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Microbiology > Chapter 19: Gram Positive, Pathogenic Bacteria > Flashcards

Chapter 19: Gram Positive, Pathogenic Bacteria Flashcards

1
Q

What are some general characteristics of Gram positive pathogenic bacteria?

A

Stain purple when Gram-stained

Two major groups based on content of DNA

Low G+C bacteria:

Cocci (Staphylococcus, Streptococcus, and Enterococcus)

Bacilli (Bacillus, Clostridium, Listeria, and Mycoplasmas)

HIgh G + C Bacteria

Rod Shaped (Corynebacteria, Mycobacteria, Proponibacteria)

Filamentous (Nocardia, Actinomyces)

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2
Q

What are some general characteristics of the Staphylococcus genus?

A

Normal member of human’s microbiota

May be an opportunistic pathogen

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3
Q

What is the general structure and physiology of Staphylococcus?

A

Gram positive cocci, nonmotile, facultative anaerobes

Cells occur in grape-like clusters

Salt tolerant- Tolerate salt of human skin

Tolerant of dessication- survive on environmental surfaces

Synthesizes catalase

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4
Q

What are the two species of Staphylococcus are commonly associated with human disease?

A

Staphylococus aures: More virulent, variety of conditions depending on site of infection

Staphylococcus epidermidis: Normal microbiota of human skin, opportunistic infection

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5
Q

How does a bacterial species become virulent?

A

Infections result when staphylococci breach body’s physical barriers

Entry of only a few hundred bacteria can result in disease

Pathogenicity results from three factors: Production of toxins, enzymes, and antiphagocytic factors

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6
Q

What are some structural defences of Staphylococcus against phagocytosis?

A

Protein A- coats the surface of the cell, interferes with humoral immune responses by inhibiting opsonization, inhibit complement cascade

Bound coagulase enzyme- converts fibrinogen into fibrin molecules, fibrin clot hide the bacteria from phagocytic cells

Slime layers (capsules)- inhibit leukocyte chemotaxis and phagocytosis, facilitate attachment of Staphyloccous to surfaces

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7
Q

Define opsonization

A

Opsonization is the neutralization of an antigen by an antibody which allows it to be engulfed by a phagocyte

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8
Q

Define the complement cascade pathway

A

Proteins in blood serum that help the immune response

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9
Q

What are the pathogenic enzymes produced by Staphylococcus?

A

Cell free coagulase- triggers blood clotting

Hyaluronidase- break down hyaluronic acid, enables the bacteria to spread between cells

Staphylokinase- dissolves fibrin threads into blood clots, allows S. aureus to free itself from clots

Lipases- digest lipisd, allow Staphylococcus to grow on skin and in oil glands

Beta-lactamase- breaks down penicillin, allows bacteria to survive treatment with beta-lactam antimicrobial drugs

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10
Q

What are the toxins produced by Staphylococcus?

A

S. aureus produces toxins more frequently than S. epidermidis

Cytolytic toxins- alpha, beta, gamma, delta, and leukocidins (lyse leukocytes), disrupt the cytoplasmic membrane of a variety of cells

Exfoliative toxins- cause skin cells to separate and slough off

Toxin-shock syndrome toxin- causes toxic shock syndrome

Entertoxins: (A,B,C, D, and E), stimulate symptoms associated with food poisoning, are heat stable

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11
Q

What are the types of disease caused by Staphylococcus?

A

Three categories of disease:

Noninvasive- Food poisioning, due to ingestion of enterotoxin-contaminated food, consumed bacteria do not continue to produce the disease, less than 24 hours

Cutaneous- Various, Scalded skin syndrome, impetigo, follicultis, sty, furuncle, carbuncle

Systemic- variety of infections when bacteria invade deeper tissues

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12
Q

What are the effects of scalded skin syndrome?

A

Exfoliative toxin causes reddened pathches of the epidermis to slough off

Blisters contain clear fluid lacking bacteria or WBCs

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13
Q

What are the characteristics of impetigo?

A

Reddened patches of skin become pus filled vsicles that eventually curst over

Generally affects children (immune system not as developed)

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14
Q

What are the characteristics of toxic shock syndrome?

A

Occurs when TSS toxin is absorbed through the skin

Characterized by fever, vomiting, red rash, low BP, loss of sheets of skin (desquamation)

Correlated with tampon use and knowledge

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15
Q

What are the other systemic diseases caused by Staphylococcus aureus?

A

Bactermia- bacteria enter into bloodstream

Endocarditis- bacteria present in the lining of the heart

Pneumonia- an inflammation of lungs where alveoli and bronchioles become filled with fluid

Osteomyelitis- bacteria invades the bones causing inflammation of bone marrow and surrounding bone

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16
Q

How is a Staphylococci infection diagnosed?

A

Detect gram positive, cluster like arrangments of bacteria

If bacteria are able to clot blood, they are coagulase positive (characteristic to S. aureus)

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17
Q

How do you treat and prevent a Staphyloccocal infection?

A

Only 5% of strains are susceptible to penicilin

Methicillin (in MRSA must treat with vancomycin)

Hand antisepsis important to prevent nosocomial infections

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18
Q

What are the general characteristics of Streptococcus?

A

Gram positive cocci, facultative anaerobes

Arranged in pairs or chains, catalase negative

Classified on the basis of antigens, types of hemolysis, cell arrangment, or physiological properties

Often categorized based on Lancefield Classification

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19
Q

What is the Lancefield classification system?

A

Streptococci species are classified using the Lancefield system

Divided into serotypes based on bacteria’s antigens

Includes serotypes A through H and K through V

Lancefield groups A and B include the significant human pathogens

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20
Q

What is the species of Group A Streptococci?

A

Group A- Streptococcus pyogenes, forms white colonies surround by a large zone of beta hemolysis

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21
Q

What are the components that make S. pyogenes pathogenic?

A

Structural components- Protein M (analgoues in funcion to Protein A), Hyaluronic acid capsule (remain hidden from phagocytic cells)

Enzymes- Streptokinase, deoxyribonucleotides, C5A peptidase (complement breaking peptide), hyaluronidase

Pyrogenic toxins (Erythrogenic toxins)- stimulate the release of cytokines (proteins) that cause fever, toxin carried on bacteriophages (only lysogneized strains are able to cause disease)

Streptolysins- lyse red blood cells, WBCs, and platelets

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22
Q

What are the group A streptococcal diseases?

A

Pharyngitis “strep throat”- inflammation of pharynx

Scarlet fever- involves lysogenized strain of S. pyogenes (Due to pyrogenic toxins) Strawberry red tongue

Pyoderma (similar to impetigo) and erysipelas- pus-producing lesions involving lymph nodes, pain, and inflammation

Streptococcal toxinc shock like syndrome (TSLS)

Necrotizing fasciitis- caused by “flesh eating bacteria” bacteria spread deep within the body along the fascia

Rheumatic fever- autoimmune, antibodies cross-react with heart antigens, inflammation leads to damage of heart valves and msucle, leads to achy joints

Glomerulonephritis- autoimmune, antibodies against group A Streptococcus accumulate in the glomeruli and nephrons of the kidneys causing inflammation, causes tea-colored urine

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23
Q

How do you diagnose, treat, and prevent a Streptococcal Group A infection?

A

Diagnosis- Gram + pair or chain found in cutaneous specimens, streptococci normally in the pharynx (not diagnostic), immunological tests

Treatment- penicillin is effective, sensitive to erythromycin, cephalosporin, and bacitracin

Prevention- antibodies against M protein provide protection

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24
Q

What are the characteristics of Group B Streptococcal strains?

A

Group B- BABY, Streptococcus agalactiae

Beta-hemolysis zones that are smaller, gram positive cocci in chains

Group specific polysaccharide cell wall antigens, resistant to bacitracin

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25
Q

How is Streptococcus agalactiae pathogenic?

A

Capsule is not protective (unlike S. pyogenes)

Often infects newborns without specific antibodies

Produces enzymes (proteases, hemolysins, hyaluronidase, etc.) whose roles are not yet understood

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26
Q

What are the diseases caused by S. agalactiae?

A

Associated with neonatal bactermia, meningitis, and pneumonia

Older, immunocomprimised patients also at risk

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27
Q

How is S. agalactiae diagnosed, treated, and prevented?

A

Diagnosis- ELISA test used to identify group B streptococcus

Treatment-Penicilin G is the drug of choice

Prevention- immunization of women can protect future children

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28
Q

What is the Viridans Group?

A

Alpha-hemolytic Streptococci (incompletely break down RBCs, WBCs, etc.)

Lack group specific carbohydrates- cannot be classified using Lancefield system

Many produce a green pigment when grown on blood media

Inhabit mouth, pharynx, GI tract, genital tract, and urinary tract

One cause of dental caries and dental plaque- Stick to dental surfaces via dextarn

If enter the blood can cause meningitis and endocarditis

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29
Q

What is the other alpha-hemolytic Streptococcus species?

A

Streptococcus pneumoniae

Gram positive cocci that most commonly form pairs

Form unpigmented, alpha hemolytic colonies on blood agar

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30
Q

What are the virulence factors of Streptococcus pneumoniae?

A

Polysaccaride capsule (required for virulence)

Phosphorylcholine- stimulates cells to phagocytize the bacteria

Protein adhesin- mediates binding of cells to epithelial cells of pharynx

Secretory IgA protease- destroys IgA (anitbodies found in the pharynx)

Pneumolysin- binds to cholesterol in the cytoplasmic membranes of epithelial cells, producing pores that result in cell lysis

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31
Q

What are the pneumoccoal diseases caused by S. pneumoniae?

A

Pneumococcal pneumonia- bacteria multiply in the alveoli, damaging the alveolar lining, allowing fluid, RBCs, and leukocytes to enter the lunds

Sinusitis and otitis media- bacteria can invade the sinuses and middle ear causing pus and inflammation

Bacteremia and endocarditis- colonize in the blood and heart

Pneumococcal meningitis- spread to the meninges

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32
Q

How is a S. pneumoniae infection diagnosed, treated, and prevented?

A

Diagnosis- gram-stain of sputum smears, confirmed with Quellung reaction (anti-capsular antibodies cause the capsule to swell)

Treatment- penicillin

Prevention- vaccine made from purified capsular material

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33
Q

What are the characteristics of the Enterococcus genus?

A

Previously classified with group D streptococcus- reclassified as a separate genus

Gram positive, unencapsulated, catalase negative, non-hemolytic

Forms short chains and pairs

Can grow up to 45 degrees Celsius, pH 9.6, and can grow in the presence of salt and bile

Found in the human colon where it is rarely pathogenic- may introduce disease if found in a different area

Enterococcus faecalis and Enterococcus faecium

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34
Q

How is Enterococcus clinically relevant?

A

Important cause of nosocomial infections

Difficult to treat because enterococci often are resistant to antimicrobials

Prevention in health care setting is difficult- patients often have weakened immune systems

35
Q

What are the characteristics of the Bacillus genus?

A

Gram positive bacilli that occur singly, in pairs, or in chains

Normally dwells in soil, is facultatively anaerobic

Form endospores and posess and protective capsule composed of polyglutamic acid which inhibits phagocytosis (not polysaccharides)

Pathogenic strains produce anthrax toxin containing three polypeptides: Edema factor, Protective antigen, and Lethal factor

36
Q

What is the epidemiology of Bacillus?

A

Primarily a disease of herbivores (zoonoses)

Humans contract via one of three routes- inhalation of spores (most deadly), incoluation of spores through break in skin, ingestion of spores

Category A bioterror agent

37
Q

What is the disease caused by Bacillus?

A

Bacillus anthracis only causes anthrax

Three clinical manifestations

Gastrointestinal anthrax- rare in humans, results in intestinal hemorraging and death

Cutaneous- produces a painless, swollen, black, crusty ulcer called an eschar which releases a toxin in blood

Inhalation- rare in fever, high fever, aches, labored breathing, high mortality rate

38
Q

How is a Bacillus infection diagnosed, treated, and prevented?

A

Diagnosis- large, nonmotile Gram-positive bailli in lung or skin sample

Treatment- ciproflaxacin and many other antimicrobials

Prevention- control of disease in animals, effective vaccine available (requires multiple doses and boosters)

39
Q

What are important characteristics of Clostridium?

A

Gram positive, anaerobic, endospore-forming bacillus

Ubiquitous in soil, water, and gastrointestinal tracts of animals and humans

Endospores allow for survival in harsh conditions

Ability to secrete potent toxins- histolytic, enterotoxins, and neurotoxins

4 important species- C.perfringens, C.difficile, C. botulinum, and C. tetani

40
Q

What are characterisitics of Clostridium perfringens?

A

Produces toxins that can cause irreversible damage to body

Food poisioning- abdominal cramps and watery diarrhea, lasts for less than 24 hours, occurs through ingestion of contaminated meat

Gas gangrene- trauma introduces endospores into body where they germinate in anaerobic environment of deep tissues (extremities)

Endospores germinate and cause necrosis, produce gaseous watse (results in bubbling or crakcing cells)

41
Q

How is a C.perfrigens infection diagnosed, treated, and prevented?

A

Diagnosis- presence of minimum bacterial load in food or feces, gas gangrene self diagnostic

Treatment- food poisoning is self limited, gas gangrene requires removel of dead tissue and administering antitoxins and antimicrobials

Prevention- dfficult to prevent because organism is so common, reheating food can destory toxin

42
Q

What are important characterisics of C. difficule?

A

Very difficult to treat

Common member of intestinal microbiota

Opportunistic pathogen in patients taking broad-spectrum antimicrobial drugs

Minor infections result in self-limiting explosive diarrhea

May cause pseudomembranous colities (sections of colon wall slough off) which can follow the use of broad spectrum antibiotics

Toxin A causes diarrhea and Toxin B is cytotoxic to colon cells (life threatening)

43
Q

How is C. difficile diagnosed, treated, and prevented?

A

Diagnosis- isolation of organism from feces of immnoassay

Treatment- discontinue causative antimicrobial drugs to resolve minor infections, serious cases treated with vancomycin or metronidazole

New, more pathogenic strain

Prevention- proper hygiene to limit nosocomial infections

44
Q

What are important characterisics of Clostridium botulinum?

A

Common in soil or water

Botulism results when the endospore germiantes and produces potent neurotoxins

Seven known botulinum toxins, A through G

45
Q

How does the botulism toxin work at the neuromuscular junction?

A

Acetylcholine is a neurotransmitter that mediates communication between neurons and othe cells

Botulism prevents the release of acetylcholine into the synaptic cleft, resulting in the prevention of muscular contraction (flaccid paralysis)

46
Q

What are the diseases of C. botulinum and how are they spread?

A

Botulism in an intoxation, not an infection

3 Manifestations:

Foodborne botulism (canned food, preserved fish)- results from ingestion of toxins, death can result from asphyixation

Infant botulism (honey)- results from ingestion of endospores- “Failure to thrive”

Wound botulism- contamination of wound by endospores

47
Q

How is a C. botulinum infection diagnosed, treated, and prevented?

A

Diagnosis- symptoms are diagnostic

Treatment- administer neutralizing antibodies against botulism toxin, administer antimicrobial durgs in infant botulism cases

Prevention- proper canning of food, infants under one year should not eat honey

48
Q

What are important characteristics of Clostridium tetani?

A

Obligately anaerobic

Ubiquitious in soil, dust, and GI tract of animals and humans

Tetanus results when endospores germinate and produce tetanus toxin- tetanospasmin

49
Q

How does tetanospasmin work?

A

Blocks the release of inhibitory neurotransmitters leading to constant contraction of muscles

50
Q

How is a C. tetani infection diagnosed, treated, and prevented?

A

Diagnosis- characteristic muscle contraction

Treatment- administer immunoglobulin against tetanus toxin, administer antimicrobial drugs, active immunization with tetanus toxoid

Prevention- immunization with tetanus toxoid, five doses beginning at 2 months of age, followed by a booster every ten years of life

51
Q

What are important characteristics of Listeria?

A

Gram positive, low G+C, non-spore-forming coccobacillus

Ubiquitous in nature; found in soil, water, mammals, birds, fish, and insects

Enters body in contaminated food and drink

Motility at lower temperatures through flagella and due to actin polymerization at 37 degrees Celsius within a human cell

Intracellular pathogen

52
Q

What makes Listeria so pathogenic? (What are its virulence factors?)

A

Virulence is directly related to the bacteria’s ability to live and spread within cells

Unique ability to survive over a wide range of temperatures from 4 to 40 degrees Celsius

Causes an uncommon but potentially serious type of food-borne infection known as listeriosis

E.g.- Listeria monocytogenes

53
Q

What are the motility characteristics of Listeria?

A

Listeria is acquired by ingestion, must find and adhere to the small intestine mucosa to infect it
Highly motile due to flagella at lower temperatures (20- 25°C)
Actin-based tumbling motility in human cells
Uses host cell actin to move within and between host cells
Polymerizes actin molecules into long stiff actin filament tails that propel the bacteria into cytoplasm

54
Q

What does Listeria produce to help it spread intracellularly?

A

Listeria binds to the surface of a phagocytic cell and triggers its own endocytosis
Adherence and invasion is mediated by membrane proteins internalins
Once inside the human cell’s phagosome, Listeria synthesizes a pore-forming cytotoxin, called Listeriolysin O (LLO)
It also produces two other enzymes, phosphatidylinositol- specific phospholipase C (PI-PLC) and phospholipase C (PC-PLC)
All enzymes help Listeria to escape from phagosome

55
Q

How does Listeria spread intracellularly?

A

Listeria is initially endocytized
The intracellular bacteria escapes the phagosome and reproduces within the phagocyte
The bacteria then polymerizes the host cell’s actin filaments at one end to form a “tail” that propels it through the cytoplasm into pseudopods
A neighboring cell then endocytizes the pseudopod
Listeria once again “tunnels” its way out of the phagosome and continues its intracellular existence

56
Q

What are the diseases caused by Listeria and how are they spread?

A

L. monocytogenes is rarely pathogenic in healthy adults
Causes high mortality in individuals developing systemic infection
Most deaths involve fetuses, newborns, or immunocompromised adults
One of the few microbes that can cross the placenta and blood brain barrier, results in miscarriage, stillbirths, or severely infected newborn
Immunocompromised adults can develop meningitis, and death
Very difficult to control during food processing as it can multiply over wide range of temperatures
Incubation period very long from 11-70 days

57
Q

How is a Listeria infection diagnosed, treated, and prevented?

A

Diagnosis- Presence of bacteria in the cerebrospinal fluid, characteristic tumbling motility (only at room temp.), Rarely seen in Gram stain
Can be cultured by cold enrichment technique

Treatment-Antimicrobial drugs like penicillin and erythromycin inhibit Listeria
Resistant to tetracycline and trimethoprim

Prevention-Difficult because organism is ubiquitousAt-risk individuals should avoid certain foods like raw vegetables, unpasteurized milk, soft cheeses, cole slaw, etc.

58
Q

What are important characteristics of mycoplasmas?

A

Smallest free-living microbes, pleomorphic
Lack cytochromes, enzymes of the Krebs cycle, and cell walls
Most have sterols in their cytoplasmic membranes
Classified as low G+C, gram positive bacteria according to genetic classification, even though they stain pink with Gram stain
Require various growth factors from a host or supplied in laboratory media
Can colonize the mucous membranes of the respiratory and urinary tracts

59
Q

What is the disease caused by Mycoplasma pneumoniae?

A

Attaches to epithelial cells lining the respiratory tracts of humans
Causes primary atypical pneumonia (walking pneumonia)
Early symptoms not typical of other types of pneumonia
Not usually severe enough to require hospitalization
Not seasonal
Spread by nasal secretions among people in close contact
Diagnosis difficult
Mycoplasmas are small and difficult to detect
Difficult to prevent
Patients often infectious without signs or symptoms
Erythromycin or tetracycline
No vaccine available

60
Q

What are other mycoplasma species of importance?

A

Three other mycoplasma associated with human diseases
M. hominis, M. genitalium, and Ureaplasma urealyticum
Often colonize the urinary and genital tracts of newborn girls

M. genitalium and U. urealyticum cause inflammation of the urethra (urethritis), Treated by erythromycin or tetracycline

M. hominis can cause pelvic inflammatory disease in women, Treated by clindamycin

61
Q

What are imporant characteristics of Corynebacterium?

A

High G+C, pleomorphic, non-endospore forming bacteria
Ubiquitous on plants, animals
Colonize on skin and respiratory, gastrointestinal, urinary, and genital tracts
Bacteria divide by binary fission (snapping division) to form characteristic V-shapes and palisade arrangements
Distinctive feature is presence of metachromatic granules
Corynebacterium diphtheriae causes diphtheria

62
Q

What are the diseases caused by Corynebacterium diphtheriae and the how is the disease spread?

A

Corynebacterium diphtheriae is transmitted from person to person via respiratory droplets or skin contact
Bacteria contains a lysogenic bacteriophage that codes for diphtheria toxin
Toxin contains two polypeptides
One polypeptide binds to a growth factor receptor on cells triggering the endocytosis of the toxin
Inside the cell, proteolytic enzymes cleave the toxin, releasing the second polypeptide into the cytosol
Enzymatically destroys elongation factor, a protein required for the synthesis of polypeptides in eukaryotes
Results in complete stoppage of polypeptide synthesis and cell death

63
Q

What are some characteristics of diphtheria?

A

Infections in immune and partially immune individuals are asymptomatic or result in mild respiratory disease
Disease most severe in non-immune patients resulting in diphtheria
Sore throat, fever, pharyngitis
Oozing of fluid composed of intracellular fluid, blood clotting factors, leukocytes, bacteria, and dead cells
This fluid thickens into a pseudomembrane
Adheres to tonsils, uvula, palate, pharynx, and larynx
Blocks the respiratory passages resulting in death by suffocation
Cutaneous diphtheria results in formation of pseudomembrane on skin
Toxin can get absorbed into the blood, leading to coma and death

64
Q

How is Corynebacteria infection diagnosed, treated, and prevented?

A

Diagnosis
Initial diagnosis on the basis of presence of pseudomembrane
Elek test – immunodiffusion assay in which antibodies against toxin react with the toxin in the sample
Culture on Loffler’s medium reveals typical colonial morphology
Treatment
Antitoxin administration to neutralize the toxin
Penicillin or erythromycin
Prevention
By vaccination
Administered as part of DTaP vaccine

65
Q

What are some important characteristics of Mycobacterium?

A

High G+C, non-endospore forming pathogen

Cell wall contains a way lipid called mycolic acid in cell wall, results in a number of unique characteristics

Slow growth

Protection from lysis after phagocytosis

Capacity for intracellular growth

Resistance to Gram statning, stain acid fast, detergents, many antimicrobial drugs, and dessication

66
Q

What are some important characteristics of Mycobacterium (continued)?

A

Grows on differential medium Lowenstein-Jensen agar

Virulent strands of M. tuberculosis have a cell wall component called cord factor- produces strands of daughter cells that remain attached to one another in parallel alignment, inhibits migration of neutrophils

Pathogen not particularly virulent- only %5 of infected people develop disease, Kill 50% of untreated patients

Two main species: M. tuberculosis and M. leprae

67
Q

What is the diseae caused by M.tuberculosis?

A

Tuberculosis- respiratory disease

Cases are declining in US due to better living conditions, pandemic in other regions of the world

Remains one of the top three killers of people worldwide today

Nearly 2 billion people are currently infected

68
Q

What are the three types of TB?

A

Primary TB- results from initial infection, formation of tubercles

Secondary TB- reestablishment of active infection after period of dormancy

Disseminated TB- results when infection spreads throughout body

69
Q

How are tubercles formed in primary tuberculosis?

A

85% of infections remain in lungs

Primary infection involves the formation of small, ahrd nodules in the lungs

5 Stages of Infection:

  1. Bacteria infects the respiratory tract via inhalation- minimum dose is 10 cells, baceteria have adhesive pili that attach to extarcellular human protein laminin
  2. Macrophages in the alveoli of ungs phagovytize the pathogens but unable to digest them as the bacteria prevents the fusion of phagosome and lysosome
  3. Bacteria replicate freely within the host cells, gradually killing them, release chemokines, bacteria are released from dead cells are phagocytized by other macrophages, asymptomatic stage
  4. Infected macrophages present antigen to T lymphocytes, which produce cytokines to trigger inflammation, tightly appressed macrophages surround site of infection, forming a tubercle
  5. Other cells deposit collagen fibers enclosing the infected macrophages within the tubercle, infected cells in the center die, releasing M. tuberculosis and producing caseous necrosis (liquid), center may become filled with air as a tuberculous cavity

If immune system able to kill all the mycobacteria, it subsequently deposits calcium around the tubercle, known as Ghon complexes

70
Q

How is tuberculosis reactivated?

A

The bacteria ruptures the tubercle, and re-establishes active infection

Bacteria sperad through lungs via bronchioles

Reactived TB found commonly in immunosuppressed individuals

71
Q

What are the effects of disseminated Tuberculosis?

A

Results when some macrophages carry the pathogens via the blood and lymph to variety of sites

Bone marrow, spleen, kidneys, spinal cord, brain

Common name for TB in the early 1900s-consumption-reflected wasting of body due to involvement of multiple sites

72
Q

How is tuberculosis diagnosed?

A

Tuberculin skin test (PPD)

Inject 0.1mL of cell wall antigens into the skin, appearance of induration (swelling) within 24-72 hours is positive

Many false positives and false negatives

Chest X-rays identify individuals with active disease

Presence of acid-fast cells and cords in sputum

73
Q

How is a tuberculosis infection treated?

A

Common antimicrobials (penicillin, erythromycin) are ineffective, mycobacterium grows so slowly taht drugs are cleared from body before being effective

Combination therapy used for months to treat disease- combination of Isoniazid, rifampin, pyrazinamide, and ethambutol for two months followed by isoniazid and rifampin alone for 4 months

Development of multi-drug resistant strins (MDR)- have to be treated with fluoroquinolones in combination with kanamucin for more than 2 yeras

Extensively drug resistant TB (XDR-TB)- resistant to all TB anti-microbials

74
Q

How is tuberculosis spread and how can it be prevented?

A

Cases in US show a strong correlation with the age, sex, and recent immigration history of a patient

High rates in new immigrants from areas of South Asia, South America, and Africa, also in AIDS patients

Directly Observed Treatment, Shortcourse (DOTS)- ingestion of TB medications is observed by a responsible person, lowers rate of drug-resistant TB and the rate of tuberculosis relapse

Prevention- BCG vaccine (composed of attenuated M. bovis strain), administered to children in all developing countries, efficicay studies vary

75
Q

What is the other type of disease caused by Mycoacterium?

A

Leprosy- caused by Mycobacterium leprae

Bacteria do not grow in cell-free culture, armadillos only other host

Bacteria grow best at 30 degrees Celsius, showing preference to grow in cooler regions of the body, like peripherlal nerve endings and skin in fingers, toes, etc.

Becoming relatively rare

Transmitted via person to person contact or break in skin

Two different forms: Tuberculoid leprosy, and lepromatous leprosy

76
Q

What is tuberculoid leprosy?

A

Non-progressive form of disease

Strong cell-mediated immunity is able to kill infected cells

Regions of skin lose sensation due to nerve damage

77
Q

What is lepramatous leprosy?

A

Develops in patients with weak CMI

Bacteria multiply in skin and nerve cells, gradually destroying tissue and leading to progressive loss of facial features, fingers, toes, etc.

Incubation period up to several years

Transmitted via person-to-person contact, not particularly virulent

78
Q

How is leprosy diagnosed, treated, and prevented?

A

Diagnosis- based on signs and symptoms of disease, Leprosy antigen skin test

Treatment- combination of antimicrobial drugs (clofazimine, rifampin, or dapsone for 12 months), lifelong treatment is sometimes needed

Prevention- limiting exposure to the pathogen, BCG vaccine provides some protection

79
Q

What are other possible mycobacerial infections?

A

Mycobacterium avium-intracellulare

Opportunistic pathogen

Most common mycobacterial infection among AIDS patients in the US

Infections result from ingestion of contaminated food or water

Can affect almost every organ and result in massive organ failuer

Treatment is difficult due to the dissmeinated nature of the infection

80
Q

What is the Buruli ulcer and what bacterial species is it caused by?

A

Caused by M.ulcerans, an emerging pathogen present in swamps

Produces a potent toxin mycoalcton that destroys cells beow the skin

Treatment- Rifampina and Streptomycin

81
Q

What are important characteristics of Propionibacterium?

A

Small, gram positive rods often found on the skin

Produce propionic acid as a by product of fermenation of carbohydrates

Propionibacterium acnes msot commonly involved in human infections- causes acne in 85% of adolescents and young adults

May be an opportunistic pathogen

Many cases require no treatment

Antimicrobial drugs help control bacterium

Retinoic acid- derivative of Vitamin A, can inhibit formation of oil

82
Q

What are important characteristics of Nocardia asteroides?

A

Common inhabitant of soils rich in organic matter

Cell wall contains mycolic acid and stains acid-fast

Appear like long hyphal cells- diagnostic

Produces opportunistic infections in numerous sites

Pulmonay infections, Cutaneous infections (may produce a myceotma characterized by swelling, pus, and sores), CNS infections

Prevention involves avoiding exposure to bacterium in soil

83
Q

What are important characteristics of Actinomyces?

A

Characterized by hypha-like, gram positive cells

Member of surface microbiota of human mucous membranes

Colonies form visible concretions resembling grains of sand known as “sulfur granules”- actually contain calcium phosphate

Opportunistic infections- respiratory, gastrointestinal, urinary, and female genital tracts, sometimes cause dental carries

Actinomycosis- results when bacteria enter breaks in the mucous membrane, formation of absecesses connected by channels in skin or mucous membranes

Diagnosis difficult as other orgniams cause similar symptoms

84
Q
A

Microbiology (10 decks)

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