Gram Positive Bacteria Flashcards
1
Q
They activate the host cell’s cytoskeletal machinery enabling bacterial entry into the cell so it can get nutrients and be protected from complement (the host’s way of popping the bacterial cell membrane), antibodies, and other body defenses.
A
INVASINS
2
Q
They are surface proteins found in the cell wall of various bacteria to enable them to bind to specific receptor molecules on the surface of host.
A
ADHESINS
3
Q
Acts on the intestinal wall (causes GI upset)
They tend to be produced by Gram-positive bacteria rather than by Gram-negative bacteria. There are exceptions, such as Vibrio cholerae.
A
Enterotoxins
4
Q
Pieces of the bacterium which are toxic to humans.
A
Endotoxin
5
Q
A protein in the cell wall of many Gram negative organisms. It is detected as foreign (an antigen) and launches an immune response.
A
Lipopolysaccharide (LPS)
6
Q
A portion of the lipopolysaccharide which is also an antigen.
A
Lipid A
7
Q
Produced by a bacterium and then released from the cell into the surrounding environment. The damage caused by an exotoxin can only occur upon release.
A
Exotoxin
8
Q
What does Hemolysin cause?
A
rupture of red blood cells
9
Q
What do Neurotoxins do?
A
disrupts nerve cells
10
Q
What does H Ag stand for?
A
The H antigen is a flagella on bacteria
11
Q
What is K Ag?
A
an antigenetic protein on the capsule of bacteria
12
Q
What is O Ag?
A
A string of sugars on the lipopolysaccharide (LPS) in bacterial cell walls.
13
Q
What do capsules do for bacteria?
A
Helps prevent phagocytosis
14
Q
How does motility help bacteria?
A
Helps to spread disease within host
15
Q
Means the organism has the ability to cause blood vessels to grow towards it to feed it.
A
Angiotropic
16
Q
What does β lactamase block?
A
An enzyme produced by some bacteria that blocks the ability of certain antibiotics (penicillin) to destroy the bacteria.
17
Q
Genes that provide tetracycline resistance
A
MDR plasmids
18
Q
Capable of transient survival even in phagocytes that exert oxidative / non-oxidative mechanisms.
A
Facultative intracellular pathogens
19
Q
An enzyme produced by some bacteria that modifies host’s proteins, causing massive fluid secretion from the lining of the lumen (in intestines causes diarrhea, in trachea causes coughing). Seen in cholera toxin, diphtheria toxin, and pertussis toxin.
A
Ribosylase
20
Q
What does Coagulase do?
A
Enzyme produced by some bacteria that causes tiny blood clots so bacteria can hide from WBC’s.
21
Q
What does IgA or IgG protease do?
A
Enzyme produced by some bacteria that prevents agglutination by antibodies.
22
Q
What does PG (prostaglandin) cause?
A
The immune response causes the host to release PG to fight the infection but the side effects are fever (pyrogenic) and inflammation.
23
Q
An enzyme produced by some bacteria that dissolves fluid between cells so bacteria can spread faster between tissue planes.
A
Hyaluronidase
24
Q
What does SOD (superoxide dismutase) do?
A
An enzyme produced by some bacteria that deactivates bleach and other substances in WBC lysosomes.
25
What does Staphylokinase do?
An enzyme produced by some bacteria that digests clots so bacteria can spread.
26
Is Staphylococcus normal flora?
Yes; that means it is part of every human’s microbiota, and can be opportunistic pathogens if the skin is broken.
27
Difference between staphylococcus from Streptococcus? Staphylococcus has…
Catalase present, which converts
H2O2 --> H2O + O2
-That allows them to deactivate hydrogen peroxide in WBC lysosomes.
28
Structure and physiology of staphylococcus.
- Gram-positive cocci, non-motile, facultative anaerobes
- Cells occur in grapelike clusters because cells division occurs along different planes and the daughter cells remain attached to one another
- Salt-tolerant-allows them to tolerate the salt present on human skin
- Tolerant of desiccation (drying)-allows survival on environmental surfaces (fomites)
29
Four species of Staphylococcus that cause disease in humans.
S. aureus
S. haemolyticus (axillae, perineum, and ingunial areas)
S. epidermidis
S. saprophyticus
30
How else does S. aureus interfere with white blood cells (WBCs)?
Inhibit chemotaxis of WBC’s.
| Having Protein A on its cell surface inhibits phagocytosis by WBC’s.
31
How does S. aureus interfere with antibody attacks?
Binds the hypervariable region of IgG antibodies.
Having Protein A on its cell surface inhibits the complement cascade (part of immune response which pops the bacterial cell membrane).
32
How does a slime layer provide defense against Phagocytosis?
Facilitates attachment of Staphylococcus to artificial surfaces.
33
How does S. aureus interfere with the action of platelets?
By producing coagulase, an enzyme that makes tiny blood clots to allow the bacteria to hide from phagocytic cells. It also produces staphylokinase, allowing it to free itself from clots when it wants to.
34
How does S. aureus spread in the body?
By producing Hyaluronidase to break down hyaluronic acid, enabling the bacteria to spread between cells. Hyaluronic acid is a fluid between body cells, and is also found in joints.
35
How does S. aureus survive on the skin surface?
By producing the enzyme lipase, which digests lipids, allowing staphylococcus to grow on the skin’s surface and in cutaneous oil glands.
36
What does S. aureus use the enzyme DNase for?
Reduces viscosity in abscesses
37
What does S. aureus use the enzyme β-lactamase for?
Breaks down penicillin and other β -lactam antimicrobial drugs.
38
Which Gram positive bacteria produce more toxins than other species?
Staphylococcus aureus
39
What are Hemolysins?
Enzymes produced by some bacteria that breaks down red blood cells so bacteria can ingest the nutrients.
40
What are enterotoxins?
Stimulate the intestinal muscle contractions, nausea, and intense vomiting associated with staphylococcal food poisoning.
41
What are 3 types of hemolysis?
1. a (alpha hemolysis). The red blood cell is only partially destroyed. Shows up as a green color on a blood agar plate.
2. b (Beta hemolysis). The red blood cell is completely destroyed. Shows up as a clear area on blood agar plate. Streptococcus (strep throat) is one organism that does this.
3. g (gamma hemolysis). RBC is not destroyed. No color change on blood agar plate.
42
Staphylococcal Diseases – What are the 3 categories?
Noninvasive Disease
Cutaneous Disease
Systemic Disease
43
What are the characteristics of noninvasive staphylococcus disease?
Food poisoning from the ingestion of enterotoxin-contaminated food.
44
What are the symptoms of staph food poisoning?
Nausea, vomiting, retching, stomach cramping, and diarrhea. In more severe cases, dehydration, headache, muscle cramping, and changes in blood pressure and pulse rate may occur.
45
What are the characteristics of cutaneous staphylococcal disease?
Various skin conditions including scalded skin syndrome, impetigo, folliculitis, and furuncles (boils).
46
What is Toxic shock syndrome-TSS?
Toxin is absorbed into the blood and causes shock that is life threatening.
47
Presence of bacteria in the blood.
Bacteremia
48
Occurs when bacteria attack the lining of the heart.
Endocarditis
49
Inflammation of the lungs in which the alveoli and bronchioles become filled with fluid.
Pneumonia
50
Infection of bone.
Osteomyelitis
51
How do you determine if Staphylococcus species is S. aureus?
S. aureus is coagulase positive
52
If a Staphylococcus is coagulase negative, how do you determine if the species is epidermidis or saprophyticus?
S. epidermidis: Novobiocin-sensitive
| S. saprophyticus: Novobiocin-resistant
53
What are the characteristics of S. epidermidis?
- Coagulase-negative
- Produces a biofilm that allows adherence to prosthetic devices. People with artificial joints need prophylactic antibiotics before other surgeries for this reason.
- Quorum-sensing
54
What is quorum-sensing?
Ability to coordinate gene expression according to the density of their local population. They will wait until there are many bacteria nearby, and then they will all start at the same time to express genes for proteins to help with the invasion. This coordinated invasion overwhelms the host defenses.
55
What drug is used to treat staphylococcal infections?
Methicillin
56
What is Methicillin?
Is a semisynthetic form of penicillin and is not inactivated by b-lactamase.
57
What does MRSA stand for?
Methicillin resistant Staphylococcus aureus
58
Where do many MRSA infections occur?
In hospitals and healthcare facilities
59
The type of MRSA with a higher incidence rate in nursing homes or long-term care facilities is known as what?
Healthcare acquired MRSA or HA-MRSA
60
What is becoming increasingly difficult to treat?
Serious MRSA infections, especially HA-MRSA infections.
61
How do you prevent infection by S. epidermidis?
- Hand antisepsis is the most important measure in preventing nosocomial infections (wash hands after patient contact)
- proper cleansing of wounds and surgical openings
- aseptic use of catheters or indwelling needles
- appropriate use of antiseptics
62
What is the structure of streptococcus?
Gram-positive cocci, arranged in pairs or chains, that are facultative anaerobes.
63
How are streptococci classified?
The Lancefield classification
64
What is the Lancefield classification entail?
- Divides the streptococci into serotype groups based on the bacteria’s antigens (M proteins)
- Human streptococcal pathogens are in Lancefield groups A and B
65
What is the Lancefield Group A pathogen?
Streptococcus pyogenes (strep throat). It is beta hemolytic, like Groups B, C, and D.
66
What is the Lancefield Group B pathogen?
Streptococcus agalactiae (normal GI flora in adults, but is the major cause of septicemia in newborns).
67
Do pathogenic strains of Streptococcus pyogenes form a capsule?
YES
68
What is pharyngitis?
Inflammation of the pharynx
69
What is scarlet fever caused by?
It is caused by erythrogenic toxin (a bacterial exotoxin) released by Streptococcus pyogenes. It causes fever, sore throat, bright red tongue, and rash.
70
Where does scarlet-fever rash begin and where does it spread to?
Begins on the chest and spreads to the rest of the body.
71
What is pyoderma?
Confined, pus-producing lesion that usually occurs on the face, arms, or legs.
72
What is streptococcal toxic shock syndrome?
Bacteremia and severe multisystem infection.
73
What do pyrogenic toxins do?
Stimulate WBCs to release cytokines, which call other WBCs to the infection site and also causes fever.
74
What 3 types of cells do streptolysins lyse?
White blood cells, Red blood cells, Platelets
75
What does Protein M do to help Group A streptococci?
Protein M helps to camouflage them from WBCs.
76
What is Necrotizing fasciitis?
Bacterial infection that destroys muscle and fat tissue and quickly spreads between tissue planes.
77
What are the early signs and symptoms of necrotizing fasciitis?
Severe pain and swelling. Often rapidly increasing, fever, redness at a wound site.
78
What is Rheumatic fever?
Streptococcal infection that has entered the bloodstream and can lead to scarring of heart valves.
79
What is Mortality of Streptococcal Toxic Shock Syndrome (STSS)?
35%
80
What are the early signs and symptoms of STSS?
Fever
Abrupt onset of generalized or localized severe pain, often in one arm or leg
Dizziness
Influenza-like syndrome
A flat red rash over large areas of the body (only occurs in 10% of cases)
81
Diagnosis of Streptococcal Toxic Shock Syndrome (STSS).
Observation of Gram-positive bacteria in short chains or pairs or immunological tests that identify the presence of group A streptococcal antigens.
Streptococci are normally in the pharynx so their presence in a respiratory sample is of little diagnostic value.
82
Treatment of Streptococcal Toxic Shock Syndrome (STSS)
Cephalosporin (third generation penicillin) is very effective.
83
Prevention of Streptococcal Toxic Shock Syndrome (STSS)
Antibodies against M protein provide long-term protection against future infection of S. pyogenes, but only if it is the same strain.
84
GROUP B STREPTOCOCCUS
Gram positive, beta hemolytic bacteria.
Common colonizer of human gastrointestinal and genitourinary tracts.
Causes serious disease in young infants, pregnant women and older adults.
The most common cause of sepsis and meningitis in infants <3 months
85
What is the leading infectious cause of neonatal sepsis in U.S.?
Group B Streptococcus (GBS) Disease
86
Where dose GBS usually live?
In gastrointestinal tract but can spread to the genital tract.
87
What are the risk factors for early-onset GBS disease?
- Obstetric risk factors
- GBS in the mother’s urine during pregnancy (marker for heavy colonization).
- Previous infant with GBS disease
- Low maternal levels of anti-GBS antibodies
88
What are the prevention of early-onset GBS disease?
Intrapartum antibiotics (IAP)
89
Intrapartum antibiotics (IAP)
- Highly effective at preventing early-onset disease in women at risk of transmitting GBS to their newborns.
- Efficacy in clinical trials: 100%.
90
Alpha-Hemolytic Streptococci
- Produce a green pigment when grown on blood agar.
- Normally inhabit the mouth, pharynx, GI tract, genital tract, and urinary tract.
- One of the causes of dental caries and dental plaques.
- If enter the blood can cause meningitis and endocarditis.
91
What organism produces alpha hemolysis?
Streptococcus pneumoniae
92
What organism normally colonizes the mouths and pharynx but can cause disease if travels to the lungs?
Streptococcus pneumoniae
93
What is pneumolysin?
Enzyme produced by some bacteria which lyses epithelial cells in the lungs.
94
What 2 diseases are caused by bacteria invading the sinuses or middle ear, often following a viral infection?
Sinusitis (sinus infection) and otitis media (middle ear infection).
95
How do you diagnose Streptococcus pneumoniae?
Gram strain of sputum smears, then Quelling reaction (anti-capsular antibodies cause the capsule to swell), confirming the presence of bacteria.
96
What would be treatment for Streptococcus pneumoniae?
Cephalosporin
97
How can you prevent Streptococcus pneumoniae?
Vaccine made from purified capsular material. Provides long lasting immunity in normal adults but is not as effective in children, the elderly, or AIDS patients.
98
Previously classified as group D streptococci but differed enough to be reclassified as a separate genus.
Enterococcus
99
Form short chains and pairs and lack a capsule.
Enterococcus
100
Found in the human colon but are rarely pathogenic at this site.
Enterococcus
101
Bacteria that normally live in the colon but can cause disease if they are introduced into other parts of the body, such as the urinary tract or bloodstream.
Enterococcus
102
What types of infections may be caused by Enterococcus?
An important cause of nosocomial infections.
103
Why is treatment for Enterococcus difficult?
Treatment is difficult because enterococci are often resistant to antimicrobials.
104
Why is prevention for Enterococcus difficult?
Prevention is difficult, especially in a health care setting, where patients’ often have weakened immune systems.
105
Describe Bacillus.
* Gram-positive bacilli, that occurs singly, in pairs, or in chains
* Forms endospores
* Typically motile
106
What is the rapid-onset emetic syndrome of B. cereus?
Rapid-onset emetic syndrome.
| Causes nausea and vomiting.
107
When does vomiting occur?
Begins one to five hours after contaminated food is eaten.
108
What is the slow-onset diarrheal syndrome of B. cereus?
Diarrhea.
| Abdominal pain occurs 8 to 16 hours after consumption of contaminated food.
109
What are treatments for symptoms caused by B. cereus?
Oral hydration
| IV fluid
110
What are the 3 ways humans can contract Bacillus Anthracis?
1. Inhalation of spores
2. Inoculation of spores into the body through a break in the skin
3. Ingestion of spores
111
What disease does Bacillus Anthracis cause?
Anthrax
112
What three clinical manifestations can Anthrax have?
Gastrointestinal, cutaneous, and inhalation anthrax
113
What are the signs and symptoms of GI Anthrax?
- Rare in humans
- Stomach pain
- Loss of appetite
- Bloody diarrhea
- Nausea
- Fever
- Vomiting blood
- Intestinal hemorrhaging and eventually death in 60% of cases
114
Signs and symptoms of Cutaneous Anthrax.
Produces a black scabby ulcer called an eschar as well as toxemia (toxins in the blood).
115
Signs and symptoms of Inhalation Anthrax.
- Similar to GI Anthrax
- Fever
- Nausea
- Vomiting
- Aches
- Fatigue
116
Symptoms of advanced Inhalation Anthrax.
- Labored breathing
- Shock
- Death
117
How does Inhalation Anthrax infect?
Rare in humans.
Spores germinate in the lungs and secrete toxins that are absorbed into the bloodstream.
Mortality rate of 75%.
118
Diagnosis of Inhalation anthrax.
Presence of large, nonmotile, gram- positive bacilli in clinical samples of the lungs.
119
What is the treatment for anthrax?
Ciprofloxacin and many other antimicrobials are effective against B. anthracis.
120
What are 2 methods of prevention?
Control the disease in animals.
| Anthrax vaccine – available but requires multiple doses and boosters.
121
What is Clostridium?
Gram-positive, anaerobic, endospore-forming bacillus
122
Where is it found?
Ubiquitous in soil, water, and the gastrointestinal tracts of animals and humans.
123
Does the presence of endospores allow for survival in harsh conditions?
Yes
124
Where does Clostridium perfringens grow?
Commonly grows in the digestive tracts of animals and humans.
125
What does C. perfringens produce?
11 toxins that have various effects on the body and can result in irreversible damage.
126
What 2 diseases does C. perfringens cause?
1) food poisoning
| 2) gas gangrene
127
What is food poisoning characterized by?
Abdominal cramps and watery diarrhea
128
How are C. perfringens endospores introduced into the body in the case of gas gangrene?
Through some traumatic event such as stepping on a sharp object that has soil on it.
129
What do the endospores cause once they begin to germinate?
They cause necrosis that is often accompanied by foul smelling gaseous bacterial waste products.
130
What indicates the involvement of Clostridium in food poisoning?
The presence of more than 10-5 bacteria in a gram of food or 10-6 cells per gram of feces.
-Gas gangrene is usually a diagnostic by itself
131
What is the treatment for most cases of food poisoning?
Ride it out; drink lots of water, eat only grains (toast) or sugars (7-Up), replace electrolytes (Pedialyte)
132
What is the treatment for gas gangrene?
Remove the dead tissue and administer large doses of Cephalosporin.
133
How does one prevent infection by Clostridium perfringens?
Proper cleaning of wounds, otherwise fairly difficult to prevent because it is so common.
134
What is Clostridium difficile?
Common member of the intestinal microbiota.
| Opportunistic pathogen in patients treated with broad-spectrum antimicrobial drugs.
135
What are the signs and symptoms of Clostridium difficile?
Minor infections can result in a self-limiting explosive diarrhea.
Serious cases can cause pseudomonas colitis.
Can result in perforation of the colon, leading to massive internal infection by fecal bacteria and eventual death.
136
How is Clostridium difficile diagnosed and treated?
Diagnosed by isolating the organism from feces or by demonstrating the presence of toxins via immunoassay.
Minor infections are usually resolved by discontinuing use of the antimicrobial drug in use.
Serious cases are treated with antibiotics.
Proper hygiene is critical for limiting nosocomial infections.
137
What is Clostridium botulinum?
Anaerobic, endospore-forming, Gram-positive bacillus
Common in soil and water
Botulism results when the endopsores germinate and produce botulism toxin.
The different botulism toxins are the deadliest toxins known.
138
What is botulism?
Botulism is not an infection, but an intoxification caused by the botulism toxin.
139
What are the 3 forms of botulism?
Food-borne botulism
Infant botulism
Wound botulism
140
Consumption of toxin in home-canned foods or preserved fish or dented cans of food. Can result in a progressive paralysis that results in death due to the inability to inhale.
Food borne botulism
141
What is the outcome of food borne botulism?
Can result in a progressive paralysis that results in death due to the inability to inhale.
142
What is infant botulism?
Results from the ingestion of endospores, which germinate, and colonize the gastrointestinal tract due to the lack of sufficient numbers of normal microbiota.
143
What are the symptoms of infant botulism?
Symptoms include constipation and “failure to thrive”, but paralysis and death are rare.
144
What food is infant botulism associated with?
It is associated with eating honey. Infants less than 1 year old should never eat honey. They do not have enough normal GI microbes to out compete Clostridium spores that are in honey.
145
What are the characteristics of wound botulism?
* Wound becomes contaminated with endospores
| * Symptoms are the same as with food-borne botulism
146
What is the diagnosis for botulism?
* Symptoms of botulism are diagnostic
| * Confirm diagnosis by culturing the organism from food, feces, or the patient’s wound
147
What are the 3 approaches to the treatment of botulism?
1. Repeated washing of the intestinal tract to remove Clostridium
2. Administer antibodies against botulism toxin to neutralize toxin in the blood
3. Administer antimicrobials drugs to kill clostridia in infant botulism cases
148
What are the preventions of botulism?
* Proper canning of food to prevent contamination
* Don’t buy dented cans of food
* Infants should not consume honey under the age of 1
149
What is clostridium tetani?
Also known as tetanus: Endospore-forming, obligately anaerobic, Gram-positive rods.
150
Where is clostridium tetani found?
Ubiquitous in soil, dust, and the GI tract of animals and humans.
151
How does tetanus occur?
* Tetanus results when the bacterial endopsores germinate and produce tetanus toxin
* Tetanus results in spasms and contractions that can result in death because patients can’t exhale
152
What does tetanus toxin (TeNT) bind to?
TeNT binds to the presynaptic membrane of the neuromuscular junction.
153
After TeNT binds to the presynaptic membrane, where is it transported to?
Spinal cord
154
What is spastic paralysis induced by?
The spastic paralysis induced by the toxin is due to the blockade of neurotransmitter release from spinal inhibitory interneurons.
155
What is the diagnosis of tetanus toxin?
* Characteristic muscular contraction
| * The bacteria are rarely isolated from clinical samples because it grows slowly and is sensitive to oxygen.
156
What are the treatments for tetanus toxin?
* Thorough cleaning of wounds to remove endospores
* Passive immunization with immunoglobulin directed against the toxin
* Administration of antimicrobials
* Active immunization with tetanus toxoid
157
How do you prevent getting the tetanus toxin?
By immunization of tetanus toxoid
158
What is Listeria and where is it found?
- It is a Gram-positive non-spore-forming, coccobacillus
| - Found in soil, water, mammals, birds, fish, and insects
159
What should individuals at risk for Listeria avoid?
At risk individuals should avoid undercooked vegetables, unpasteurized milk, undercooked meat, and all soft cheeses.
160
Where is Corynebacterium diptheriae found?
Ubiquitous on plants and in animals and humans
161
What does cutaneous diphtheria cause?
Cutaneous diphtheria causes cell death and formation of a pseudomembrane in the trachea that causes suffocation.
162
How is Diphtheria (Corynebacterium diptheriae) diagnosed?
Initial diagnosis is based on the presence of pseudomembrane.
Absolute identification is based on the Elek test.
163
How does the Elek test help identify gram positive bacteria?
Antibodies against diphtheria toxin react with toxin in a sample of fluid from the patient.
164
How is Diphtheria treated?
Administration of antitoxin to neutralize toxin before it binds to cells.
165
What antibiotics are used to Diphtheria?
Penicillin and Erythromycin kills the bacteria
166
How do you prevent Diphtheria?
Immunization with the DPT vaccine
TDap ages 11+
DTap ages 6 weeks+
167
Which bacterium cell wall contains a waxy lipid called mycolic acid?
Mycobacterium
168
What advantage does a cell wall of mycolic acid provide?
- Slow growth
- Protection from lysis once the bacteria are phagocytized
- Capacity for intracellular growth
- Resistance to gram-staining, detergents, many antimicrobial drugs and desiccation
169
What are three main mycobacterium diseases?
Tuberculosis
Leprosy
Opportunistic infections in AIDS patients
170
What is Tuberculosis?
Respiratory disease caused by Mycobacterium tuberculosis.
171
Virulent strains of M. tuberculosis contain what cell wall component that is necessary to cause the disease?
Cord factor
172
What are the three types of tuberculosis?
Primary, Secondary and Disseminated TB
173
What are the differences between the three types of TB?
Primary results from the initial infection with M. tuberculosis.
Secondary: Reestablishment of an active infection after a period of dormancy.
Disseminated results when the infection spreads throughout the body.
174
How is Tuberculosis diagnosed?
Tuberculin skin tests identify individuals with previous exposure to M. tuberculosis. A hard and red swollen bump will be present at the test site in 48 hours.
175
How do you treat Tuberculosis?
Common antimicrobials are not effective in treating M. tuberculosis. A combination therapy must be used for a 9-18 months to treat the disease.
176
How do you treat Tuberculosis?
Common antimicrobials are not effective in treating M. tuberculosis. A combination therapy must be used for a 9-18 months to treat the disease.
177
How is M. tuberculosis prevented?
Prophylactic antibacterial drugs are used to treat patients who have converted from a negative skin test to a positive skin test or were exposed to active cases of TB.
Immunization with BCG vaccine is used in countries where TB is common.
178
What causes Leprosy (Hansen’s disease)?
Caused by Mycobacterium leprae. Transmission is contact person to person or break in the skin. Bacteria have never been grown in cell-free culture. They can only be grown on foot pads of mice or armadillo scales. Cases of leprosy are becoming epidemic.
179
Two different types of Leprosy
Tuberculoid leprosy
| Lepromatous leprosy
180
Non-progressive disease that is characterized by loss of sensation in regions of the skin.
Tuberculoid leprosy
181
Produces gradual tissue destruction that results in the loss of facial features, digits and other body structures.
Lepromatous leprosy
182
How is Leprosy diagnosed?
Diagnosed based on signs and symptoms.
•Tuberculoid leprosy- loss of sensation in skin lesions
•Lepromatous leprosy-disfigurement
183
How is leprosy treated?
Combination of antimicrobial drugs. Lifelong treatment is sometimes needed. These medicines cause severe birth defects, so women must have their fallopian tubes tied (sterilization) before treatment can begin.
184
Prevention of leprosy
Primarily prevented by limiting exposure to the pathogen. BCG vaccine provides some protection.
185
Mycobacterial infections in AIDS patients are a result of ingestion of what?
Contaminated food or water
186
Mycobacterial infections in AIDS patients can result in what?
Massive organ failure
187
What gram positive bacteria are common in soils rich in organic matter?
Nocardia asteroides
188
Nocardia asteroides produce opportunistic infections in which sites?
1. Pulmonary infections (from inhalation of the bacteria, which then produce pneumonia)
2. Cutaneous infections (bacteria in wounds)
3. Central nervous system infections (meningitis results from spread of bacteria in the blood.)
189
Prevention of nocardial disease involves avoiding what substance?
Exposure to the bacterium in soil.
190
Actinomyces israelii is most commonly associated with what type of infections?
Crainiofacial infections (eg., post-dental procedure) , soft tissue infections (after human bite wounds) and maxillary osteomyelitis.
191
Is actinomyces israelii a normal flora or parasite?
The organism can be a normal flora of the normal host.
192
What is a furuncle?
Infected hair follicle --> abscess/ boils
| Usually caused by Staph auerus
193
What are carbuncles?
Larger than a furuncle; usually it is a mass of furuncles
Infected hair follicle --> abscess/ boils
Usually caused by Staph auerus
194
What is cellulitis?
Soft tissue infections that spreads quickly between tissue planes and can lead to septicemia (blood poisoning) and death
195
What causes scalded skin syndrome?
Exfolatin toxin from Staph aureus
