Exam 3 Chapter 39 Flashcards
1
Q
What makes up the Chain of Infection?
A
Agent, Virulence, Exposure, Dose, Susceptibility
2
Q
What is the Agent in the Chain of Infection?
A
Agent - pathogen, bug that could cause us trouble
3
Q
What is the virulence in the Chain of Infection?
A
Magnitude of harm it can do to its host
4
Q
What is the Exposure in the Chain of Infection?
A
Pathogen transmission
5
Q
What is the Dose in the Chain of Infection?
A
Dose = Initial innoculum to the host
6
Q
What is the susceptibility in the Chain of Infection?
A
ability of the host to fight the pathogen or pathogens
(can look at immune system status, pathogenosity or virulence of the bug, host nutrision, host stress level)
7
Q
Name and describe the stages in the course of infection and disease
A
Incubation period = period where the intensity of symptoms is zero and the initial exposure of microbe
8
Q
What is the prodromal stage in the course of infection and disease?
A
Initially start to feel bad, host is contagious
9
Q
What is the period of invasion course of infection and disease?
A
Time where you have the symptoms and signs you have the disease
Height of infection
10
Q
What is the convalescent period?
A
getting better and decreasing the intensity of symptoms
11
Q
What happens if there is a height of infection and your body cannot fight it off anymore?
A
Death
12
Q
What bacteria causes Chlamydial Pneumonia?
A
Chlamydophila pneumoniae
Gram Negative coccoid
13
Q
How is Chlamydial pneumoniae transmitted?
A
Airborne Routes
elementary bodies infect, reticulary bodies repliate
Non sexually transmitted
14
Q
What are elementary bodies?
A
Infect new hosts
15
Q
What are reticular bodies?
A
- metabolically inactive except passing pathogen on, once inside host
- Are metabolically active, but non infectious. Need to convert back to elementary bodies to infect
16
Q
What are the clinical manifestations of Chlamydophila pneumoniae bacteria?
A
fever, productive caugh, and mild pharyngitis, bronchitis, and sinusitis
17
Q
Describe the diagnosis, treatement and prevention for Chlamydophila pneumoniae?
A
- observation of symptoms and a microimmunofluorescence test (infect with fluorescent antibodies)
- Antibiotic therapy
18
Q
What are macrolyte?
A
affect 50S ribosomal that inhibits protein synthesis
19
Q
What are the common airborne bacterial diseases?
A
- Chlamydial pneumonia
- Diphtheria - Exotoxin Mechanism
- Legionnaires’ Disease
- Meningitis
- Mycobacterium Infections (M. avium complex = MAC)
- Tuberculosis (TB)
- Mycoplasmal pneumonia
- Pertussis
- Streptococcal Diseases (Streptococcal pharyngitis)
- Post-streptococcal Diseases (Glomerulonephritis = Bright’s disease and rheumatic fever)
20
Q
What bacterium is Diphtheria caused by?
A
Corynebacterium diphtheriae
= Gram positive bacilli
21
Q
What are varialence factors?
A
Help the camofage and make it so human cells do not recognize as a disease
22
Q
Explain how Diphtheria works?
A
Lysogenized strains of Diphtheria produce an exotoxin that inhibits protein synthesis and is responsible for pathogenesis
23
Q
What is Diphtheria resistant to?
A
Resistant to drying
24
Q
How is Diphtheria transmitted by?
A
Airborne transmission by nasopharyngeal (NP) secretions - crwding increase likelihood of transmission
25
What age group is Diphtheria observed in?
Usually observed in individuals \> 30 years old with weakened immunity to diphtheria toxin and living in tropical areas
26
What is cutaneous diphtheria?
- infection at woonds or skin lesion
- Slow- healing ulceration (tend to look gray when healing due to pseudomembrane)
27
How does one diagnose Diphtheria?
Pseudomembrane in throat or bacterial culture
(throat cultures can cause it to dislodge and block airway)
28
What is the treatment for Diphtheria?
-- Antitoxin neutralizes unabsorbed exotoxin in patient's tissues
-- antibiotic therapy
29
What else can Diphtheria invade?
Can invade circulatory system, cardiac, kidney, nervous system and inhibit protein synthesis in that area
30
What is the prevention of Diphtheria?
The main prevention is mainly vaccinations:
- the diphtheria/tetanus/pretussis vaccine to children (DTap)
- Non-immunized adolescents and adults (Tdap)
- Booster in adolescents and adult is the diphtheria/tetanus vaccine (Td) every 10 years
Schedule:
1. DTap at 2, 4 and 6 months of age
2. booster at 12-18 months
3. Booster at 4 - 6 years
4. Tdap vaccine at 11 - 12 years
5. Booster of Td at 10 years
6. Tdap vaccine during second half of each pregnancy
31
What bacteria is responsible for Legionnaire's Disease?
Legionella pneumophila
fastidious, Gram - Negative = rod shaped
32
How is Legionella pneumophila harbored?
by free-living amoebae and ciliated protozoa
33
How is Legionnaires' Disease spread?
Airborne transmission from environmental reservoir to human host
\*Soil, aquatic ecosystems, air-conditioning systems and shower stalls (LOVE WATER)
34
What has Legionella been known to cause?
Can cause an inflammatory reaction (pneumonia) in the lungs called legionellosis
35
What causes localized tissue destruction with Legionellosis?
Reproduction of bacterium in alveolar macrophages
- Hits the lungs
- Produce cytotoxic exoprotease = (produce a distructive enzyme to breakdown lungs)
36
What are the clinical manifestations of Legionnaires' Disease?
- Fever, cough, headache, neuralgia (muscle pain), and bronchopneumonia
- Serve in immunocompromised people/elderly
- Pontiac fever: nonpneumonic form, flu- like symptoms, resolves by itself (less severe)
37
What is the treatment, prevention and control for Legionnaires' Disease?
- Isolation of bacteria and immunodiagnostics
- Symptomatic/supportive therapy and antibiotic therapy
- Eliminate nosocomial spread (if we have large amount of people, break groups up)
- Identification/elimination of environmental source
38
What symptoms does meningitis cause?
Inflammation of brain or spinal cord meninges (membranes)
39
What are the causes of the Meningitis?
- Bacterial and viral = most common but can get fungal or parasite
- Bacterial may be diagnosed by gram stain of cerebrospinal fluid (CSF)
- culture of CSF may or may not grow bacteria
40
What are the major bacterial causes of Meningitis?
1. Streptococcus pneumoniae
2. Neisseria meningitidis (sterotypes)
3. Haemophilus influenza (serotype b)
41
Which of the three bacterial causes of Meningitis is most common in 5 year and younger individuals?
## Footnote
1. Streptococcus pneumoniae
2. Neisseria meningitidis (sterotypes)
3. Haemophilus influenza (serotype b)
3. Haemophilus influenza (serotype b)
42
What does N. meningitidis (meningococcus) cause?
Epidemic meningitis
(mainly upper respiratory system therefore can get into spinal cord)
43
How is Meningitis transmitted?
Respiratory droplets
44
What are the clinical manifestations of Meningitis?
- Initial respiratory illness or sore throat interrupted by one of the following:
1. Vomiting, headache, lethargy, confusion, and stiffness in neck and back
(There is viral meningitis and not much treatment but the bacterial version is the most concerning strain)
2. May be fatal
45
What is the clinical manifestation of Aseptic Meningitis Syndrome?
Similar to bacterial meningitis but show no microbial agent in gram-stained specimen and in culture
46
What is the treatment, prevention and control of Meningitis?
- Must rule out bacterial diagnosis
- Treatment difficult
1. S. pneumoniae
- Vaccine and antibiotics
2. N. meningitidis
- Antibiotics (also prophylactic), vaccine
- recommended for college students, others
3. H. influenzae
- pneumonia and meningitis kill 3 million worldwide/year
- Vaccine (Hib) reduced cases to 1/100,000
47
Where is Mycobacterium bacteria found in?
Soil, water and house dust
one of the oldest documented diseases
Grows very slowly and people do not know they have something and have an unusal cell wall = acid fast (special stain)
48
Why is Mycobacterium Infections difficult to treat?
- mycolic acid in cell wall is protective waxy material that is acid fast (will stain a faint blue)
- Resistant to penetration of some antibiotics (rice shaped)
49
What is mycobacterium infections referred to as?
M. avium complex (MAC)
## Footnote
- normal inhabitants of soil and water
- Infect variety of insects, birds, and other animals
50
What is the portal of entry for the Mycobacterium Infection?
Respiratory and gastrointestinal tracts
- Most common cause of mycobacterial infections in the U.S.
51
What are the clinical manifestations for M. avium complex (MAC)? (Mycobacterium infection)
1. pulmonary infection (similar to tuberculosis)
- Usually observed in elderly patients with preexisting pulmonary disease
2. Gastrointestinal infection
- Common in AIDS patients
- fever, malaise, weight loss, and diarrhea
52
What is the treatment, prevention, and control of M. avium complex (MAC)? (Mycobacterium Infections)
- Isolation from sputum, blood, or bone marrow (variety of samples - for sputum - 3 samples)
- Acid-fast strain, and immunodiagnostic tests (changes in antibody levels)
- multiple drug therapy
53
What is the bacteria that causes Tuberculosis (TB)?
Mycobacterium tuberculosis (Mtb), M. bovis, M. africanum
54
What is the important facts to know about Tuberculosis (TB)?
- ~1/3 world's population infected
- worldwide distribution
- many are also HIV positive (over 50% of TB deaths worldwide are in AIDS patients)
- U.S. elderly, homeless, alcoholics, prisoners, and immigrants are some commonly infected groups
55
What is the transmission of Tuberculosis (TB)?
- Majority is person to person spread of droplet nuclei in respratory tract
- Also transmitted from infected animals and their products
- Reactivation of old, dormant infections
56
Explain the speed that the Tuberculosis (TB) develops?
Disease develops slowely
57
What are the virulence factors for Tuberculosis (TB)?
Unique toxic cell envelope components (Unique lipids and glycolipids that make toxins that kill the host cell and survive phagocytosis because of this)
- Mycolic acid, lipoarabinomannan, trehalose dimycolate, phthiocerol dimycocerosate
- Kill eukaryotic cells and protect the bacterium from lysozyme and osmotic lysis
58
How does Tuberculosis survive phagocytosis?
1. Kill macrophages
2. resistant to oxidative killing
3. Inhibit diffusion of lysosomal enzymes
59
Explain the course of the tuberculosis (TB) disease and how it survives
- Lung macrophages that have phagocytosed M. tuberculosis often die in the attempt to kill the bacteria
- Survives by forming tubercles:
- Composed of bacteria, macrophages, T cells and human proteins
- Subsequent changes in tubercle may occur
60
When viewing on a skin or x-ray test, how does primary tuberculosis show up?
Skin -
X ray -
61
When viewing on a skin or x-ray test, how does delayed-type hypersensitivity and cell-mediated immunity tuberculosis show up?
Skin +
X ray -
62
Name and describe the stages of primary tuberculoses. Skin and X ray test results?
**1. Disseminated tuberculosis (Skin -, X ray +)**
A direct extension of primary tuberculosis. Spread throughout the body.
**2. Latent-dormant tuberculosis (Skin +, X ray -)**
The usual outcome. Most persons remain in this condition for life and suffer no ill effets. (activates after many years to then go into Active tuberculosis stage)
**3. Active tuberculosis (skin +, X ray +, sputum +)**
A slow progressive extensition of tuberculosis with erosion into the air passages and blood vessels. Death if not treated
63
What is the basis for the tuberculin (TB) skin test?
Develop cell-mediated immunity (sensitized T cells)
64
What is the incubation period for TB infection?
4-12 weeks
65
What are the symptoms of TB infection?
- Fever, fatigue, weight loss
- Cough: Characteristic of pulmonary involvement, many result in expectoration of bloody sputum (coughing up blood)
66
How are the ways that TB is diagnosed?
- Observation of acid-fast bacteria
- Chest X-ray, Mantoux, or tuberculin skin test
- DNA -based tests
- QuantiFERON TB gold (brand new-blood test drawn in 3 tubes, advantage = saves patient from coming back in to see if they react to skin test)
67
What is the antimicrobial theroapy for TB?
- Multi-drug-resistant strain (MDR-TB)
- Extensively drug resistant strains (XDR-TB)
- Resistance develops due to naturally occuring chromosomal mutations and natural selection of resistant Mrb due to lack of adherence to tratement protocol
68
What is the prevention and control of TB?
- Rapid, specific therapy to interrupt spread, retreatment of patients with MDR-TB, immunization, improved sanitation and housing, and reduction in homelessness and drug abuse
- Directly observed therapy (DOTS)
- antibiotics for 6-9 months
69
70
What is the bacteria that causes Mycoplasmal Pneumonia?
Mycoplasma pneumonia
causes _atypical pneumonia_ as opposed to consistent signs and sumptoms of typical pneumonia
71
How is Mycoplasmal Pneumonia transmitted?
By close contact and airborne droplets
Worldwide distribution
72
Explain the structure of M. pneumoniae
- lacks cell wall
- Resistant to beta-lactam antibiotics
- attach to lower respiratory tract cells
- produces peroxide, which may be toxic factors
73
Explain the clinical manifestation for Mycoplasmal pneumonia
- Mild in infants and more serious in older children and young adults
- headache, weakness, low fever, charactereistic cough, and pneumonia that presists for weeks
74
Explain the diagnosis for Mycoplasmal pneumonia
- Rapid immunological tests
- Isolation from respiratory secreations -\> _"Fried egg"_ appearance of organisms on agar
75
What is the treatment, prevention and control for Mycoplasmal Pneumonia?
- Likely cause when other bacteria and virsuses cannot be detected and immunodiagnostic tests
- Antibiotic therapy
- No preventitive measures
76
What is another name for Pertussis?
Whooping cough
77
What is the bacteria that causes Pertussis?
i.e. Whooping cough
= Bordetella pertussis
(gram negative bacilli or coccobacilli)
78
Explain the transmission of Pertussis
ie Whooping cough
- Highly contagious disease that primarily affects children
- Transmission by droplet inhalation
- can be recovered from dried mucus for up to 3 days
79
Explain the toxins of Pertussis
i. e. Whooping Cough
- Toxins cause _nitric oxide production_:
**1. pertussis toxin** = most important toxin - stops protein synthesis
**2. tracheal cytotoxin** = dermonecrotic toxin - destroys epithelial tissue
80
How long is the incubation period for Pertussis
i.e. Whooping cough
Incubation period is typically 7-10 days but may range from 5-21 days and as long as 41 days
81
What is the infectious period for Pertussis for:
1. Adolescents and adults
2. Infants
1. Adolescents and adults are infectious until 21 days after onset of paroxysmal cough
2. Untreated infants may remain infectious for 6 weeks or longer
82
What are the clinical manifestations for Pertussis?
- 7 to 14 day incubation
- Initial cold- like symptoms/ inflamed mucous membranes
- followed by prolonged coughing sieges with inspiratory whoop
- permanent or long- lasting immunity develops
83
What is the treatment, prevention and control of Pertussis?
- Bacterial culture, fluorescent antibody staining, and serological tests
- Antibiotic therapy
- Immunization with DPT for younger or Tdap acellular vaccines for older children and adults
84
What is the bacteria that causes Streptococcal Diseases?
Streptococcus pyogenes
Gram positive cocci
- one of the most important pathogens
group A beta-hemolytic streptococci (GAS)
85
What are the virulence factors for Streptococcus pyogenes?
- Extracellular enzymes that break down host molecules
- Streptokinases - dissolve clots
- Streptolysin O and S - kill host leukocytes (defense)
- capsules and M proteins for attachment
86
What is the transmission for Streptococcal diseases?
Respiratory droplets, direct or indirect contact
widely distributed, some carriers
87
How is Streptococcal diseases (streptococcus pyogenes) diagnosed?
- Based on clinical laboratory findings
- Rapid diagnostic tests available
88
What does the M protein of Streptococcus pyogenes look like?
Hair pins- hold in place
89
What is the common infection strep throat called, how is it spread and where does it infect?
- Called = Streptococcal pharyngitis
- Spread = by droplets of saliva or sasal secreations
- Infection = in throat (pharyngitis) or tonsils (tonsillitis)
90
What are the symptoms of streptococcal pharyngitis?
i. e. Strep throat
- Symptoms of disease not diagnostic becasue many viral infections have similar presentation
91
What are the physical manifestations of streptococcal pharyngitis?
i. e. Strep throat
- redness, edema, exudate and lymph node enlargement in throat
92
How is streptococcal pharyngitis diagnosed?
rapid kits
93
How is streptococcal pharyngitis treated and controlled?
- Antibiotics important for childred to lessen chance of complications (rheumatic fever and glomerulonephritis)
- control by preventing contact with contaminated material or infected individuals
94
What are post-streptococcal diseases?
Glomerulonephritis (Bright's disease) and rheumatic fever
Nonsupportive (nonpus-producing)
Most serious problems associated with streptococcal infections in U.S.
95
When do Post-streptococcal diseases come on?
1-4 weeks after an acute streptococcal infection
96
What is Glomerulonephritis?
Inflammatory disease of renal glomeruli (a type III hypersensitivity)
97
What are the clinical manifestations of Glomerulonephritis?
- edema, fever, hypertension, and hematuria
- may spontaneously heal or may become chronic
98
What is the diagnosis of Glomerulonephritis?
clinical history, physical findings, and confirmatory evidence of prior streptococcal infection
99
What is the treatment for Glomerulonephritis?
antibiotic therapy (to kill residual bacteria), otherwise no specific therapy
100
What is the Autoimmune disease involving heart valves, joints, subcutaneous tissues and central nervous system?
Rheumatic Fever
101
What are the clinical manifestations for Rheumatic Fever?
vary widely, making diagnosis difficult
102
What is the treatment, prevention and control of Rheumatic Fever?
- therapy directed at decreasing inflammation and fever, and controlling cardiac failure
- treatment with salicylates and corticosteroids
103
What are Arthropods?
- Indirectly harm--transmit... not produce
- some are true parasites
- some inflict direct harm via bites, stings, or other activities
- can carry more than one type of pathogen
104
Explain Arthropod-Borne Diseases
- Generally rare
- Some are of historical interest (such as plaque and typhus)
- Some newly emerged (such as Lyme disease and erlichiosis)
105
What is the bacteria for Lyme disease?
- LD or Lyme borreliosis
- Most common tick-borne disease in the U.S
106
What is lyme disease caused by in the US and Europe and Asia (most common)?
- Borrelia burgdorferi = U.S
- B. garinii and B. afzelii = Europe and Asia
107
How is Lyme disease transmitted?
- From animal reservoirs by ticks (lxodes scapularis and I. pacificus)
- deer, field mice and woodrats
108
What are the clinical manifestations and stagest of Lyme disease?
- Clinical manifestations vary with three stages of disease:
**_- Initial (localized stage) :_** develops 1 week to 10 days after infection with an expanding, ring-shaped skin lesion with flu-like symptoms
**_- Disseminated :_** Occurs weeks or months after infection with neurological abnormalities, heart inflammation and arthritis (lyme arthritis may be autoimmune to joint MHC which are similar to bacterial antigens)
**_- Late Stage :_** occurs years later and has demyelination of neurons, behavioral changes and symptims resembling Alzheimer's disease and multiple sclerosis
109
What are the two families of ticks that cause Lyme disease? how do they differ?
1. hard ticks = ixodidae
2. soft ticks - argasidae
- Differ by feeding habits. Soft ticks complete their meals in a matter of minutes or a few hours. Hard ticks feed slowly, taking up to 7-9 days
110
How is Lyme disease diagnosed?
- serogical testing (Lyme ELISA or Western blot)
- Isolation of spirochete from patient
- Detection of Borrelia DNA (PCR)
111
How is Lyme disease treated, prevented and controlled?
- Antibiotic therapy most effective in early stages
- tick control and avoiding ticks
112
What is the bacteria that causes Plague? (G+ or G-)
Yersinia pestis - gram negative
113
How is plague transmitted?
- rodent to human
- bite of infected flea, direct contact with infected animal or product, inhalation contaminated air borne droplets
114
What happens once the Plague gets into the body?
- multiply in blood and lymph
- survive and proliferate in phagocytic cells
- enlarge lymph nodes (buboes)
115
Explain the plague infectious cycle
116
What are the virulence factors for Plague?
- proliferates in phagocytes, not killed
- Type III secretion systems deliver yersinal outer membrane proeins (YOPS) into cells which shut down defense mechanisms
117
What is the select agent for plague?
- Y. pestis
- potential bioterrorism threat
118
What are the clinical manifestateions for plague?
- subcutaneous hemorrhages, fever, and buboes (hence name bubonic plague)
- High mortality if untreated
- Pneumonic plague arises from
* primary exposure to infectious respiratory droplets of infeted persons or cats
* secondary to hematogenous spread in a patient with bubonic plague
119
What is the diagnosis of plague?
Diagnosis made in reference labs which use direct microscopic examinations, cultures and serological tests and PCR
120
What is the treatement, prevention and control for plague?
- antibiotic therapy
- Ectoparasite and rodent control, isolation of human patients, prophylaxis of exposed persons, immunization of persons at high risk
121
What is the cause of Rocky Mountain Spotted Fever?
- Rickettsia rickettsii
122
How is Rocky Mountain spotted fever transmitted?
By ticks!!!
* Transovarian passage - transmission of bacteria from generation to generation of ticks through their eggs
* Passage by tick feeding or by defectation of tick and rubbed into skin
123
How is Rocky Mountain Spotted Fever reproduced?
in epithelial cells and macrophages
124
What is located on tissue? what is located in blood stream?
Macrophage = on tissues
Monocyte = blood stream (largest)
125
What are the clinical manifestations of Rocky Mountain Spotted Fever?
- Vasculitis and sudden onset of headache, high fever, chills and skin rash
- Can destory blood vessels in heart, lungs or kidneys, leading to death
126
How is Rocky Mountain Spotted Fever diagnosed?
observation of signs and symptoms and serological tests
(sends patient into DIC - throwing clots - deceminated intravascular coagulation)
127
How is Rocky Mountain Spotted Fever treated, prevented and controlled?
- antibiotic therapy and symptomatic/supportive therapy
- tick control and avoidance of ticks
128
Is it possible for arthropods to carry more than 1 type of pathogen?
YES
129
What is direct contact dieseases? explain
- Most involve skin or underlying tissues
- some can become disseminated
130
What is Gas Gargrene caused by?
or called Clostridial Myonecrosis
- Caused by: Clostridium perfringes
* Gram positive, spore- forming rod
* Secretes toxin and tissue damaging enzymes
131
What does gas gangrene infect?
a necrotizing infection of skeletal muscle or clostridial myonecrosis
132
How is Gas Gangrene transmitted?
by contamination of injured tissue by spores from soil or bowel microbiota
133
What are the clinical manifestations of Gas Gangrene?
- severe pain, edema, drainage, muscle necrosis
134
How is Gas Gangrene diagnosed?
recovery of appropriate clostridial species and characteristic disease symptoms
135
What is the treatment, prevention and control of Gas Gangrene?
* surgical debridement, administration of antitoxin, antibiotic therapy and hyperbaric oxygen therapy
* Prompt treatment of all wound infections and amputation of limbs
136
How is Group B streptococcal disease cause? bacteria?
Streptococcus agalactiae or group B streptococcus (GBS)
Gram Positive
137
What does group B streptococcal disease cause for neonatal and newborns?
- sepsis, meningitis and pneumonia
138
How is group B Streptococcal disease transmitted?
Directly from person to person with many people being transient carriers
- vagina may be source for newborns
139
What are the clinical manifestations for Group B streptococcal disease?
- Early onset disease
* Presents within first few hours after birth
* may be severe meningitis or death
- Late onset disease - rare
140
What is teh diagnosis for Group B streptococcal disease?
Gram Positive, beta - hemolytic, streptococcal bacteria growth from cultures of otherwise sterile body fluids
141
What is the treatment, prevention and control for Group B streptococcal disease?
- detect pregnant carriers
- antibiotics
142
What are mycobacterial skin infections?
- Leprosy
- Tattoo- associated Mycobacterial Infections
143
What is another name for Leprosy? where is it most commonly found?
Hansen's disease, most common in tropics
144
What is Leprosy caused by and how is it invading?
Mycobacterium leprae
- invades peripheral nerve and skin cells, becoming obligate intracellular parasites
145
How is Leprosy transmitted and spread?
Humans are only significant reservoir (obligate intracellular parasite)
* Transmitted after prolonged exposure to infected individual
* probably spread in nasal secretions
146
What are the clinical manifestations of Leprosy?
* Incubation usually 3 to 5 years
* initial symptoms is slightly pigmneted skin eruption
* development of disease throught to be related to strength of cell0mediated immune response to bacterium
147
What are two common forms of Leprosy (describe)
**_Tuberculosis (neutral) leprosy_**
* Mild, nonprogressive form
* associated with delaying-type hypersenstivity
* damaged nerves and regions of skin surrounded by a border of nodules
**_Lepromatous (progressive) leprosy_**
* Individuals do not develop hypersensitivity
* skin tissue killed, leading to progressive loss of facial features, fingers, toes
* disfiguring nodules form on body
148
What is the diagnosis for Leprosy?
direct fluroescent antibody staining of biopsy specimens, serodiagnostic tests, DNA amplification and ELISA (more difficult to stain so cannot just do gram staining)
149
What is the treatment prevention and control for Leprosy?
- Long term antibiotic and drug therapy, and immunotherapy with vaccine
- identification and treatment of patients and prophylactic therapy for uninfected household members
150
What is the bacteria for Tattoo-associated Mycobacterial Infections?
- Mycobacterium chelonae
151
Explain the transmission and manifestations for Mycobacterium chelonae
- emerging agent in tattoo-associated infections
- skin lesions, papules, pustules, plaques
152
How is tattoo associated mycobacterial infections diagnosed and treated?
- culture, bacterial staining
- long-term antibiotic treatment, steroids
153
What is Peptic Ulcer disease and gastritis caused by?
Helicobacter pylori (H. pylori)
Gram negative
154
Explain what the Peptic Ulcer disease and gastritis bacterium does
H. pylori (gram negative) = Class 1 carcinogen!!!!
* Colonizes gastric mucus-secreting cells (common for ulcer disese)
* Produces urease, which acts to increase pH
* Releases toxins that damage epithelial mucosal cells
155
How does H. pylori Disease (Peptic Ulcer disease and gastritis) colonize?
Colonizes gastric mucus-secreting cells, beneath gastric mucosa by aid of suface fimbriae (adhesions)
* Binds sialic acid in gastric epithelial cells
Produces ureases which hydrolyses ammonia and provides a local alkaline environment
Proteases, phospholiases, cytokines, and cytotoxins increase inflammation
156
How is H. pylori Disease (Peptic Ulcer disease and gastritis) transmitted?
Probably person to person
common source has not been ruled out
157
How is H. pylori Disease (Peptic Ulcer disease and gastritis) diagnosed?
Culture of gastric biopsy specimens, examination of stained biopsies, serological testing, urea breath test, tests for ammonia in urine, and detection of urease activity in biopsies
158
How is H. pylori disease (Peptic Ulcer disease and gastritis) treated, prevented and controlled?
a combination of drugs to decrease stomach acid and antibiotics to kill the bacteria
159
What is the organims for Chlamydia STD?
chlamydia trachomatis
Gram negative small rods
MOST FREQUENT REPORTED STD
160
What is the bacterial microorganism for gonorrhea STD?
Neisseria gonorrhoea
Gram negative diplococci
can affect the mucous membranes of the genitourinary track, eye, rectum and throat
161
What is the bacterial microorganism for syphillis STD?
Treponema pallidum
Spirochete-gram stain not used due to difficulty. Prefer dark-field of lesions exudate. Serology-VDRL or RPR testing
A contagious, ulcerative disease
162
What are the clinical manifestations for Chlamydia disease?
In males
* asymptomatic or urethral discharge, and itching and inflammation of genital tract
In femails
* sometimes asymptomatic
* may cause PID
* if pregnant, can lead to miscarriage, stillbirth, inclusion conjunctivitis, and infant pneumonia
163
How is Chlamydia disease diagnosed?
demonstration of leukocyte exudate, exclusion of urethral gonorrhea by gram stain and culture, rapid diagnostic tests
164
How is chlamydial diseases treated?
antibiotic therapy
165
What causes Gonorrhea? and how does the bacterial attach?
Neisseria gonorrhoeae
gram negative, oxidase-positive diplococcus
(referred to as gonococcus)
Attaches to microvilli; phagocytosed by mucosal cells
166
What is the conjunctivitis of the newboar called? Mother to child during birth...
ophthalmia neonatorum
167
What are the virulence factors for Gonorrhea?
- Attach to microvilli or mucosal cells by pili and proein II adhesions
- survive phagocytosis by neutrophils
- fibrosis results and may lead to stricture or urethral closing
168
What are the clinical manifestations of Gonorrhea?
symptoms in men
* Urethral discharge of yellow, creamy pus, and painful, burning urination
Symptoms in femails
* vaginal discharge beginning 7 to 21 days after infection
169
What results from the infection of the fallopian tube and surrounding tissue from Gonorrhea?
Pelvic inflammatory disease (PID)
- major cause of sterility and ectopic pregnancies
170
What is the disseminated gonococcal infections?
involvement of joints, heart and throat
171
What is teh diagnosis for gonorrhea?
culture of bacterium followed by gram stain, oxidase test and determination of cell and colony morphology; DNA probe test
172
What is the treatment, prevention and control for Gonorrhea?
Antibiotic therapy (penicillin resistance common)
Public education, diagnosis and treatment of asymptomatic infividuals, condom use, and quick diagnosis and treatment of infected individuals
173
What is the cause of syphilis?
Treponema pallidum subsp.pallidum
174
What are the types of syphilis?
venereal syphilis - sexually transmitted
congenital syphilis - aquired in utero (from mom)
175
What is the diagnosis for syphilis?
clinical history, microscopic examination and serology
176
What is the treatment, prevention and control for syphilis
antibiotic therapy most effective in early stages
public education, prompt treatment of new cases, follow-up on sources and contacts, sexual hygiene and use of condoms
177
What are the stages of syphilis
Primary/shanker - lesions on genital area
Secondary - lesions all over body
Thertiary stage - 2 to 3 years but up to 10 years after exposure (can lead to demensia and mind loss)
During military take over, syphilis took over and become very common
178
What is staphylococcal disease caused by?
members of the genus Staphylococcus
Gram positive cocci
occurring singly, pairs, tetrads or grape-like clusters
179
How would you describe the genus staphylococcus and where does it normally inhabit?
facultative anaerobes and usually catalase positive
normally inhabitants of upper respiratory tract, skin, intestines and vagina
180
What are the two main type sof staphylococcal diseases?
S. aureus - coagulase positive, pathogenic
S. epidermidis - coagulase negative, less pathogenic but nosocomial opportunists (common on skin and does not cause too much problems, if right place at right time it can become pathogen)
181
What contributes to pathogenicity of staphylococcal diseases?
Teichoic acid and peptidoglycan
182
What is staphylococcal diseases harbored by?
asymptomatic carriers or active carriers (have the disease)
- spread by hands, inanimate objects or expelled by respiratory tract, or through blood
\*\*May produce disease in almost every organ and tissue\*\*
- Immune comprimised most at risk!
183
What are the virulence factors for staphylococcal diseases?
- Exotoxins and enzymes involved in invasiveness
- toxin genes may reside on plasmids and on chromosome
Examples:
* enterotoxin - food intoxication
* bacteremia and abscess formation
184
what is an exotoxin?
organism produces a toxin that travels to other areas of the body
185
what is beta lactamase physiological action?
Produced by staphylococci
breaks down beta-lactam antibiotics
186
What is catalase physiological action?
Produced by staphylococci
converts hydrogen peroxide into water and oxygen and reduces killing by phagocytosis
187
What is coagulase physiological action?
Produced by staphylococci
Reacts with prothrombin to form a complex that can cleave fibrinogen and cause the formation of a fibrin clot; fibrin may also be depositited on the surface of staphylococci, which may protect them form destruction by phagocytic cells; coagulase production is synonymous with invasive pathogenic potential
188
What is DNase physiological action?
Produced by staphylococci
Destroys DNA
189
What is enterotoxins physiological action?
Produced by staphylococci
Are divided into heat-stable toxins of six known types (A, B, C1, C2, D, E); resonsible for the gastrointerestinal upset typical of food poisoning
190
What are exfoliative toxins A and B (superantigens) physiological action?
Produced by staphylococci
Cause loss of the surface layers of the skin in scalded-skin syndrome
191
What is Hemolysins physiological action?
Produced by staphylococci
Alpha hemolysin destroys erythrocytes and causes skin destruction. Beta hemolysin destroys erythrocytes and sphingomyelin around nerves
192
What is hyaluronidase physiological action?
Produced by staphylococci
Also known as spreading factor; breaks down hyaluronic acid located between cells, allowing for penetration and spread of bacteria
193
What is panto-valentine leukocidin physiological action?
Produced by staphylococci
Inhibits phagocytosis by granulocytes and can destroy these cells by forming pores in their phagosomal membranes
194
What is lipases physiological action?
Produced by staphylococci
breaks down lipids
195
What is nuclease physiological action?
Produced by staphylococci
Breaks down nucleic acids
196
What is protein A physiological action?
Produced by staphylococci
Is antiphagocytic by competing with neutrophils for the Fc portion of specific opsonins
197
What is proteases physiological action?
Produced by staphylococci
Break down proteins
198
What is toxic shock syndrome toxin-1 (a superantigen) physiological action?
Produced by staphylococci
Is associated with the fever, shock and multisystem involvement of toxic shock syndrome
199
Explain staphlococcal lesions (localized abscess)
- S. aureus infects a hair follicle, tissue necrosis results
- coagulase is produced forming a fibrin wall around leasion, limiting spread
- Liquefaction of necrotic tissue in center of leasion occurs; abscess spreads
- may be a furuncle (boil) or carbuncle (coalescing of multiple furuncles)
- Bacteria may spread from area via lymphatics or bloodstream (bacterimia)
200
Explain Staphylcoccal Scalded Skin Syndrome (SSSS)
- caused by strains of S. aureus that carry a plasmid-borne gene for exfoliative toxin (exfoliation)
- Epidermis peals off revealing red area underneath
- Staph gets right under the epidermis of skin and starts producing toxins
201
What is the diagnosis for Staphylcoccal Scalded Skin Syndrome (SSSS)?
isolation/identification of Staphylococcus involves commercial kits
202
What is the treatment, prevention and control for Staphylcoccal Scalded Skin Syndrome (SSSS)?
* Isolation and identification based on catalase test, coagulase test, serology, DNA fingerprinting and phage typing
* Antibiotic therapy
* many drug-resistant strains
* Personal hygiene, food handling, and aseptic management of lesions
203
Explain staphylococcal disease toxic shock syndrome (TSS)
* caused by S. aureus strains that release toxic shock syndrom toxin and other toxins
* Some cases occur in femails who use superabsorbant tampons
* disease results from body's response to staphylococcal superantigens (T cells fight own body)
* Tell body T cells we have a problem and kick into overdrive
204
What are the clinical manifestations for staphylococcal disease toxic shock syndrome (TSS)?
Low blood pressure, fever, diarrhea, extensive skin rash, and shedding of skin
205
Explain Streptococcal disease superficial types of diseases
* Contact superficial cutaneous diseases:
* Cellulitis
* Diffuse, spreading infection of subcutaneous tissue
* redness and swelling
* Impetigo
* Also caused by S. aureus
* Superficial cutaneous infection commonly seen in children
* crusty lesions and vesticules surrounded by red border
* Erysipelas
* acute infection of dermal layer of skin
* red patches that may occur periodically at same site for years
206
Explain the Streptococcal Invasive diseases
May reach underlying muscles
* caused by certain virulent strains of S. pyogenes
* Rapidly progressive
* carry genes for exotoxins
* superantigens (select agent)
* Tissue-destroying protease
* Clinical manifestations
* Necrotizing fasciltis ("flesh eating"): destruction of sheath covering skeletal muscles
* Myositis: inflamation and destruction of skeletal muscles and fat tissue
* toxic shock-like syndrom (TSLS): precipitous drop of blood pressure, failure of multiple organs and high fever
207
Explain Tetanus and what it is caused by?
Caused by Clostridium tetani
* anaerobic, Gram Positive Spore former
* Endospores found in soil, dust, hospital environments, and mammalian feces (rusty metal)
* Produces tetanospasmin in low oxygen tension environments
* causes prolonged muscle spasms
* Also produces tetanolysin, a hemolysin
208
What is the method for getting Tetanus?
Portal of entry - skin wounds
209
How is Tetanus diagnosed?
clinical history of wound infection and muscle stiffness
210
What is the treatment, prevention and control for Tetanus?
antibiotic therapy and treatment with antitoxin
active immunization with toxoid (DPT vaccine) and proper care of wounds contaminated with soil, prophylocatic use of antitoxin
211
What are the clinical manifestations of Tetanus?
Early in disease
* Tension or cramping and twisting of skeletal muscles and tightness of jaw muscle
Advanced disease
* trismus ("lockjaw"), characteristic facial expressions, board-like rigidity of trunk, tonic convulsions, and backward bowing of back
* Death usually results form spasms of diaphragm and intercostal respiratory muscles
212
What is pink eye?
conjuctivitis
- defined as inflammation of the bulbar and/or papebral conjuctiva (the transparent lubricating mucous membrane that covers both surfaces of the eye).
- has many etiologies, including infection from various bacteria, fungi, and viruses, as well as toxic and allergic insults
- Common about 1% of all primary care office visits in US are related to conjuctivitis
- 30% have bacterial conjunctivitis, though 80% are treated with antibiotics
- Most common bacteria:
Staphylococcus, streptococcus, corynebacterium, Haemophilus, Pseudomonas, and Moraxella species
213
What are the common bacteria that cause conjunctivitis?
Pink eye
## Footnote
- Most common bacteria:
Staphylococcus, streptococcus, corynebacterium, Haemophilus, Pseudomonas, and Moraxella species
214
What is an inflammation of stomach and intestinal lining?
Gastroenteritis
215
What is it when a food is a source of pathogen?
food poisoning
216
What is it in food-borne infections that make it different?
pathogen must colonize host
217
What is food intoxication?
Ingestion of toxin - through bacteria may have died, the toxins they produced make you sick
* enterotoxins - disrupt functioning of intestinal mucosa causing nausea, vomiting, and/or diarrhea
218
What is the general way to prevent food borne and water borne diseases?
sanitation measures
219
What is the reservoir for the organism Aeromonas hydrophilia?
Waterborne Bacterial Pathogen
Free-living
sometimes associated with gastroenteritis, cellulitis and other diseases
220
What reservoir does the organism Campulobacter jejuni?
Waterborne Bacterial Pathogen
Bird and animal reservoirs
Major cause of diarrhea; common in processed poultry; a microaerophile
221
What reservoir is for Helicobacter pylori?
Waterborne Bacterial Pathogen
Free-Living
Can cause gastrititis, peptic ulceers, gastric aderocarcinomas
222
What is the reservoir for Legionella pneumophilia?
Waterborne Bacterial Pathogen
Free-living and associated with protozoa
Found in cooling towers, evaporates, condenses, showers, and other water sources
223
What reservoir for Leptospira spp.?
Waterborne Bacterial Pathogen
Infected animals
Hemorrhagic effects, jaundice
224
What is the reservoir for Mycobacterium spp.
Waterborne Bacterial Pathogen
Infected animals and free-living
COmplex recovery procedure required
225
What is the reservoir for Pseudomonas aeruginosa?
Waterborne Bacterial Pathogen
Free-living
Swimmer's ear and related infections
226
What is the reservoir for Salmonella enteriditis?
Waterborne Bacterial Pathogen
Animal intestinal tracts
COmmon in many waters
227
What is teh reservoir for Vibrio cholerae?
Waterborne Bacterial Pathogen
Free-living
FOund in many waters, including estuaries
228
What is the reservoir for vibrio parahaemoyticus?
Waterborne Bacterial Pathogen
Free-living in coastal waters
causes diarrhea in shellfish consumers
229
What is the reservoir for Yersinia enterocolitica?
Waterborne Bacterial Pathogen
Frequent in animals and in the envirionment
Waterborne gastroenteritis
230
What is the bacteria responsible for Botulism?
Clostridium botulinum
and obligate anaerobic, endospore-forming
Gram positive rod (on select agent list)
231
Explain the presence of Botulism
Most common source of infection is insufficiently heated home-canned foods
* Endospores not killed, then germinate and produce toxin
* if food inadequately cooked, toxin remains and causes disease
232
What does Botulism impact?
Botulinum toxin
neurotoxin that binds to synapses of motor neurons
233
What is the diagnosis for Botulism?
Diagnosis restricted to reference laboratoris
* Demonstration of toxin in patient's serum, stool, or vomitus or C. botulinum in stool cultures
234
Explain Botulism in Infants
Most common form
* Endospores ingested, germinate, reporduce and produce exotoxin
* constipation, listlessness, general weakness, and poor appetite; death may reslut from respiratory failure
235
What is the treatment, prevention and control for Infant botulism?
* symptomatic/supportive therapy and administration of antitoxin
* safe food processing practices and not feeding honey to babies under one year of age
236
What is the bacteria responsible for Gastroenteritis?
Campylobacter jejuni
gram negative
curved rod found in intestinal tract of animals (e.g. chickens, turkey, and cattle)
causes campylobacteriosis
237
How is Gastroenteritis transmitted?
to humans by contaminated food or water, contact with infected animals or anal-oral sexual activity
238
What is the manifestation of Gastroenteritis?
C. jejuni invades epithelium of small intestine, secretes and exotoxin, causes inflammation, ulceration and bloody stool
239
How is Gastroenteritis diagnosed?
culture in low oxygen, high CO2 atmosphere
240
What is the treatment, prevention and control of Gastroenteritis?
* Symptomatic/supportive therapy and antibiotic therapy in severe cases
* good personal hygiene, safe food handling practices
241
What is the comma-shaped bacteria?
Vibrio cholerae (cholera)
Gram - negative bacteria
242
How is Cholera aquired?
ingesting food or water contaminated by fecal matter from patient or carrier
243
What is a natural reservoir for V. cholerae (cholera)?
shellfish are natural reservoirs
244
How does cholerae adhere to organisms?
adhere to intestinal mucosa of small intetine and secrete the toxin choleragen
245
What happens in the presence of the choleragen toxin?
Results in a massive loss of water and electrolytes
- Production of "rice-water stools"
246
How is cholerae diagnosed?
culture form feces with subsequent identification by agglutination reactions
247
What is the treatment, control and prevention for cholerae?
- oral rehydration
- antibiotic therapy
248
What is another name for Escherichia coli - Gastroenteritis?
Traveler's diarrhea
249
What is E. coli - Gastroenteritis (Traveler's diarrhea) caused by?
* Caused by certain viruses, bacteria or protozoa normally absent from traveler's environment
* E. coli is one of major causative agents
* Six categories or strains are recognized
* most other E. coli is non-pathogenic
250
What are the pathogenic E. coli strains (name and special feature)?
* Enterotoxigenic E. coli (ETEC)
* heat stability - produces one or both enterotoxins repsonsible for diarrhea
* Enteroinvasive E. coli (EIEC)
* multiplies within intestinal epithelial cells and may produce a cytotoxin and an enterotoxin
* Enteropathogenic E. coli (EPEC)
* Causes effacing lesions - destruction of brush boarder microvilli in intestinal epithelial cells
* Enterohemorrhagic E. coli (EHEC)
* produces effacing lesions and hemorrhagic colitis, releases shiga-like toxins
* Enteroaggregative E. coli (EAEC)
* Forms "stacked brick" appearance of epithelial cells, toxins not been identified
* Diffusely adhering E. coli (DAEC)
* Adheres in a uniform pattern to epithelial cells, particular problem in immunologically naive or malneurished children
251
What is the diagnosis for Traveler's Disease?
Past travel history and symptoms, isolation and identification of causative agents using DNA probes, tests for virulence factors and PCR
252
What is the treatment, prevention and control of Traveler's Disease?
- Symptomatic/supportive therapy and antibiotic therapy
- Avoiding contaminated food and water
253
What is the cause/bacteria for Salmonellosis?
caused by \>2,000 Salmonella serovars
Gram negative
Non-spore forming rods
254
How is Salmonellosis transmitted?
to humans by contaminated foods such as beef products, poultry, egg products and water
255
What does the Salmonellosis disease impact and what are the symptoms?
Disease results from food-borne infection
* bacteria in intestinal mucosa produce enterotoxin and cytotoxin
Symptoms include abdominal pain, cramps, diarrhea, nausea, vomiting and fever
256
How is Salmonellosis diagnosed?
isolation of organism from food or patients' stool
257
How is Salmonellosis treated?
Fluid and electrolyte replacement
good food handling practices, proper refrigeration, adequate cooking
258
What bacteria is responsible for Typhoid Fever?
Salmonella enterica
subspecies enterica serovar Typhi
Gram negative rod
259
How is Typhoid Fever aquired?
by ingestion of food or water contaminated by feces in infected humans or person to person contact
260
What is another version of Typhoid Fever
Paratyphoid fever
- Milder form of disease
261
How does the Typhoid Fever bacteria spread?
From small intestine to lymphoid tissue, blood, liver and gallbladder
262
What are the symptoms of Typhoid Fever?
Fever, headache, abdominal pain, anorexia, and malaise
263
What happens in Typhoid Fever carriers?
In carriers (eg. Typhoid Mary) bacteria grow in gallbladder and reach intestine through bile duct
264
how does one diagnose Typhoid Fever?
demonstration of typhoid bacilli in blood, urine, or stools
serology (Widal test)
265
How does one Treatment, prevention and control of Typhoid Fever?
* Antibiotic therapy
* vaccine for high risk individuals
* purification of drinking water, prevention of food handling by carriers, and isolation of patients
266
What bacteria causes shigellosis?
Bacillary dysentery
* caused by four species of genus Shigella
* Gram negative, non-spore forming rods
* intracellular parasites, multiply in colonic epithelium
267
What does shigellosis cause?
inflammatory reaction in mucosa
humans are the only host
watery stools often contain blood, mucus and pus
268
How is shigellosis diagnosed?
biochemical characteristics
serology
269
How is shigellosis treated, prevented and controlled?
antibiotic therapy
prevention by use of good personal hygiene and a clean water supply
270
What is the virulence in shigellosis?
* endotoxin
* Exotoxins play role in disease progression
* Shiga toxin
* targets glomerular epithelium and may lead to kidney failure
* Type III secretion system delivers virulence factors into epithelial cells
271
What does Staphylococcal food poisoning result from?
Ingestion of improperly stored or cooked food (eg. ham, processed meats, chicken salad, ice cream and hollandaise sauce) in which staphylococcus aureus has grown and released enterotoxin
272
What does staphylococcal food poisoning produce?
* Bacteria produce heat-stable enterotoxins in food
* properly cooking the food will not destroy toxin; intoxications can result from thoroughly cooked food
273
What are the symptoms of Staphylococcal Food Poisoning?
Include abdominal pain, cramps, diarrhea, vomiting and nausea
274
How is Staphylococcal Food Poisoning diagnosed?
* Based on symptoms or laboratory identification of bacteria from food
* enterotoxins can be detected in foods by animal toxicity tests
275
What is the treatment, prevention and control for Staphylococcal Food Poisoning?
* Fluid and electrolyte replacement
* avoidance of food contamination, and control of personnel involved in food preparation and distribution
276
What is Zoonotic Diseases?
* Diseases transmitted from animals to humans
* A number of important human pathogens begin as normal flora or parasites of animals and then adapt to cause disease in humans
277
What is Anthrax caused by?
Bacillus anthracis (select agent)
Gram positive, aerobic endospore forming
Endospores viable in soil and animal products for decades
plasmid encodes genes for anthrax toxin
278
How is Anthrax transmitted?
By direct contact with infected animals or their products
portal of entry determines form of disease
BIOTERRORISM AGENT
279
What is the virulence of Anthrax?
B. anthracis envades immune system by
* Capsule which inhibits phagocytosis
* synthesis of coomplex exotoxin
* protective antigen - forms hole for entry of other toxins
* edema factor - fluid release and edema
* lethal factor - inhibits cytokine production
* Macrophages die, release toxic contents leading to septic shock, death
280
What are the forms of Anthrax disease?
* **_Cutaneous (_**most common)
* Infection through cut or abrasion of skin
* Manifestiations: 1-15 day incubation
* skin papule that ulcerates, headache, fever and nausea
* Antibiotic therapy effective if caught early
* **_Pulmonary anthrax_**
* Woolsorter's disease (sheared lambs - direct animal contact)
* inhalation of endospores
* Resembles influenze
* if bacteria reach the bloodstream, usually fatal
* **_gastrointestinal anthrax_**
* ingestion of endospores
281
How is Anthrax diagnosed?
* Presumptive ID in sentinel labs of laboratory response network (LRN)
* Gram-stained smear of skin lesion, cerebrospinal fluid or blood; also growth and biochemical characteristics of culture
* confirmatory diagnosis by PCR and serology
282
How is Anthrax Treatment, prevented and controlled?
* Antibiotic therapy and symptomatic/supportive therapy
* Immunization of animals and persons at high risk
283
What is Brucellosis (Undulant Fever) caused by?
Brucella spcies (B. abortus, B. melitensis, B. ovis, B. suis, or B. canis) (select agents)
- Elk to cattle hurds can infect humans
- Brucella spp. are tiny Gram-negative coccobacilli
284
How are humans infected with Brucellosis?
* Ingestion of Brucella contaminated food or water
* inhalation of organism
* bacterial entry into body through skin wounds
285
What are the symptoms of Brucellosis?
* Presents as non-specific, flu-like symptoms
* In undulant form, symptoms include undulant fevers, arthritis and testicular inflammation in males
* In chronic form, symptoms include chronic fatigue syndrome, depression and arthritis
286
What causes Psittacosis (ornithosis)?
Chlamydophilia psittaci
enters respiratory tract, transported to and reproduces in liver and spleen and then invades lungs
287
Explain the details of Psittacosis (Ornithosis), how is it transmitted?
Infectious disease of birds
* Transmitted to humans by direct contact with infected birds or by inhalation of dried bird excreta
* occupational hazard in poultry industry
288
What are the clinical manifestations of Psittacosis (ornithosis)?
Inflammation and hemorrhaging of lung tissue and pneumonia
289
How is Psittacosis (ornithosis) diagnosed?
Isolation from blood or sputum, or by serology
290
How is Psittacosis (ornithosis) treated, prevented and controlled?
antibiotic therapy
chemoprophylaxis for pet birds and poultry
291
What causes Q fever (Select Agent)?
Coxiella burnetii
intracellular Gram- Negative bacterium
proliferates in lungs
servives outside host by forming endospore-like body
Q = quiry because do not know what is going on
292
How is Q fever transmitted?
- Ticks between animals
- Contaminated dust to humans
- Occupational hazard among slaughterhouse workers, farmers and veterinarians
293
What are the clinical manifestations of Q Fever?
* Mild respiratory symptoms and acute onset of severe headache, muscle pain, and fever
* endocarditis can develop 5 to 10 years later
294
How is A Fever Diagnosed?
In reference labs using immunofluorescence
295
What is the treatment, prevention and control of Q fever?
* Serological tests
* antibiotic therapy
* vaccination of high risk individuals and pasturization of cow and sheep milk in areas where disease is endemic
296
What is Tularemia caused by?
Francisella tularensis (Select Agent - Category A)
297
How is Tularemia spread?
From animal reservoirs by serveral mechanisms (from rabbits)
* Arthropod bites
* direct contact with infected tissue
* inhalation of aerosolized bacteria
* ingested of contaminated water or food
298
What are the clinical manifestations of Tularemia?
incubation 2 to 10 days
primary ulcerative lesion at infective site, enlarged lymph nodes and high fever
299
How is Tularemia diagnosed?
PCR, culture of bacteria and immunodiagnostic tests
300
How is Tularemia treated, prevented and controlled?
- antibiotic therapy
public education, protective clothing, vector control and immunization for high- risk individuals
301
What are opportunistic diseases?
Microbes that are otherwise members of the normal microbiota but become pathogens are referred to as opportunists and cause opportunistic disease
302
What is the bacteria for Antibiotic - Associated Colitis (pseudomembranous Colitis)?
Clostridium difficile (C. difficile associated diarrhea - CDAD)
* uncomplicated diarrhea
* pseudomembranous colitis
* viscous collection of inflammatory cells, dead cells, necrotic tissue, and fibrin that obstructs the intestine
* toxic megacolon
* inflammation resulting in intestinal tissue
303
What is C. difficile?
Anaerobic spore forming bacillus found in the intestines of some healthy people
* Numbers in check by other normal intestinal microbiota
* excessive antibiotic use eliminates normal microbiota and allows C. difficile to overgrow
* most common: amoxicillin, ampicillin, clindamycin, cephalosporins
304
What are the virulence factors of C. difficile?
Multiplies and produces toxins
Toxin A (enterotoxin causing diarrhea)
Toxin B (cytotoxin kills cells)
305
what are the clinical manifestations and treatment for C. difficile?
Inflammation, diarrhea, fever, nausea, cramping
most common cause of diarrhea in hospitalized patients
treatment is with antibiotics
306
What is Bacterial vaginosis caused by?
* Gardnerella vaginalis
* Gram positive or gram variable pleomorphic nonmotile rods
* Mobiluncus spp
* Gram-negative anaerobic rod
307
Explain the Bacterial vaginosis disease, details and transmission
Typically a mild disease, characterized by
* copious, frothy, fishy-smelling vagina discharge
* varying degrees of pain/itching
Microbes are present in vagina and rectum of 20-40% of healthy women, suggesting an opportiunistic etiology
* transmission from person to person through intimate contact can occur, however
308
How is Bacterial vaginosis diagnosed and treated?
* Diagnosis via microscopic observation of _clue cells_ - vaginal epithelial cells covered in bacteria
* Treatment with metronidazole clears the infection
309
How are Dental diseases acquired?
Acquired enamel pellicle
* formed when enamel absorbs acidic glycoproteins from saliva
* colonized by various bacterial species to form plaque
Coaggregation
* attachment of different species of bacteria to each other
* based on cell-to-cell recognition
310
What is the main species involved in periodontal disease?
Porphyromonas gingivalis
311
