Brainscape's Knowledge GenomeTM

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


See full index

Fall 2013 > Microbiology - Exam #3 > Flashcards

Microbiology - Exam #3 Flashcards

1
Q

What is regulation of gene expression?

A

Microorganisms are able to control HOW MUCH of each building block it makes

  • On simple media, they make all amino acids
  • On complex, they get all them from the media (don’t make)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Feedback Regulation?

A

Since it is a series of enzyme reactions, the cells either turn ON or OFF enzyme synthesis or enzyme ACTIVITY (FR specifically);
Turning off inhibits the beginning of the reaction to that specific products;
Conserves energy when not needed

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

What is Negative Transcription Regulation?

A

Involves the binding of a repressor to the operator to prevent transcription;
Ex = Lactose Operon

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

The Lactose Operon has DNA that encodes for what enzymes?

A
  • LacZ (beta-galatosidase);
  • LacY (permease);
  • LacA (transacetylase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

The Lactose Operon has DNA that encodes for what regulatory protein?

A

Lac I (repressor protein)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How is transcription of the Lactose Operon controlled?

A

Regulatory protein BINDS to DNA =

  • LacI = REPRESSOR;
  • Operator = DNA site BOUND by LacI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the OFF State of the Lactose Operon?

A

-NO Lactose present for cell use;
-Repressor is BOUND to DNA at operator;
-VERY llittle transcription of LacZ, LacY, and LacA genes
(**Normal conditions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the ON State of the Lactose Operon?

A
  • Lactose PRESENT;
  • High lactose causes accumulation of ALLOLACTOSE (inducer);
  • RNA polymerase CAN interact with promoter DNA and cause HIGH levels of transcription of enzymes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is Allolactose?

A
  • Inducer of the lactose operon;
  • Created by a side rxn of beta-galactosidase when there is a high conc. of lactose outside the cell;
  • Alters the repressor so it can’t bind to the operator DNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a Mutation?

A
  • A change in the DNA sequence of a chromosome;
  • Change in a NUCLEOTIDE PAIR compared to a WILD TYPE or the initial strain;
  • Occurs spontaneously or by a mutagen (radiation, chemicals)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a Mutant?

A

-Organism that has a mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of Induced Mutations?

A
  • UV Light
  • NItrous Acid
  • Base analogs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does UV Light cause an Induced Mutation?

A
  • induces adjacent THYMINE molecules to link together → THYMINE DIMER;
  • No DNA replication, and organism will die
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does Nitrous Acid cause an Induced Mutation?

A
  • Converts DNA Adenine to Hypoxanthine.
  • Hypoxanthine complemented by C → Give AT to GC base pair change.
  • Mutation beings upon replication and H will replace in the sequence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How do Base Analogs cause induced mutations?

A
  • Substances bearing a chemical RESEMBLANCE to nitrogenous bases;
  • Can inhibit DNA replication;
  • Ex: 5-Bromouracil, Acyclovir (herpes drug)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are they types of Mutations?

A
  • Base-pair change;
  • Deletion – LOSS of DNA;
  • Insertion – GAIN of DNA
  • Insertion-Deletion cause Frame Shift Mutations (can come from benzopyrene or fungi toxin, Aflatoxin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are Point Mutations?

A
  • Affect ONE base pair in a gene=

- Substitution or Deletion/Insertion

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

What is a Silent Mutation?

A

still codes for the same amino acid (redundant codon)

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

What is a Missense Mutation?

A

codes for a different amino acids with a different codon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is a Nonsense Mutation?

A

Codes for a stop codon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are DNA Repair Enzymes?

A

LOCATE and REPAIR alteration (mismatched bases) and distortions (thymine dimers) of the DNA;

  • Mismatch repair;
  • Damage/excision repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is a Mismatch Repair?

A
  • First proof-reading by DNA polymerase as it is synthesizing → Will delete the mismatch and start over with correct coding;
  • Highly efficient
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is Damage/Excision Repair?

A

Nucleases that cut out of damaged DNA which is repaired by DNA polymerases → Each side of the damage is cleaved, cutting out the damage, and then DNA polymerase will bind and resynthesize the correct segment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are Transposable Genetic Elements?

A
  • Insertion sequences;

- Transposons (jumping genes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are Insertion Sequences?

A

(Transposable)
Small segments of DNA about 1000 base pairs;
-Forms a COPY of ITSELF;
-Can move (trans-locate) elsewhere on the chromosome;
-Cause of some SPONTANEOUS mutations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are Transposons (jumping genes)

A 
(Transposable)
-LARGER than insertion sequences and often carry drug resistant genes.  
Transposons move from 
-Plasmid to plasmid
-Plasmid to chromosome
-Chromosome to plasmid
(Ends have INVERTED REPEAT sequences)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is Ames Mutagen Test?

A

•Purpose to look for REVERTANT mutants of a Histidine requiring strain on media WITHOUT Histidine
-Back to ORIGINAL histidine form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What is Bacterial Recombination?

A

Involves genetic (DNA) exchange between two organisms =

  • Donor cell – CONTRIBUTES chromosomal DNA or plasmid DNA
  • Recipient cell – RECOMBINES with chromosome or now harbors the plasmid DNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

How can genetic information in bacteria be transferred?

A

-Vertically and Horizontally (laterally)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the 3 methods of bacterial recombination in prokaryotes?

A
  • Transformation (DNA from environment);
  • Conjugation (Active cell-cell transfer);
  • Transduction (from phage infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What is Transformation?

A
  • Taking up pieces of DNA from the environment and rehoming DNA into the prokaryotes chromosomes;
  • Cell that can be transformed are COMPETENT;
  • EX:Haemophilus, Streptococcus, Bacillus, Neisseria.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What is Competence?

A

-often EXPRESSED when cells are in a high cell density (late LOG phase);
There is INCREAED expression of a competence factor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How was Natural Competence found?

A
  • Classic transformation experiment by Griffth and Avery et al;
  • Demonstrated that DNA was the transforming factor;
  • They transformed a AVIRULENT Streptococcus pneumonia strain to VIRULENT with heat-killed virulent cells.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What did Griffith’s Experiment state?

A
  • Type R (Rough) LIVE cells, AVIRULENT, took up the DNA of the S (Smooth) DEAD cells which were VIRULENT.
  • RECOMBINATION of S (donor) DNA with R (recipient) chromosome converted R cells into S (virulent) cells. = TRANSFORMATION…actually DNA.
  • Dead donor cells took in the DNA and transformed cell now has some of the recipient DNA
  • R → S transformation through the uptake of DNA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is Conjugation?

A

-Mechanism of gene TRANSFER;
oInvolves single stranded DNA TRANSFER DIRECTLY from one cell to another by a “rolling circle” mechanism of DNA replication.
-Involves a conjugative plasmid (F in E. coli) that carries the genes necessary for the DNA transfer.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What is the F plasmid (conjugation)?

A
  • F factor or fertility factor;
  • HAVE F cells are POSITIVE (male)
  • Do NOT have F cells are NEGATIVE (female_
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What is the Sex Pili?

A
  • Made by F POSITIVE cells;

- External protein filaments that allows donor (F+) to form contact with recipient (F-)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

How the is the F plasmid transferred?

A
  1. F+ donor (male) synthesizes sex pili;
  2. Pili contacts F- (female) and pulls the cells together;
  3. Rolling DNA replication, and F plasmid is transferred as single-stranded DNA molecule;
  4. DNA synthesis of F+ in BOTH donor and recipient (now also F+)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What else can be transferred by Conjugation?

A
  • Chromosomal DNA;

- High frequency of recombination strains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Conjugation can occur between which GRAM-NEGATIVE bacteria?

A
  • Escherichia and Shigella
  • Salmonella and Serratia
  • Escherichia and Salmonella
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is INTERGENIC Transfer?

A

Genetic transfer between various species of bacteria =

  • transfer of antibiotic-resistance genes carried on plasmids.
  • introduction of drug-resistant transposons between Genera
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is Transduction?

A
  • Phage (donor) packages DNA into its phage head and then transfers this DNA by phage particle infection into a host (recipient);
  • Either Generalized or Specialized transduction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is Generalized Transduction?

A
  • Donor strain is infected by a VIRULENT Generalized transducing phage;
  • Phage expresses genes, replicates its DNA, and packages it in its head which eventually LYSES
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Where do Transducing Phage Particles come from?

A
  • Phage head packaging mechanism sometimes fill the phage heads with chromosomal DN;.
  • DNA pieces from ANY PORTION of the donor chromosome can be packaged
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

How are generalized transducing particles transferred to the recipient?

A
  • Recipient infected with generalized transducing particles;
  • Small linear DONOR DNA enters the cytoplasm;
  • DNA donor fragment recombines with recipient’s chromosomes replacing genes it contains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are diseases of the UPPER Respiratory Tract?

A
  • Streptococcal diseases
  • Diphtheria
  • Pertussis (whooping cough)
  • Meningococcal meningitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What are diseases of the LOWER Respiratory Tract?

A
  • Tuberculosis
  • Pneumonias (typical and atypical)
  • Legionnares’ disease
  • Q fever
  • Psittacosis and Chlamydial Pneumonia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is Pathogenicity?

A
  • Qualitative;

- Indicates that bacterium CAN cause disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What is Virulence?

A
  • Quantitative;
  • Measure of disease potential;
  • Function of the number of bacteria with which a host must be infected multiplied by the bacteria’s virulence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What affects the number and virulence of bacteria?

A

the number and virulence of the bacteria to produce disease is LESSENED by the host’s resistance capacity (HEALTH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the Structure of the Upper Respiratory System?

A

consists of the nose and throat, including the middle ear and auditory tubes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the Structure of the Lower Respiratory System?

A

consists of the larynx, trachea, bronchial tubes, and lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Strep. Pyogenes - Basic

A
  • Strep throat, strep pharyngitis;

- Red pharyngeal lining, pus, pain swallowing, enlarged tonsils and lymph nodes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Corynebacteium diphtheriae - Basic

A
  • Diphtheria;

- Mild sore throat, slight fever, swelling in neck, toxin production damages organs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Bordetella pertusis - Basic

A
  • Pertussis (Whooping cough);

- Cold-like symptoms, mucus, coughing spasms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Neisseria meningitidis or Hemophilus influenzz - Basic

A
  • Meningitis;
  • Membrane covering brain and spinal cord (meninges) is inflamed, sever headache, sudden high fever, stiff neck;
  • Children under 4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

What is Pharyngitis (upper)?

A

Sore, inflamed throat

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What is Laryngitis (upper)?

A

Inflammation of the larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

What is Tonsillitis (upper)?

A

Inflammation of the tonsils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What is Sinusitis (upper)?

A

Infection of the paranasal sinus cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What is Epiglottis (upper)?

A

Inflammation of the flaplike structure of cartilage that prevents material from entering the larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What is Strep. pyogenes?

A
  • Aerotolerant anaerobe;
  • G-POSITICE cocci in chains;
  • Found in THROAT flora and SKIN of carries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What are the Virulence factors of Strep. pyogenes?

A
  • Beta-hemolytic;
  • M protein;
  • Erythogenic toxins;
  • Invasion enzymes (steptokinase dissolves blood clots and Hyaluronidase allows tissue penetration)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

What is Hemolytic?

A

“Blood-digesting” ability of streptococci;

  • Alpha = PARTIAL destruction of red blood cells;
  • Beta = COMPLETE destruction of red blood cells;
  • Gamma = NO effect on red blood cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Classifying Strep by Cell Wall Carbs

A

Group A through O streptococci;

Strep. pyogenes = Group A, beta-hemolytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What is the M-Protein of Strep?

A
  • Located in the cell wall and pili of strep;
  • Encourages adherence to pharyngeal tissue;
  • Retard phagocytosis by body’s immune cells;
  • Over 100 specific types
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

What is the primary disease of Strep. pyogenes?

A
  • Strep Throat from airborne droplets expelled from coughing/sneezing;
  • High fever, swollen lymph nodes/tonsils, red throat;
  • Can infect middle ear (Ottis media)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What is Scarlet Fever?

A
  • Strep throat with a skin rash;
  • Rash from production of ERYTHOGENIC toxin by prophage with toxin genes;
  • Usually only get scarlet fever ONCE because body will make antibodies against toxin (antitoxin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How does the prophage Erythrogenic toxin cause a rash?

A
  • Toxin damages capillaries results in blood leaking through the walls
  • Give pink-red blush on neck, chest on soft-skin areas of arms.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the 2 life cycles of a bacteriophage?

A
  • Lytic (replication, making more phage);

- Lysogeny (phage DNA integrates into chromosome and become DORMANT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What is a PROPHAGE?

A

Integrated viral genome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

What are Lysogens or Lysogenic Cells?

A

Cells that have phage in the chromosome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

What is INDUCTION LYSOGENIC Phage?

A
  • A change in the environmental conditions can cause the prophage to come out of the chromosome;
  • Phage will enter LYTIC cycle and make more that are released upon LYSIS (cell breaking)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What is Lysogenic Phage Conversion?

A
  • Cells gain new properties, for example altered surface components, when they become a LYSOGEN of a phage =
  • Strep will produce EXOTOXIN for scarlet fever;
  • C. Diphtheria produces EXOTOXIN for diphtheria;
  • C. Botulinum produces Botulinum toxin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What is Rheumatic Fever?

A
  • Characterized by fever and inflammation of the SMALL blood vessels;
  • Complication of UNTREATED Strep. pharyngitis;
  • Can cause permanent scarring of heart valves (Rheumatic Heart Disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How does Rheumatic Heart Disease occur?

A

Damage arises from the reaction of the body’s antibodies (AUTOIMMUNE response) to streptococcal antigens (M protein) that cross react to similar proteins on heart muscle.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is GLOMERULONEPHRITIS?

A

Complications like rheumatic fever where damage to KIDNEYS arises from BODY’S ANTIBODIES reacting with streptococcal antigens BOUND to the kidney;
-(Untreated Strep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is ERYSIPELAS?

A

-Skin infection;
-REDDISH PATCHES on skin often with HIGH FEVER;
-Involves lymph nodes, may have pus filled lesions
-Common faces of children.
(Untreated strep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

What is NECROTIZING FASCIITIS?

A

-Rare flesh-eating disease with extensive tissue destruction;
-Strep spreads deep within fascia (fibrous layers that hold muscles together)
-Damages from pyrogenic toxin that increases body temp;
-Toxin and bacteria make super antigen that makes immune system add to damage
(Untreated Strep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is Puerperal sepsis (Childbirth fever)?

A

UTERUS becomes infected during the birth process with Streptococcus
(Untreated strep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What is Septicemia?

A

“blood poisoning” when streptococci gets into and spreads throughout the body through the BLOOD SYSTEM
(Untreated strep)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What causes DIPHTHERIA?

A
  • Agent = Corynebacterium diphtheriae;
  • G-POSITIVE , NONSPORE-forming club-shaped RODS with lysogenic corynephage that contain the genes for an EXOTOXIN production;
  • Causes extreme local inflammation;
  • Swelling in neck causes pseudomembrane;
  • Produces toxin what damage receptor-specific organs (heart, nerve, kidney damage)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is a Pseudomembrane that comes from Diphtheria?

A
  • A membrane composed of fibrin and dead human and bacterial cells,
  • Diphtheria from Greek word for leather because of the tough grayish membrane that forms in throat;
  • Pseudomembrane may interfere with airway.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What causes Pertusis (Whooping Cough)?

A
  • Agent: Bordetella pertussis → encapsulated Gram NEGATIVE COCOBACILLUS;
  • NON-INVASIVE by destructs CILIATED Epithelium;
  • Dense masses of bacteria in trachea and bronchia;
  • ENDOTOXIN upon cell’s death and host’s CYTOTOXIN cause loss of ciliated cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What are the 3 stages of Pertussis?

A
  1. Initial = CATARRHAL (common cold-like, fever, cough);
  2. Second = PAROXYSMAL (attempts to clear throat accumulations by cough);
  3. Third = Sporadic coughing for several weeks (100 day cough)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Why is it called Whooping Cough?

A

“Whoop” - spasmodic coughing episodes due to irritation of laryngeal surfaces stimulating strong cough reflexes.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is Meningitis?

A
  • Inflammation fo the meninges (layers that cover brain and spinal cord);
  • Cerebrospinal fluid between the layers is typically sterile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is Encephalitis?

A

-Inflammation of the BRAIN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What causes Meningococcal Meningitis?

A
  • Agent: Neisseria meningitides – Gram NEGATIVE DIPLOCOCCUS;
  • Attachment pili, endotoxin, capsule;
  • Carried by human ASYMPTOMATIC carries, nose and throat flora;
  • Spread by airborne droplets (Respiratory, blood to CNS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Haemophilus influenzae b

A
  • Aerobic, Gram-negative bacterium.;

- HAEMOPHILUS MENNGITIS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is Haemophilus Meningitis?

A
  • Respiratory tract disease from which the organism moves to the BLOOD and then to the MENINGES. ;
  • Stiff neck, severe headache;
  • Children 6 months to 2 yrs;
  • Treated with Rifampin, Cefotaxime;
  • Acceular vaccine combined with DTaP given to children at Tetramune
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is Tuberculosis (lower)?

A

Chronic LUNG disease characterized by low grade fever, weight loss and destruction of lung tissue → may spread to bone, CNS, or kidneys in late stages)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Mycobacterium tuberculosis

A
  • ACID FAST POSITIVE, ROD-shaped bacteria with a waxy, mycolic acid, cell wall that is resistant to drying and disinfectants;
  • Can survive phagocytosis inside microphages and enter deep lung tissue;
  • Produce Tubercles (lumps from bodes immune system trying to limit)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

How is a Tubercle formed?

A
  1. Mycobacterium tuberculosis is INHALED to the lungs.
  2. Bacilli enters the alveolus
  3. The bacilli multiply within macrophages.
  4. Body’s immune system dispatches other macrophages.
  5. Wall off infected cells – forms tubercle. (note: bacteria are NOT killed)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

How is Tuberculosis Spread?

A
  • Aerosol droplets from respiratory secretion of people with active lung infection (coughing, sneezing, speaking);
  • ~22% infection rate (prolonged, frequent contact at higher risk);
  • 30% primary tuberculosis;
  • Organism remains infectious when dried in dust
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is ASYMPTOMATIC Laten Tuberculosis?

A
  • 90% infection arrest and lung lesions heal;

- DORMANT bacilli can produce tuberculosis in 2 to 23% of these latent cases, but often MANY years after infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is ACTIVE Tuberculosis?

A

10% develop ACTIVE disease usually within 3 month;
If ACTIVE tubercles develop throughout the body the disease is called Miliary Tuberculosis (milium = “seed”) → consumption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Control of Tuberculosis

A
  • Tuberculin skin test and follow up x-ray;

- Multiple antibiotics for 6-9 months due to slow growing bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Multi-drug resistant tuberculosis (MRTB)

A

-Strains resistant to 2 or more drugs, and some to ALL antibiotics;
-AIDS population of the US;
-HIgher than normal death rate;
-Caused by patients who stopped taking meds prematurely
(Estonia, Latvia, Russia, China, India, Iran)

100
Q

Tuberculosis BCG Vaccine

A
  • Attenuated (weakened) Mycobacterium bovis (from cows);
  • Bacille Calmette Guerrin (BCG);
  • NOT approved in the US
101
Q

Tuberculosis Whole Blood Test

A

QuantiFERON®-TB Gold test (QFT-G) ;

  • Detects both LATENT tuberculosis infection (LTBI) and tuberculosis disease;
  • Approved by FDA in 2005;
  • Blood samples mixed with antigens and incubated to 16-24 hours;
  • Amount of interferon-gamma (IFN-gamma) is measured
102
Q

Tuberculosis Whole Blood Test Results

A
  • Infected = White blood cells release IFN-gamma in response to the TB antigens;
  • QFT-G results based on AMOUNT of IFN-gamma released in response to antigens
103
Q

What is Bronchitis or Bronchiolities?

A

infection affecting the BRONCHI

104
Q

What is Pneumonia?

A

general descriptive term which refers to the presence of FLUID build-up in the LUNGS

105
Q

What is the key to Bacterials Pneumonias?

A

Fluid build up in the alveoli of the lungs (hollow cavity)

106
Q

What is Pneumococcal pneumonia? (lower)

A
  • serious respiratory infection which leads to difficulty breathing and sputum production.;
  • Present at all ages by mortality highest among the elderly;
  • Symptoms = High fever, sharp chest pain, difficulty breathing, rust-colored sputum (blood from alveoli of lungs)
107
Q

Step. pneumonia (bacteria)

A
  • Gram POSITIVE, oval diplococcus in chains;
  • NORMAL flora of upper respiratory passgaes;
  • “Self-infection” when immune defenses are lowered;
  • Over 80% bacterial cases
108
Q

What are the types of Pneumonia?

A
  • Lobar pneumonia – ENTIRE LOBE of the lung.
  • Double pneumonia – BOTH left and right lungs
  • Bronchopneumonia – infection in the BRONCHIOLE respiratory passage.
109
Q

What is the treatment for Pneumonia?

A
  • Penicillin OR Tetracycline and Chloramphenicol;
  • Resistant strains are treated with Erythromycin, Cefotaxmine or Ceftriaxone;
  • FDA licensed a vaccine for 23 stains (90 strains identified on capsule component)
110
Q

What is the other GRAM POSITIVE Pneumonia bacteria?

A
  • Staph, aureus (positive, cocci, clusters);
  • 10% bacterial cases;
  • Nosocomial pneumonia (hospitals);
  • Uncommon in healthy adults but can develop in SUSCEPTIBLE (weakened immunity, young, drug abusers) after viral influenza
111
Q

What is the common Gram NEGATIVE Pneumonia bacteria?

A
  • Haemophilus influenza (negative, cocci, capsules)
  • 10% “typical” cases;
  • Can become SYSTEMIC and causes Ottis Media of the middle ear and Sinusitis
112
Q

What is KLEBSIELLA Pneumonia? (lower)

A

A = Klebsiella pneumoniae (Neg, encapsulated rod);

  • 5% of cases;
  • Primary: characterized by gelatinous reddish-brown sputum; Organism grows over lung surfaces;
  • Secondary: Nosocomial of the already sick;
  • Can also affect female urinary tract
113
Q

What is SERRATIA Pneumonia? (Lower)

A

A = Serratia marcescens (Neg, rod);

  • RED pigment;
  • ONLY causes disease in immune compromised patients;
  • Common Nosocomial infection;
  • Infects lungs, bronchial tubes AND urinary tract, eyes, joints/bones
114
Q

What is MYCOPLASMAL Pneumonia (Walking Pneumonia)? (lower)

A

A = Mycoplasma pneumniae (PLEOMORPHIC, NO cell wall so can’t be treated with Penicillins)

  • Primary Atypical Pneumonia;
  • Mild and difficult to diagnose;
  • Treated with Erythromycin and Tetracycline
115
Q

Why Mycoplasmal Pneumonia called Primary Atypical?

A 
Primary = Occurs in HEALTHY individuals (pneumococcal pneumonia usually secondary);
Atypical = differs from typical pneumonia
116
Q

What is the CAST screening for Mycoplasmal Pneumonia?

A
  • Cold Agglutinin Screening Test;
  • Antibodies produced against M. pneumonia agglutinates Type O blood at 4C by not 37C;
  • Organism on blood agar looks like a “fried egg”
117
Q

What is Legionnaires Disease (Legionellosis)? (lower)

A

A = Legionella pneumonphilia;

  • Pneumonia caused by an environmental contaminant, which may include the additional symptoms of gastrointestinal disturbance;
  • Spread by Aerosols;
  • Fever, dry cough, some diarrhea and vomit;
  • Treated with Erythromycin
118
Q

Legionella pneumonphilia (Legionnaries)

A
  • Negative rod, but doesn’t stain well b/c unusual cell wall;
  • Can survive phagocytosis in immune compromised causing ABSCESS and TISSUE DEATH;
  • Grow in water of cooling towers and hot water lines, natural waters and fountains;
  • RESISTANT to chlorine;
  • Can grow inside waterborne protozoa
119
Q

What is Q Fever? (lower)

A

A = Coxiella burnetii (a Rickettsia) = small, only grows on living tissue;

  • Mild respiratory disease lasts 1-2 weeks (headache, high fever, dry cough);
  • Found in livestock (dairy cows, goats, sheep);
  • Western US;
  • Treated with Tetracycline
120
Q

C. burnetti (Q fever)

A

-Parasite of cattle ticks which spreads the disease;
-Microbes are shed in feces, milk and urine.
Humans get it =
by ingesting UNPASTEURIZED MILK and
-by inhaling AERORLS of microbes in DAIRY BARNS

121
Q

What are Chlamydia?

A

-Subgroups of rickettsiae and are among the SMALLEST bacteria ( 0.25 μm);
-Grow ONLY in LIVING HUMAN cells (cellular parasites)
oChlamydia psittaci – cause psittacosis.
oChlamydia pneumoniae – cause chlamydial pneumonia.

122
Q

What is Psittacosis? (lower)

A
  • affects PARROTS, PARAKEETS and other BIRDS;
  • Spread through inhaling dried droppings or dust from infected birds;
  • Resembles the flu (headaches, cough, lung infected patches);
  • Tetracycline treated;
  • 30 day quarantine for Psittacine birds in US so uncommon
123
Q

What is Chlamydia Pneumonia? (lower)

A
  • Spread by respiratory droplets and causes mild “Walking Pneumonia” (fever, headache, cough, infection of lower lung lobe);
  • Tetracycline treated;
  • May injure blood vessels and cause ARTERIOSCLEROSIS and HEART ATTACK
124
Q

What are the food and waterborne diseases?

A
  • Typhoid fever;
  • Salmonella;
  • Shigella;
  • Cholera;
  • E. Coli diarrheas;
  • Peptic ulcers;
  • Listerosis;
  • Brucellosis
125
Q

Salmonella typhi and TYPHOID FEVER

A
  • Shed in HUMAN feces only - stays alive a long time in water, sewage and some foods;
  • Disseminated infection (wide spread, ~1/2 from foreign travel);
  • Mortality;
  • Spread by 5 F’s = flies, food, fingers, feces, fomites
126
Q

Salmonella typhi (bacteria)

A
  • Negative rod, acid resistant, high resistance to environmental conditions;
  • Invasive - multiply in PHAGOCYTIC cells, not intestine (unlike salmonella);
  • Isolated in blood, urine and feces;
  • 1-5% recovered become CHRONIC CARRIERS with organism in gallbladder and shed for months
127
Q

Who was Typhoid Marry?

A

Mary Mallon also known as Typhoid Mary;

  • first person in the US to be identified as a HEALTHY CARRIER of typhoid fever;
  • Cook in NY who infected 47 people, 3 died;
  • Tracked by George Soper and had her forcibly quarantined where she died
128
Q

What are the symptoms of Typhoid Fever?

A
  • Incubation about 2 wks;
  • Pass through stomach and into small intestine where it invades tissue (blood invasion, deep ulcers and blood stools);
  • High fever (104° F) and continual headache;
  • 2nd/3rd wks, fever decline and diarrhea appears
129
Q

What is the treatment for Typhoid Fever?

A
  • Chloramphenicol antibiotics;
  • RESISTANT strains (have R-factors) are treated with 3rd-gen Cepholosporins (Ceftriaxone);
  • Vaccine = killed S. typhi (risky/effective only several yrs);
  • TY21 vaccine = attenuated (weakened) viruses that carry SALMONELLA antigens;
  • Typhin Vi = capsule polysaccharide vaccine from S. typhi
130
Q

Salmonella enterica/ Salmonella typhimurin and SALMONELLA

A
  • Inhabitants and multiply in intestinal epithelial cells;

- Can enter bloodstream causing nausea and diarrhea

131
Q

What is Salmonella?

A

Infection of the intestinal tract (gastroenteritis/enteritis)=

  • bacteria enter the EPITHELIAL (mucosa) cells of intestine.
  • MULTIPLY in VESCICLES in cells.
  • Either results in epithelial cell death due to LYSIS;
  • Or enter the blood stream (low probability) causing septicemia (bacterial infection of the BLOOD STREAM)
132
Q

What are the Agents of Salmonella?

A

*Salmonella enterica and its SEROTYPES =
oS. enteridis
oS. typhimurium
oS. Heidelberg
oS. newport
-NEGATIVE,, facultatively anerobic rods.
- ~ 2000 serotypes cause HUMAN DISEASAE.
-Genus name from Daniel Salmon
-INTESTINAL tracts of humans and animals.

133
Q

What are the Symptoms of SALMONELLA?

A 
INCUBATION period 1 – 3 days  
oDiarrhea
oStomach cramps
oNausea and vomiting
oFever
-Commonly last for 2-7 days. 
-mild or severe. 
-BLOOD or OTHER BODY SITES may become INFECTED.
-CAN HAVE Salmonellosis but have NO SYMPTOMS
134
Q

How is SALMONELLA spread?

A
  • Need to INGEST 10,000 bacteria to become sick,
  • but INFECTIVE DOSE may be as small as 1000.
  • Some RAW FOODS and FECES → comes out in the feces of infected people and animals!
  • Foods such as raw chicken, turkey, beef, pork, other meat, EGGS, and unpasteurized milk products.
  • INFECTED people and animals (reptiles (like iguanas and turtles), ducks, chickens can also have in their FECES)
  • INFECTED people in recovery may carry the bacteria in their FECES for SEVERAL WEEKS
135
Q

Salmonella as a foodborne disease

A
  • Most reported;
  • CDC gets about 40,000 cases/yr;
  • Estimated 2-4 million cases with 500-2000 deaths;
  • Diagnosed by isolation in stool or rectal swabs with differential media
136
Q

How is Salmonella prevented and treated?

A
  • Good sanitation to prevent contamination;
  • Proper refrigeration to prevent growth;
  • Cooking foods to internal temp (140F);
  • Treat = oral rehydration for diarrhea; antibiotics useless unless becomes systemic
137
Q

Shigella spp. and Shigellosis

A
  • Shed in feces;
  • Shiga toxin;
  • Multiply in intestinal epithelial cells and spreads;
  • Dysentery
138
Q

What is SHIGELLOSIS?

A

A = Shigella

  • Bacterial dysentery;
  • Most cases on watery diarrhea WITHOUT blood or mucus in stool;
  • Spread when humans digest organism from feces contaminated water or hands;
  • Veggies, eggs, shellfish, dairy (products that come into contact with water);
  • Treat dehydration with salt solution;
  • Antibiotics sometimes, work, but many resistant
139
Q

Shigella (bacteria)

A

oSh. sonnei (US diarrhea)
oSh. dysenteriae (tropical area -mortality)
oSh. flexneri
oSh. foydii
-NEGATIVE, facultative anaerobic rods.
-Japanese microbiology Kiyoshi Shiga identified in 1898.

140
Q

What is the reservoir SHIGELLA?

A
  • Intestines of humans, apes and monkeys;
  • Closely related to intestinal E.coli;
  • Can shed for a month or more after recovery;
141
Q

What is the virulence factor for SHIGELLA?

A
  • Enter epithelial (mucosa) cells of the intestine.
  • Multiply in VESICLES inside cells and INVADE NEIGHBORING cells AVOIDNG the immune defenses.
  • After 2-3 days, release of ENTEROTOXINS (Shiga toxin) encourages water release by the EPITHELIAL CELLS → diarrhea;
  • Not affect by stomach acidity and proliferate in small intestine and can damage large intestine
142
Q

What is Dysentery from Shigella?

A
  • Syndrome manifested by waves of intense abdominal cramps and frequent passage of small-volume, bloody mucoid stools;
  • Due to damage to the large intestine
143
Q

Vibrio cholerae and CHOLERA

A
  • Exotoxin causes diarrhea and large loss of water and electrolytes;
  • NO invasion of tissue
144
Q

What is CHOLERA?

A

A = Vibrio cholera;

  • EXTENSIVE DIARRHEA, fluid is colorless and water (rice water);
  • 3-5 gal loss per day;
  • Sudden loss of fluid/electrolytes causes shock and death;
  • Blood becomes so viscous vital organs (like brain) can’t function and cause coma;
  • NON invasive, no fever
145
Q

Vibrio cholera (bacteria)

A
  • Negative, slightly curved rod;
  • Robert Koch;
  • Found in contaminated food and water (raw oysters);
  • EXOTOXIN with two components
146
Q

What are the components of the CHOLERA Exotoxin?

A
  • Toxin bind to the EPITHELIAL LINING of the SMALL intestine induces formation of cyclic AMP from ATP in cytoplasm
  • Results in epithelial cells DISCHARGING a large amount of fluids and electrolytes.
147
Q

How is CHOLERA treated?

A
  • Restore body’s water balance!;
  • Intravenous injection of salt solutions;
  • Oral rehydration solution (ORS) solution of ELECTTROLYTES and GLUCOSE.
  • TETRACYCLINE may be used to kill the bacteria.
148
Q

What is E. Coli (bacteria)?

A
  • G. NEGATIVE, rod;
  • One of the MOST PROLIFIC microorganisms of human and animal intestines;
  • Watery diarrhea’ typical traveler’s diarrhea
149
Q

What are the Virulence factors for E. Coli?

A
  • Sspecialized fimbriae that allow them to bind to certain intestinal epithelial cells;
  • Enterotoxic strans (NON-INVASIVE) produce enterotoxins similar to cholera which induces FLUID LOSS in SMALL intestine.
  • Enteroinvasive strains PENETRATE the intestinal epithelium (INVASIVE) and damage the LARGE intestine.
150
Q

What are the 5 classes of E. Coli that cause diarrheal disease?

A
  • Enterogenic (ETEC);
  • Enteroinvasive (EIEC, invade, no toxin);
  • Enteropathogenic (EPEC);
  • Enterohemorrahagic (EHEC)
  • Enteroaggrevative (EAggEC-persistent diarrhea in children)
151
Q

Enterotoxigenic E. Coli - NON INVASIVE

A

-ETEC cause of diarrhea in infants and travelers in UNDERDEVELOPED countries or regions of POOR SANITATION.
-Makes ENTEROTOXINS include:
o the LT (heat-labile) toxin (similar to Cholera toxin) and/or the ST (heat-stable) toxin, the toxin genes occur on the same or separate plasmids
-Major SYMPTOMS ETEC infections include diarrhea without fever

152
Q

Enteropathogenic E. Coli (INVASIVE)

A
  • EPEC induce a watery diarrhea similar to ETEC,
  • ENTEROTOXIN (similar to that of Shigella) → DO NOT produce LT or ST toxins
  • Diarrhea and other symptoms caused by bacterial INVASION of host cells and interference with normal cellular signal transduction
  • Cause of infant and traveler’s diarrhea in MEXICO and in NORTH AFRICA.
153
Q

What i Traveler’s Diarrhea (Montezuma’s Revenge)?

A
  • 50 – 60% travelers diarrhea caused by ETEC & EPEC E. coli strains;
  • Diarrhea within 2 weeks of traveling and the diarrhea last from 1 up to 10 days;
  • Disease typically SEL-LIMITING;
  • Treat oral rehydration;
  • Severe cases my need antimicrobial drugs
154
Q

Enterohemorrhagic E. Coli (INVASIVE)

A

-E. coli O157:H7- is EHEC serotype;
-Exists in the intestine of cattle, but don’t cause disease;
-Colonizes the INTESTINE and produces an ENTEROTOXIN;
Toxin is PHAGE ENCODED and its production is enhanced by iron deficiency

155
Q

What are the symptoms of Enterohemorrhagic E. Coli (EHEC)?

A
  • DIARRHEA with copious BLOODY discharge but NO FEVER → causes an inflammation of the colon with bleeding (hemorrhagic colitis);
  • Other complications, usually in children less than 5 and elderly=
  • Toxin can affect kidneys leading to blood in the urine (hemolytic uremic syndrome (HUS).
  • Can lead to kidneys failure, seizures, coma, colonic perforation, liver disorder, cardiomyophathy
156
Q

What was the E. Coli outbreak in Germany in 2011?

A
  • E. Coli O104:H4;
  • New strain that has properties of BOTH Enteroaggrevative that cause DIARRHEA and Enterohemolytic that cause hemolytic uremic syndrome (HUS, bloody urine);
  • Resistant to the widest range of antibiotics
157
Q

What are the virulence factors for E. Coli O104:H4 (germany outbreak)?

A
  • Combines the virulence factors of Shiga toxin of E. Coli O157 and
  • Mechanism for sticking to intestinal cells of Enteroaggrevative which causes diarrhea in poorer countries;;
  • Strain resistant to most anitbiotics and they won’t help slow HUS (hemolytic uremic syndrome) once Shiga toxin has been released
158
Q

What causes Peptic Ulcer disease?

A
  • H. pylori = Negative, microaerophilic curved rod (low oxygen levels);
  • Can survive stomach acidity;
  • Burrows through stomach’s mucus lining and attaches to the stomach wall;
  • Secretes enzyme UREASE;
  • Secretes toxin that destructs tissue and forms ulcer
159
Q

What is Urease produced by H. pylori?

A
  • Enzyme that splits Urea into ammonia and CO2;

- Ammonia helps neutralize stomach acid and inflammation of the stomach results

160
Q

How is a Peptic Ulcer diagnosed?

A
  • Detection of H. pylori;
  • 1996 BREATH TEST was approved;
  • Patient drinks a UREA solution fortified with harmless carbon-13 isotope;
  • H. prylori breaks urea down rapidly, carbon-13 as CO2 detected in breath.
161
Q

How are Peptic Ulcers treated?

A
  • Tetracycline clarithromycin (Biaxin) or Omeprazole (Prilosec).
  • Often taken with Bismuth subsalicylate (Pepto-Bismol) which has antibacterial properties.
162
Q

Campylobacter jejuni and CAMPYLOBACTEROSIS

A
  • GASTROENTERITIS from raw milk and POULTRY;
  • Mild diarrhea to sever GI distress;
  • Fever, abdominal pain and bloody stools;
  • Typically recover WITHOUT treatment;
  • When Severe (high fever, bloody stools) treated with Erythromycin
163
Q

Campylobacter jejuni (bacteria)

A
  • Spirally-curved microaerophilic Gram-negative rod that moves by means of single polar flagella
  • INTESTINAL TRACTS of many animals (dairy cattle, CHICKENS and turkeys)
  • Raw milk, contaminated water;
  • Almost all retail CHICKENS
164
Q

How does Campylobacter jejuni affect the GI tract?

A
  • Colonizes the small or large intestine causing inflammation and occasionally mild ulceration;
  • Toxin causes diarrheal symptoms
165
Q

Listeria monocytogenese and LISTEROSIS

A
  • Main danger is to FETUS:
  • Transmitted from contaminated FOOD;
  • Vey difficult to diagnose;
  • Treated with Ampicillin and/or Tetracycline
166
Q

Listeria monocytogenes (bacteria)

A
  • Small, POSITIVE, rod;
  • Found in the SOIL and INTESTINES of animals (birds, fish, barn animals, dairy cattle and pets);
  • Transmitted to humans through fecal matter and food;
  • INVADES GI epithelium;
  • NOT destroyed when ingested by phagocytic cells, but proliferate and can move from one macrophage to another evading immune defenses.
167
Q

What foods have been associated with Listerosis?

A
  • Delicatessen cold cuts (hot dogs) and soft cheeses (Brie, Camembert, feta and blue-veined cheeses) were associated with a number of cases;
  • Summer 2011 – cantaloupes (muskmelons)
168
Q

How does Listerosis manifest in disease?

A
  • HEALTHY adults often have NO symptoms or mild flu-like symptoms;
  • Immune suppressed, PREGNANT, or those with cancer have affinity for growth in the central nervous system
169
Q

What is Listeric Meningitis?

A
  • Listerosis in highly susceptible (pregnant, immune compromised);
  • Characterized by headaches, stiff neck, delirium and coma;
  • During PREGNANCY can cause miscarriage or mental damage to newborn;
  • Others may have respiratory distress, diarrhea, back pain, and other nonspecific symptoms
170
Q

Brucella species and BRUCELLOSIS

A
  • Undulant fever = Fever associated with bacterial infection spikes in the evening and is lower in the day time
  • Animal workers;
  • Cattle
171
Q

What are the Brucella species that cause Brucellosis?

A
  • *Brucella abortus (cattle, elk, bison) = yellowstone park outbreak in elk and bison;
  • B. suis (swine)
  • B. mellitensis (goats and sheep)
  • B. canis (dogs)
172
Q

Brucellosis in Cattle

A
  • Bacteria favors INTRACELLULAR growth → Can GROW IN MACROPHAGES macrophages that engulf them.
  • Travel to organs via the BLOODSTREAM
  • Likes REPORUDCTIVE ORGANS → especially the UTERUS;
  • PREGNANT animals ABORT their young = Contagious abortion
173
Q

Vibrio parahemolyticus (food/waterborne bacteria)

A
  • Negative rod;
  • Gastroenteritis;
  • Exotoxin that causes mild cholera-like diarrhea;
  • SEAFOOD, especially shrimp
174
Q

Vibrio vulnificus (food/waterborne bacteria)

A
  • Negative rod;
  • Gastroenteritis;
  • Eating RAW OYSTERS and calms;
  • Dangerous for people with liver disease
175
Q

Yersinia entercolitica (food/waterborne bacteria)

A
  • Negative rod;
  • Gastroenteritis;
  • Inhabits the intestinal tract of animals;
  • Grows at refrigerations temps;
  • Mild abdominal pain and diarrhea
176
Q

Plesiomanas shighelloides (food/waterborne bacteria)

A
  • Negative rod;
  • Gastroenteritis;
  • Gut of tropical fish
177
Q

Aeromonas hydrophilia (food/waterborne bacteria)

A
  • Negative rod;
  • Gastroenteritis;
  • Common in soil and water;
  • Has an enterotoxin
178
Q

What are the SOILBORNE bacterial diseases?

A
  • Anthrax
  • Tetanus
  • Gas Gangrene
  • Leptospirosis
  • Melioidosis
179
Q

What are the ARTHROPODBORNE Bacterial diseases?

A
  • Bubonic Plague
  • Tularemia
  • Lyme Disease
  • Relapsing fever
180
Q

What are the RICKETTSIAL ARTHROPODBORNE diseases?

A
  • Rocky Mountain spotted fever
  • Epidemic typhus (typhus fever)
  • Endemic typhus
181
Q

Bacillus anthracis and ANTHRAX

A 
3 forms = 
-Cutaneous;
-Inhalation;
-GI;
Easily septicemic and proliferates in the blood
182
Q

Bacillus anthracis (soilborne bacteria)

A
  • Aerobic, endospore-forming Gram. POSITIVE, long rods (Koch);
  • Spores found in contaminated soil and ingested by grazing animals;
  • Spores survive in soil for several decades;
  • Infected animal carcasses are infective
183
Q

How is Anthrax spreads to humans?

A
  • Humans (accidental hosts) are infected by handling infected animal hair, skin, or waste;
  • Either Cutaneous, Inhalation (Woolsorter’s disease) or GI
184
Q

What is Cutaneous Anthrax?

A

-One endospore in a skin abrasion can start disease → Spores geminate, vegetative cell multiply;
-Skin infection starts as raised, itchy BUMP then develops a VESICLE and then painless ULCER with black necrotic (dying) center;
-Lymph glands may swell;
-Necrotic ulcer may spread infection to blood and cause SEPTICEMIA (in 5-20% and may be fatal);
~20% untreated result in DEATH;
-PENICILLIN treatment

185
Q

What in Inhalation Anthrax?

A
  • Humans may become infected by the INHALATION OF ENDOSPORES (biological warfare)
  • Thousands of spores have to be inhaled before a person becomes ill;
  • Initially resembles common flu/cold;
  • Progress to severe breathing problems and shock;
  • 24hrs after respiratory distress typically DEATH;
  • Only treated with Ceprofloxaxin
186
Q

What is Gastrointestinal Anthrax?

A
  • Result from ingestion of contaminated meat. → NOT possible in USA
  • ACUTE INFLAMMATION of the INTESTINAL tract.
  • Initial signs of nausea, loss of appetite, vomiting, fever FOLLOWED by Abdominal pain, vomiting of blood and severe diarrhea.
  • Intestinal anthrax result in DEATH in 25% to 60% of cases.
187
Q

What is the CAPSULE virulence of Anthrax?

A

-Unique capsule consisting of poly-D-glutamate polypeptide → ALL VIRULENT B. anthracis forms this capsule.
On culturing smooth[S] and rough[R] variants occur.
•S is VIRULENT
•R is AVIRULENT
-PROTECT against bactericidal components of serum and phagocytes → Important in the establishment of the infection.

188
Q

What is the TOXIN virulence of Anthrax?

A
  • Diffusible EXOTOXINS;.
  • The level of the lethal toxins in the circulation INCREASES RAPIDLY quite LATE in the disease, and it closely parallels the concentration of organisms in the blood;
  • DEATH is apparently due to the toxins causing oxygen depletion, secondary shock, increased vascular permeability, respiratory failure and cardiac failure.
189
Q

What is the Human Anthrax vaccine? (93% effective)

A
  • Preparation of the protective antigens recovered from the culture filtrate of an avirulent, nonencapsulated strain of Bacillus anthracis;
    -Contains ONLY a part of the EXOTOXIN.
    (BioPort, Corporation, Lansing Michigan).
190
Q

What is in the works for a new Anthrax vaccine?

A

-Health and Human service contract with VaxGen for new vaccine;
-Contains purified recombinant protective antigen (rPA), a protein that elicits ANTIBODIES that NEUTRALIZE anthrax toxins, and provide protective immunity;
rPA vaccine is effective in providing PROTECTION against AEROSOL exposure to deadly anthrax SPORES.
-Clinical testing has shown the rPA vaccine to be safe in humans.

191
Q

Keys to Anthrax

A
  • NOT contagious;
  • Caught early, easily treated with antibiotics;
  • “Inhalation anthrax” from an envelop is not a real threat;
  • Endospores need advanced equipment for warfare;
  • Bombs would kill endospores;
  • Spores can survive for years and are RESISTNAT to DISINFECtANTS, BAKING (need160 C [320 F] for at least 2 hrs – to kill) and MICROWAVING;
  • Spores DESTROYED in BOILING WATER for ten minutes, and treatment with OXIDIZING AGNTS such as hydrogen peroxide or Clorox (Bleach)
192
Q

Clostridium tetani and TETANUS

A
  • Toxin causes uncontrolled muscle contraction/stiffness;
  • Facial and swallowing muscles affected first (Lockjaw and Opisthotonus);
  • Then, spasmodic inhalation or seizures in the diaphragm and rib muscles that lead to reduced inhalation and DEATH
193
Q

How are the facial and swallowing muscles affect by Tetanus?

A
  • Lockjaw = spasms of the jaw cause teeth to clench, “fixed smile”;
  • Opisthotonus = severe hyperextension and spasticity in head, neck and spinal column into a complete bridging/arching position
194
Q

Clostridium tetani (soilborne bacteria)

A
  • Positive, anaerobic, ENDOSPORE-formings rods (NO oxygen);
  • Found in endospore contaminated SOILS
  • VEGETATIVE bacteria found in intestines of many animals and humans;
  • Vegetative Bacteria within intestine DOES NOT cause disease but its the SPORES excreted in FECES to the SOIL
195
Q

How is TETANUS treated?

A
  • PENICILLIN to destroy the organisms;
  • With Sedatives and muscle relaxants → Often the patient is placed in quiet, dark room;
  • Tetanus ANTITOXIN neutralizes toxin
196
Q

What is the Tetanus vaccine?

A
  • Tetanus toxoid part of diphteria-tetanus-pertussin vaccine [DPT or DTaP].
  • BOOSTER shot with Td vaccine recommend every 10 years.
197
Q

Clostridium perfringens and GAS GANGRENE

A
  • Endospores contaminated an open wound;
  • Toxins destroy adjacent tissue;
  • Intense pain/swelling at the wound site
  • Foul odor from dead tissue (Necrotic)
  • Initial site turns DULL RED, then GREEN and finally BLUE-BLACK.
  • Toxins may damage heart and nervous system;
  • Treated with antibiotics, debridement, amputation or exposure in a hyperbaric oxygen chamber.
198
Q

C. perfringens (soilborne bacteria)

A
  • Positive, anaerobic ENDOSPORE forming rod (NO Oxygen);
  • Grows in the necrotic tissue;
  • Ferments CARBS in the tissues and produces gases (CO2 and H) that swell tissue;
  • Secretes enzymes that kill more tissue;
199
Q

What are the enzymes secreted by C. perfringens that cause Gas Gangrene?

A
  • Lecithinase – enzyme dissolves cell membranes;
  • Hyaluronidase – enzyme dissolves cement holding tissue together (Hyaluronic acid);
  • Hemolysins – enzymes destroy red blood cells;
  • Neurotoxins also released.
200
Q

What is the meaning of Gangrene?

A
  • Gangrene is the DEATH of soft tissue or NECROSIS;
  • Resulting from the Loss of Blood Supply (tissue becomes ANAEROBIC)
  • Blood flow may be the result of DEAD TISSUE or sometimes complication of DIABETES.
  • Dry gangrene (non-bacterial) is like blackened tissue caused by frost bite
201
Q

Leptospira interrogans and LEPTOSPIROSIS

A

Headaches, muscle aches, fever, kidney failure:

  • Incubation of 1-2 weeks, with abrupt aches, chills and fever that disappear;
  • Few days later, fever again as organs become infected
  • Small number of cases cause kidneys and liver to be seriously infected (Well’s disease);
  • Occupational disease of sewer workers, farmers, meatpackers, and vets;
  • Infected animals and flood contaminated waters
202
Q

Leptospira interrogans (soilborne bacteria)

A
  • Spirochete (hook on one end like a question mark) with axial filaments and undulating movement;
  • Infected animals (rodents and dogs) shed in URINE;
  • Enter body through the skin such as a small abrasion of the soft tissue of the foot;
  • Colonize kidney tubules;
  • Treated with PENICILLIN, unless kidneys are failing;
  • Diagnosed by pathogens in blood and spinal fluid
203
Q

Yersinia pestis and BUBONIC PLAGUE

A
  • Rat FLEA bite or feces;
  • Lymph infection; Large swelling of regional lymph nodes;
  • Black Death because of the characteristic blacking areas on the skin caused by hemorrhages -Bubonic plague comes from the BUBOES, that form in the lymph nodes in the groin and armpit regions.
204
Q

Yersinia pestis (arthropodborne bacteria)

A
  • Non-motile, Negative rod, stains heavily at poles (safety-pin look);
  • Multiplies in bloodstream within PHAGOCYTES, localizes in the LYMPH NODES;
  • Produces CAPSULE at body temperatures.
  • New cells can EVADE phagocytes.
  • ENDOTOXIN release leads to shoc;
  • Infected rodents and rat fleas (Zoonosis);
  • Endemic of the Western US
205
Q

What is the treatment for Bubonic Plague?

A
  • Tetracycline and streptomycin;

- Vaccine contains killed Y. pestis for high-risk groups

206
Q

What is the cycle of Bubonic Plague?

A
  1. Flea drinks rat blood that has bacteria
  2. Bacteria multiply in flea
  3. Flea gut clogged with bacteria
  4. Flea bites human, regurgitates blood into open wound
  5. Human is infected
207
Q

Frncisella tularensis and TULAREMIA

A
  • TICK;
  • “Rabbit fever”;
  • One of the MOST INFECTIOUS pathogenic bacteria (requires as few as 10 organisms to infect)
  • Initial symptoms mild and nonspecific, except for insect bite ulcer (tick) and local inflammation;
  • Lymph nodes enlarge;
  • Can produce Septicemia pneumonia and abscesses throughout the body
208
Q

Francisella tularemia (arthropodborne bacteria)

A
  • Negative, rod with bipolar staining;
  • 1911, plague-like disease from ground squirrel in Tulare, CA (Edward Francis);
  • Humans infected by ticks. animal fur in contact with a skin abrasion, or inhalation leading to pulmonary symptoms;
  • Treated with Tetracycline, Streptomycin and/or Gentamycin with prolonged administration because contained in phagocytes
209
Q

Borrelia burgdorferi and LYME DISEASE

A
  • Deer TICK vectors;
  • Spreading of “bulls-eye” rash from the initial bite; Heat and nervous symptoms, JOINT involvement;
  • Asymptomatic = mammals (rodents) and infected ticks (Ixodes scapularis and Ixodes pacificus);
  • *Systemic Immune Complex Inflammatory Disorder;
210
Q

Borrelia burgdorferi (arthropodorborne bacteria)

A
  • Spirochete;
  • Diagnosed based on symptoms = rash expanding and spirochetal antibodies in blood
  • Early stages treated with Penicillin, later requires massive amounts of antibiotics;
  • LYMEric vaccine is 3 stages (1st, 1 month, 1 yr) but removed from market
211
Q

How is Lyme Disease a Systemic Immune Complex Inflammatory Disorder?

A

(1) spreading of “bull-eye” rash from initial bite.
(2) Joint involvement (arthritis-like symptoms).
(3) DAMAGE to cardiovascular and nervous systems. → Late chronic – irregular heartbeats, migraine headaches, hearing and vision abnormalities, loss of muscle tone.

212
Q

Borrelia recurrentis and RELAPSING FEVER

A
  • Spirochete;
  • Human pathogen = BODY LOUSE:
  • Spread human to human;
  • No cases in the US (Africa, China, South America, overcrowd, poverty)
213
Q

Borrelia hermsii, Borrelia turicatae and RELAPSING FEVER

A
  • Spirochete;
  • Wild rodents and ticks (remain infective for life and pass through generations);
  • Passed to human through infected tick bite;
  • Western US and Canada (high rodents)
214
Q

What are the symptoms of Epidemic Relapsing Fever?

A
  • Fever, shaking, headaches, drenching sweats which lasts from 2-9 days and alternates with a period of 2-4 days without fever, after which fever returns.
  • Relapses varies from 1-10 or more. → Bacteria make different surface antigens that evades immune system
  • FIRST onset of fever is often accompanied by a RASH.
  • Relapsing fever CAN BE FATAL if not treated
  • TETRACYCLINE or ERYTHROMYCIN
215
Q

Rickettsia rickettsii and ROCKY MTN. SPOTTED FEVER

A
  • TICKBORNE disease characterized by a rash, fever and headache;
  • Originally called “black measles:
  • Howard Taylor Ricketts;
  • Snake RIver Valley Idaho (1896) where is was frequently fatal
216
Q

Rickettsia rickettsii (rickettsial arthropodborne bacteria)

A
  • Very small, lives insides the cells of the host;
  • Mainly in the cels that line small/medium blood vessels where they multiply and cause cell death;
  • Zoonosis from American Dog Tick and Rocky Mtn. Wood TIck
  • Transmitted to vertebrate host through tick saliva;
  • No lab tests, just used symptoms and antibody-detection (Weil-Felix Test looks for clumping Proteus OX19)
217
Q

What is the rash of Rocky Mtn. Spotted Fever?

A
  • Rash begins as pink spots called MACULES.
  • Progresses to pink-red pimplelike spots known as PAPULES.
  • Spots fuse and form MACULOPAPULAR rash which become DARK RED → type of rash characterized by a flat, red area on the skin that is covered with small confluent bumps.
  • Rash BEGINS on hand and feet, progressively SPREADS to the BODY trunk.
218
Q

Rickettsia prowazekii and EPIDEMIC TYPHUS (Typhus Fever)

A
  • LOUSEBORNE disease characterized by hIgh fever (104), high mortality due to damaged blood vessels around organs;
  • Rash stars on trunk and spreads to extremities
  • Typhus fever = bad sanitation;
  • “jail fever”, “ship fever”
  • Killed many of Napoleons army;
  • Transmitted to human through head and body LICE (natural human parasites);
219
Q

Rickettsia typhi and ENDEMIC TYPHUS

A
  • FLEA disease; Similar to Epidemic Typhus with low mortality;
  • “Murine Typhus”, (mouse);
  • Spread by rats/rodents FLEA;
  • “Mexican Typhus” in the SW US;
  • Mild fever, persistent headache;
  • Rash covers trunk but not extremities;
  • Spontaneous recovery;
  • Tetracycline or Chloramphenicol and remove rodents
220
Q

Rickettsia tsutsugamushi and SCRUB TYPHUS

A
  • Miteborne disease with fever and a rash;
  • tsutsuga = disease;
  • mushi = mite;
  • Outbreaks U.S. service men in the Pacific during World War II.
221
Q

Rickettsia akari and RICKETTSIALPOX

A
  • Akari (Greek) for mite.
  • MITES in the fur of MICE.
  • Fever and skin rash similar to that of chickenpox.
  • Considered a BENIGN disease because fatalities are rare.
222
Q

Bartonella (Rochalimaea) quintana and TRENCH FEVER

A
  • WORLD WAR II;
  • One of few rickesttsiae that can be cultivated OUTSIDE of living cells.
  • Spread through head and body LICE.
  • Fever, chills headache and severe pain in the tibia.
  • MACULOPAPULAR rash may or may not appear on the trunk.
  • Symptoms may reappear at 5 day intervals and thus the disease is also called 5 day fever.
  • Mortality rates are very LOW
223
Q

Rickettsia conorii and TICKBORNE FEVERS

A
  • Also: Boutonneus fever, Marseilles fever, Nigerian typhus, South African tick bite;
  • TICK → Wild rodents harbor disease in nature.
  • A MILD FORM of Rocky Mountain spotted fever
  • Mediterranean countries, Africa, India, SW Asia
224
Q

Brill-Zinsser Disease

A

-Recurrence of an earlier case of TYPHUS in which Rickettsia prowazekii has been dormant in the patient for many years.

225
Q

Ehrlichia species and EHRILCHIOSIS

A
  • TICK, flu-like disease;
  • Human granulocytic ehrilchiosis (HGE) can be fatal;
  • Mainly tickborne disease of DOGS;
  • Headaches, malaise, fever and some liver disease.
  • Resembles Rocky Mountain spotted fever except that the rash does not develop in most (80%) patients
  • Lowering of white blood cell count (leukopenia) due to WHITE BLOOD CELL LYSIS.
226
Q

E. chaffeensis – human MONOCYTIC ehrlichiosis [HME]

A

-Transmitted LONE STAR TICK found Southeastern, Mid-Atlantic and South Central United States.

227
Q

E. phagocytophilia (E. equi) – human GRANULOCYTIC ehrlichiosis [HGE].

A

Transmitted by DEER and DOG TICKS found in Wisconsin, Minnesota, Connecticut.

228
Q

What are STD’S?

A 
Diseases of reproductive system transmitted by sexual activity:
•Syphilis
•Gonorrhea
•Chlamydia
•Ureaplasmal urethritis
•Chancroid
229
Q

What is the Norma MIcrobiota of the Urinary Tract?

A

Urine in bladder and upper urinary tract are normally STERILE

230
Q

What is found in the Female Vagina?

A

Populated by acid-forming lactobacilli:

  • Estrogen cause glycogen to accumulate in the cells lining of the vagina.
  • Lactobacilli convert the glycogen to lactic acid, and pH of the vagina becomes acidic.
  • Only acid-tolerant normal microbiota grow in the vagina.
231
Q

How do antibiotics cause Vaginitis?

A
  • Antibiotics can eliminate the normal microbiota and lead to vaginitis. → INFLAMMATION of the vagina
  • Often associated with growth of Candida albicans (yeastlike fungus) → Candidiasis
  • Growth of Gardnerella vaginatis – Gram neg– organism commonly found in the vagina.
232
Q

What is the Human Dilemma surrounding STD’s?

A
  1. Humans require sexual activity to procreate → The PRIME DIRECTIVE of all life.
  2. STDs require sexual activity for their transmission.
  3. Powerful reward systems are built into the performance of the STD-transmission act (sexual intercourse).
    Thus: STD microbes best viewed as deadly hitchhikers on a natural process that our very survival requires.
233
Q

Treponema pallidium and SYPHILIS

A
  • Initial chancre;
  • 3 stages (primary, secondary, and tertiary);
  • Negative spirochete;
  • Human to human (sex);
  • Average is three week before one see any symptoms (but it can be up to three months);
  • Fluorescence or Dark-field microscope detects spirochetes, then antibodies found in blood
234
Q

Primary Syphilis

A

-A lesion at the initial site of infection → An open sore called a CHANCRE.
-Usually on the penis or wall of vagina.
-Painless and the initial lesion heals up spontaneously.
-Many syphilis infections are cured by our NATURAL HOST defense system at this stage;
(Penicillin)

235
Q

Secondary Syphilis

A

-Organisms travel to other parts of the body.
-Causes SKIN RASHES (that may be mistaken for measles, rubella, or chickenpox) and hair loss visible in eyebrows;
Brown sores are characteristic
-At this stage patient is highly infectious.
(Penicillin)

236
Q

Tertiary Syphilis

A

-Organism invades the NERVOUS SYSTEM.
-Hallmark tertiary syphilis is the GUMMA, soft, gummy granular lesion.
-Due to weakening of major blood vessels causing them to bulge and burst.
-Other lesions can occur in brain that lead to insanity, blindness and eventual death.
(Penicillin less effective)

237
Q

What occurs with Syphilis in pregnant women?

A
  • UNTREATED pregnant woman with active syphilis will pass the infection to her unborn child.
  • About 25 % of these pregnancies result in stillbirth or neonatal death.
  • Between 40 to 70 % of such pregnancies will yield a syphilis-infected infant with poor bone formation, meningitis or Hutchinson’s triad → a combination of deafness, impaired vision and notched, peg-shaped teeth
238
Q

Neisseria gonorrhoeae and GONORRHEA

“Clap = brothel”

A
  • Negative, coccus with double been shape (gonococcus)
  • Bacteria attaches to URETHRA using a special pili.
  • Person-to-person contract during sexual intercourse.
  • Very fragile organisms survives only brief period outside body, easily killed most antiseptics and disinfectants.
  • One day to two weeks till first symptoms
  • Penicillin, but some resistant;
  • Look for G neg. discharge from urogenital tract with IMMUNOASSAY Rxns
239
Q

What occurs in Female Gonorrhea?

A
  • Female symptoms are usually a mild vaginites similar to other vaginal infections.
  • Often goes unnoticed and untreated.
  • Infected females are the major reservoir of continued infection.
240
Q

What occurs in Male Gonorrhea?

A
  • Pus and swelling in the urethra that cause painful and frequent urination;
  • Yellowish discharge at tip of penis
241
Q

What does Gonorrhea cause in both?

A
  • Gonorrhea often leads to STERILITY in BOTH sexes if left UNTREATED→ There is no immunity and a cured individual can catch the disease repeatedly;
  • Can also infect the mouth, throat (gonococcal pharyngitis) and anus/rectum (gonococcal proctitis).
  • May infect the eyes, particularly of babies at birth (gonococcal ophtalmia), and can lead to BLINDNESS.
242
Q

Chlamydia trachomatis and CHLAMYDIA

A
  • Pain on urination, watery discharge, leads to infertility;
  • 75% women and 25% men have NO symptoms;
  • Very small bacteria that lives inside infected cells;
  • Sexual contact;
  • Symptoms in 1-2 weeks
243
Q

What are the infection complications from Chlamydia?

A
  • Grows in the male and female URETHRA. → Often called nongonococcal urethritis (inflammation of the urethra).
  • This inflammation may cause STERILITY.
  • Will also infect the EYE = Chlamydial ophthalmia (redness and irritation around the lining of the eye)
244
Q

Chlamydia in Females

A
  • FEMALES- if inflammation spreads to the UTERINE TUBES and causes SCARRING
  • Can also effect the PELVIC REGIONS.(uterus, cervix and uterine tubes or ovaries)
  • Called Pelvic Inflammatory Disease (PID) → PID can also be cause by N. gonorrhea
245
Q

Chlamydia in Males

A

-MALES- if inflammation spreads to the EPIDIDYMIS.

246
Q

How is Chlamydia detected?

A

Since 1983 two fast and simple laboratory tests have been available to detect C. trachomatis.
A. Fluorescent antibody test using monoclonal antibodies against C. trachomatis
B. Immunoassay test with antibodies against C. trachomatis
-Tetracycline and/or erythromycin.

Fall 2013 (6 decks)

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