A
  1. arthropod bite introduces spirochetes which then multiply in many tissues and
    result in Bacteremia.
  2. Each attack is terminated as antibodies arise
  3. This process may occur several times in an untreated host
  4. The relapses are due to the ability of Borrelia to undergo multiple cyclic antigenic variations
36
Q

about relapsing fever
1. incubation period ……….
2. Relapsing fever, is characterized by……………….
3.Acute episodes are characterized by………………
4. each attack is terminated as antibodies rise. Relapses occur
………. and several relapses may occur (3-10 times)

A
  1. (3-7) days
  2. recurrent acute episodes of fever followed by periods of remission of increasing duration
  3. high fever, chills, headache, muscle pains, photophobia & cough. Fever
    persists for 3-6 days (spirochetes in the blood)
  4. (7- 10) days later
37
Q

illustrate Laboratory diagnosis of Relapsing Fever

A

-Specimen: blood during febrile attack.

1-Direct demonstration of Borreliae in
peripheral blood smears:
a) Giemsa’s stain shows large spirochetes with irregular loosely coils, highly flexible, and motile between RBCs.
b) Direct Immunofluorescence:
detect Ag
c) Dark-field microscopy:
periodically check for spirochetes motility

2.PCR:detection of nucleic acid

3.Culture:
They are microaerophilic organisms that
can be cultured in fluid media containing blood, serum or tissues.

38
Q

treatment of relapsing fever

A

tetracycline, erythromycin, and penicillin are effective. Spontaneous recovery after 10 relapses can occur

39
Q

illustrate how to prevent relapsing fever

A
  1. personal hygiene
  2. delousing & Insecticides for eradication of ticks
  3. Anti-rodent measures
40
Q

about Lyme disease
1. It is caused by …………..
2. transmitted to human by ………..
3. clinical picture ……….
4. diagnosis………
5. treatment………
6. virulence factor …….

A
  1. Borrelia burgdorferi
  2. the bite of a small tick
  3. spreading annular skin rash called erythema migraines along with flu- like symptoms (fever, fatigue, headache, and muscle and joint pain).
  4. Serology ( ELISA or indirect fluorescent antibody (IFA) assay) for rising Ab titer
    - CSF or joint fluid can be obtained, but culture usually is not recommended. These specimens can be used to
    detect B. burgdorferi DNA by PCR.
  5. oral tetracyclines and penicillin

6.- multiple protein attachment to the host cell
- change in surface Ag in ticks & humans = evade immune system

41
Q

about Rickettsial infection
1. Causative organism……..
(list its character)

A
  1. Rickettsiae spp
    Small, aerobic, coccobacilli that are obligate intracellular parasites
    * They may reside in the cytoplasm or within the nucleus of the cell that they invade
    * They have typical Gram-negative cell walls
    * All of these organisms are maintained in animal and arthropod reservoirs.
    * They are transmitted by arthropod vectors (e.g., ticks, mites, lice or fleas) and humans are accidentally infected with these organisms
42
Q

list groups of rickettsia with its organism

A
  1. Spotted fevers:
    - R. ricketsii
    - R. akari
  2. Typhus Group:
    - R. prowazekii
    - R. typhi
    - R. tsutsugamushi.
  3. Others:
    - Coxiella burnetti
43
Q
  1. disease of R. ricketsii…………….
  2. disease of R. Akari…………
  3. disease of R. prowazekii…….
  4. disease of R. typhi……….
  5. disease of R. tsutsugamushi………….
  6. disease of Coxiella burnetti………
A
  1. rocky mountain
  2. Rickettsial pox
  3. Epidemic typhi
  4. Endemic typhi
  5. Scrub typhi
  6. Q fever
44
Q

list Arthropod vectorof each one :
1.R. ricketsii…………….
2. R. Akari…………
3. R. prowazekii…….
4. R. typhi……….
5.R. tsutsugamushi………….
6. Coxiella burnetti………

A
  1. Ticks
  2. Mites
  3. Lice
  4. Fleas
  5. Mites
  6. None
45
Q

list Mammalian Reservoir each one :
1.R. ricketsii…………….
2. R. Akari…………
3. R. prowazekii…….
4. R. typhi……….
5.R. tsutsugamushi………….
6. Coxiella burnetti………

A
  1. Dogs, rodents
  2. Mice
  3. Humans
  4. Rodents
  5. Rodents
  6. Cattle, sheep, goats
46
Q

illustrate pathogenesis of rickettsia

A
  • They preferentially infect endothelial cells lining the small blood vessels.
  • The bacteria lyse the phagosome membrane with a phospholipase and get into the cytoplasm where they replicate
  • The typical lesion is vasculitis
  • Pathogenesis is primarily due to destruction of the endothelial cells
    by the replicating bacteria
  • resulting in leakage of blood and subsequent organ and tissue damage
  • Damage to the blood vessel of the skin results in characteristic rash.
47
Q

illustrate Clinical manifestation of rickettsia

A

fever
headache
myalgia
rash

48
Q

illustrate treatment of rickettsia

A
  • The treatment of choice for all rickettsial diseases is : tetracycline
    -the second choice: chloramphenicol
49
Q

illustrate prevention & control of rickettsia

A

1- Louse control measures for prevention of epidemic typhus.
2- Rodent control measures for prevention of murine typhus, rickettsial pox and scrub typhus.

50
Q

discuss Laboratory Diagnosis of rickettsia

A
  • The primary laboratory diagnostic tool is serology.
  • 1-Serological diagnosis: Detection of specific antibodies (IgM and IgG) by EIA.
    1. Detection of Rickettsial antigen in tissue: Skin biopsies from the
      center of petechial lesion can be examined for the presence of
      Rickettsial antigen by I.F.
    1. Detection of Rickettsial DNA: By PCR
51
Q

plague cause ……….
caused by ………..

A
  • (Black Death)
  • Yersinia pestis
52
Q

Transmation of plague in human differ from the animal. illustrate

A
  1. in animals :
    - enzootic in wild rodent : transmitted among them by fleas
    - epizootic occur intermittently :
    infection can spread to domestic rodent
    transmitted among them by rat flea fleas (urban plague )
  2. in humans :
    - mainly flea bite carried by rodent : dogs& cats may bring infected fleas into home
    - direct contact with contaminated tissue s from infected animals
    - infectious droplet from patient with pneumonic plague
53
Q

illustrate virulence factor of plague

A
  1. Polypeptide capsule (F1 capsular antigen) formed at 37˚C: antiphagocytic
  2. Endotoxin.
  3. Plasminogen activator: that has temperature-dependent coagulase
    activity (20–28°C, the temperature of the flea) and fibrinolytic activity (35–37°C, the temperature of the host). This factor is involved in dissemination of the organism from the flea bite
    injection site
  4. exotoxins
  5. YOPs (yersinia outer protein)
  6. Two proteins known as V antigen and W antigen. The V and W antigens allow the organism to survive and grow intracellularly.
54
Q

illustrate pathogenesis of plague in both flea & human

A

In flea:
- Y. pestis, multiply in the gut and, helped by the coagulase at 27˚C, block its proventriculus thus starving the flea for blood. It attempts to feed more often but end up giving back infected blood into the wound of the bite

In human:
- the inoculated org. produce antiphagocytic F1 protein that resist phagocytosis
- spread & clinical types :

a- bubonic plague (commonest): organism spread by lymphatics to regional LNs which become enlarged &painful (buboes)= necrosis

b- septicemic plague :
org. multiply in blood & disseminated, endotoxin release = DIC, IV thrombosis Capillary fragility , hemorrhages in the skin which also result in black patches (black death)

c-pneumonic plague:
* 1ry pneumonic plague: Severe hemorrhagic bronchopneumonia
after inhalation of the organism. It can be spread by aerosols in bioterrorism.
* 2ry pneumonic plague : spread to the lungs via the blood stream. It is highly infectious and sputum is often blood stained & contains large numbers of Y. pestis bacilli

55
Q

discuss Laboratory Diagnosis of Plague

A

Done in Biological Safety Level 3

a. Specimens include:
1- Blood for blood culture in septicemic plague.
2- Aspirate from lymph node (buboes) in bubonic plague.
3-Bronchial Lavage in pneumonic plague.

b. Rapid diagnosis
1-ELISA (detect F1 capsular antigen)
2- PCR (detect F1 capsular gene)

c. Direct microscopic examination & Culture
* Gram stain: short Gram negative bacilli.
* Leishman`s stain: small capsulated bipolar stained violet coccobacilli
* Direct immune fluorescence is more specific

Culture
* The organism can grow on sheep blood agar or sulphite agar medium forming small shiny non hemolytic colonies after 24 – 48 hours incubation at 27oC which is the optimum temperature for growth.
* It gives non-lactose fermenting colonies on MacConkey’s agar medium.

Colonies are further identified by:
* Morphology based on Gram and Leishman`s stain stained films
* Biochemical reactions
* Definite identification is best made by immunofluorescence .

*Serological Diagnosis Used in case of negative cultures. Detection of a rising titre in two sequential specimens confirms the diagnosis

56
Q

prevention & treatment of plague

A
  • Treated The treatment of choice is a combination of :
    streptomycin and a tetracycline such as doxycycline, although streptomycin alone can be used.
  • Prevented with rodent and flea control and good hygiene
57
Q

………, ………., …. are highly infectious need Biosafety level 3 and they are intracellular organism

A

-Brucella,
- Yersinia pestis,
- Francisella tularensis

58
Q

about Tularemia
1. It is ……
2. It has been isolated from more than 100 different species of ……………, eg rabbits, deer, and a variety of rodents.
3. All infections are transmitted to ……… from …….(No ………… infection)
4. Causative organism………….
5.Important Properties:
-The organisms are ………, small pleomorphic Gram ………rods with bipolar staining
- They are strict aerobes. They do not grow on ordinary bacteriological media
6. source of infection :………….
7. mode of infection :
- ……………
- ……………
- …………..
8. human is accidental dead end host no human to human Transmation
9. Virulence factors:
- ………….
-………….
-………….

A

1.enzootic (endemic in animals)
2.wild animals
3. humans /animals /human to human
4. Francisella tularensis.
5. capsulated /negative
6. rabbit: enzootic & cause outbreak
7.
- contact with infected rabbit
- bites of ticks or flea
- rare form :
a. inhalation of aerosolsb.
b. ingestion of contaminated meat
9.
-intracellular survival
- Symptoms are caused primarily by
endotoxin.
- No exotoxins have been identified

59
Q

illustrate pathogenesis of tularemia

A
  • It is an intracellular organism that multiplies within phagocytic cells and spreads to different parts of the
    body via lymphatics and blood vessels.
  • Dissemination of the organisms through the bloodstream permits focal lesions to develop in numerous organs.

microbiology (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions