Chapter 8 - Infectious Diseases Flashcards
(276 cards)
1
Q
Categories of infectious agents?
A
a. prions
b. viruses
c. bacteria
d. fungi
e. parasites
2
Q
Prions:
- Pathology involves ____ encephalopathies ___ inflammation.
- The normal prion protien is associated with?
A
GERD:
- Pathology involves spongiform encephalopathies withoutinflammation.
- The normal prion protein is associated with neuronal development and prevention of cell death.
3
Q
Prions:
When they undergo a conformational change they become ___ and form? What does this induce?
A
Prions:
When they undergo a conformational change they become insoluble and form amyloid plaques. These accumulate in the brain and induce neuronal degeneration leading to dimentia and death
4
Q
Prions:
Genetic prion disease?
Infectious?
A
Prions:
Genetic: Cruetzfeldt-Jakob
Infectious: iatrogenic CJD, Kuru, and new variant CJD
5
Q
Prions:
The human form of Bovine spongiform encephalopathy (BSE) is called?
A
Prions:
BSE human form = new variant CJD
6
Q
Viruses:
_____ intracellular parasites with what genome?
What is the genome enclosed in?
Envelope?
A
Viruses
Obligate intracellular parasites with DNA or RNA as genome
Enclosed in a capsid
The capsid may be enveloped or not
7
Q
Protection from infectious agents:
Skin:
What are two exceptions that can penetrate nondamaged skin?
A
Protection from infectious agents:
Skin:
a. Schistosoma can penetrate
b. Dermatophytes thrive on keratinized tissue
8
Q
Protection from infectious agents:
GI:
What provides protection?
When does infection occur?
A
Protection from infectious agents:
GI:
Protection: acid secretion, bile, normal flora, mucous, defensins, IgA, and digestive enzymes
Infection occurs when immunity is compromised or microbes adapt
9
Q
Protection from infectious agents:
Respiratory tract:
What provides protection?
When does infection occur?
A
Protection from infectious agents:
Respiratory tract:
Protection: ciliary activity, mucous, normal flora, IgA, and phagocytes
Infection occurs when immunity is compromised or microbes adapt
10
Q
Pathogen entry:
Skin:
How can they enter?
A few examples?
A
Pathogen entry:
Skin:
Enter though direct contact, bites, burns, wounds, etc.
Examples: Dermatophytes, HPV, staph, strep
11
Q
Pathogen entry:
Transplacental:
Examples of things that can infect the fetus?
A
Pathogen entry:
Transplacental:
Rubella, HIV, CMV, HBV, HCV, T. pallidum, L monocytogenes, S. agalactiae, Toxoplasma gondii
12
Q
Pathogen entry:
Common routes of transmission?
A
Pathogen entry:
a. transplacental or during birth
b. skin
c. respiratory tract (cough/sneeze –> aerosol droplets)
d. urine/feces
e. blood/tissue
f. skin/intimate contact
13
Q
STD:
The common sexually transmitted viruses?
A
STD:
HIV, HTLV1, HBV, HDV, HCV, HSV, and CMV (all with V, most with H)
14
Q
STD:
Sexually transmitted bacteria?
A
STD:
C. trachomatis, N. gonorrhoeae, H. ducreyi, mycoplasma, and ureaplasma
15
Q
STD:
C. trachomatis and N. Gonorrhoeae cause?
A
STD:
Cause urethritis, epidiymitis, cervicitis, and PID
16
Q
STD:
T. Pallidum causes?
H. Ducreyi causes?
Mycoplasma and Ureaplasma both cause?
A
STD:
T. Pallidum - syphilis
H. ducreyi - chancroid
Mycoplasma/ureaplasma - urethritis
17
Q
STD:
Klebsiella granulomatis:
Gram ____. Is a major cause of?
Begins as a ___ papule –> ____ (early disease) –> multiple lesions _____ (active) –> heals with ___.
A
STD:
Klebsiella granulomatis:
Gram negative. Is a major cause of genital ulceration
Begins as a painless papule –> ulcerates (early disease) –> multiple lesions coalesce (active) –> heals with scarring
18
Q
STD:
Sexually transmitted fungi? Causes?
Sexually transmitted parasite? Causes?
A
STD:
Fungus: C. Albicans - vaginitis
Parasite: Trichomonas vaginalis - urethritis and vaginitis
19
Q
Trophism:
What disseminates to the skin?
What disseminates to the brain?
A
Trophism:
Skin - chickenpox, yaws
Brain - poliomyelitis
20
Q
Trophism:
What infects the lungs?
What infects the kidneys?
A
Trophism:
Lungs - measles and rubella
Kidney - hematogenous pyelonephritis
21
Q
Trophism:
What affects the salivary gland?
What affects the liver?
A
Trophism:
Salivary gland - mumps and rabies
Liver - yellow fever and hepatitis B
22
Q
Virus-mediated tropism/cell injury:
Tropism is determined by:
Location of what 2 things?
As well as the local ____.
A
Virus-mediated tropism/cell injury:
Tropism is determined by:
Location of receptors for the firus and transcription factors required by the virus
As well as the local environment (temp, pH, etc)
23
Q
Virus-mediated tropism/cell injury:
Injury/death:
- Virus replication resulting in cell ___
- Inhibition of _____ synthesis
- Insertion of viral proteins into the host ___. What does this cause?
A
Virus-mediated tropism/cell injury:
Injury/death:
- Virus replication resulting in cell lysis
- Inhibition of macromolecular synthesis
- Insertion of viral proteins into the host membrane. This disrupts integrity, promotes cell fusion, and loss of cellf function.
24
Q
Bacteria-mediated tropism/cell injury:
What are some bacterial adhesins?
What is bacterial resistance mediated by?
A
Bacteria-mediated tropism/cell injury:
Adhesins - pili, fimbriae, LTA, capsule and receptors for host matrix proteins
Resistance may be mediated by - capsules, pili, M-proteins, proteases, antigenic mimicry, antigenic change, and intracellular growth**
25
Bacteria-mediated tropism/cell injury:
Effective intracellular growth may involve inhibition of ____ \_\_\_\_ fusion, escaping from the \_\_\_, blocking the host ___ \_\_\_\_ pathways, and rearranging \_\_\_.
Bacteria-mediated tropism/cell injury:
Effective intracellular growth may involve inhibition of _phagosome-lysosome_ fusion, escaping from the _phagosome_, blocking the host _signal transduction_ pathways, and rearranging _actin_.
26
Bacteria-mediated tropism/cell injury:
Intrinsic toxins?
All of these are ____ and can induce cellular \_\_\_.
Bacteria-mediated tropism/cell injury:
Intrinsic toxins - LPS, LTA, PG, TA, and LOS
All of these are _proinflammatory_ and can induce cellular_ necrosis_
27
Bacteria-mediated tropism/cell injury:
Examples of secreted exotoxins?
Some are superantigens: what do they do?
Bacteria-mediated tropism/cell injury:
Exotoxins - cholera, enterotoxin, Ef/LF from B. anthracis, tetanus, proteases, and hemolysins
Superantigens non-selectively activate T cells
28
What is this bacterial infection that is associated with skeletal muscle necrosis?
V. vulnificus
29
What is this bacteria associated with adrenal hemorrhage and necrosis? (also known as Waterhouse-Friedrickson syndrome)
N. meningitidis
30
Fungal-mediated tropism/cell injury:
Tissue damage is associated with:
1. The host inflammatory response via ___ and \_\_\_.
2. Secreted \_\_\_\_
3. Metabolic ___ products and exotoxins
4. What is physical damage mediated by?
Fungal-mediated tropism/cell injury:
Tissue damage is associated with:
1. The host inflammatory response via _granulomas_ and _abscesses_.
2. Secreted _proteases_
3. Metabolic _end_ products and exotoxins
4. Physical damage mediated by filament penetration of cells and tissues
31
This is c. albicans forming microabscess in the \_\_.
lung
32
Parasite mediated tissue tropism/cell injury:
Most infections are _____ and the most common modes of entry are?
What is tropism related to?
What causes tissue damage?
Parasite mediated tissue tropism/cell injury:
Most infections are _exogenous_ and enter via ingestion or direct penetration
Tropism is related to the stages in the life cycle and host species infected
Damage - toxic end pdts, mechanical damage, or cell lysis
33
This shows septate hyphae with acute angle branching: what is it?
This is aspergillus
34
This is showing broad, aseptate hyphae with right angle branching as well as invasions of vasculature and the airways. What is this?
This is mucormycosis
35
This is blastomyces dermatitidis: with thick walled ____ and neutrophilic infiltrate and broad based \_\_\_.
Thick walled _yeast_ and neutrophilic infiltrate and broad based _buds_
36
What is this?
What is in the spherule?
This is coccidioides immitis
There are endospores in the spherule
37
Immune evasion by infectious agents:
There is replication in inaccessible sites to the host immune response: Where is this?
Agents change or shed \_\_\_\_.
Immune evasion by infectious agents:
Inaccessible - lumen of intestine and keratinized epithelium
Agents change or shed _antigens_
38
Immune evasion by infectious agents:
There is rapid replication before an immune response can be established:
1. ___ sporozoite infection of hepatocytes
2. Trypanosoma cruzi infection of ___ \_\_\_
3. ___ infection of GI epithelium
Immune evasion by infectious agents:
Rapid replication
1. _Plasmodium_ infection of hepatocytes
2. Trypanosoma cruzi infection of _skeletal muscle_
3. _Shigella_ infection of the GI epithelium
39
Immune evasion by infectious agents:
Form "shields" of?
Types of intracellular growth?
Immune evasion by infectious agents:
capsules, parasite cysts, granulomas, encapsulated abscesses, and coating themselves with host proteins
Growth: spread laterally, interfere with signal transduction, prevent MHC expression, and inhibit Ag presentation to T cells
40
Immune evasion by infectious agents:
What inhibits protease activity?
What blocks MHC synthesis?
What blocks TAP transport?
Immune evasion by infectious agents:
Inhibits protease: EBV, CMV
Blocks MHC synthesis: Adenovirus, CMV
Blocks TAP transport: HSV
41
Mechanisms of antigenic variation:
For given type give example:
1. High mutation rate?
2. Genetic reassortment?
Mechanisms of antigenic variation:
For given type give example:
1. High mutation rate - HIV, influenza
2. Reassortment - influenza, rotavirus
42
Mechanisms of antigenic variation:
For given type give example:
1. Genetic rearrangement/recombination?
2. Diverse serotypes?
Mechanisms of antigenic variation:
For given type give example:
1. Recombination - Borrelia, Neisseria, Plasmodium
2. Serotypes - rhinoviruses, S. pneumoniae
43
Infection in the immunosuppressed host:
Hypogammaglobulinemia:
1. Recurrent sinopulmonary infections and/or otitis due to?
2. Gastroenteritis caused by? (3)
3. 2 other infections?
Infection in the immunosuppressed host:
Hypogammaglobulinemia:
1. Sinopulmonary - S. pneumoniae and H. influenzae
2. GE - giardia, rotavirus, and cryptosporidium
3. Enterovirus and P. aeruginosa
44
Infection in the immunosuppressed host:
T cell defects (SCID, DiGeorge):
Name some disease in which the host is suceptible to getting.
Infection in the immunosuppressed host:
T cell defects:
Candida, pneumocystis, viral pneumonia, aspergillosis, slamonellosis, and CMV
45
Infection in the immunosuppressed host:
Complement deficiencies:
Infections by?
Infection in the immunosuppressed host:
Complement:
Infections by Nisseria, s. pneumoniae, and h. influenzae
46
Infection in the immunosuppressed host:
Phagocyte or chemotactic deficiencies:
Susceptible to?
Infection in the immunosuppressed host:
Phagocyte:
Susceptible to s. aureus, Gram- bacilli, and aspergillus
47
Infection in the immunosuppressed host:
Transplant:
Within one month, what is the greatest risk for with an allograft?
1-6 months after?
\>6 months?
Infection in the immunosuppressed host:
Transplant:
1 month - CMV
1-6 months - CMV, HHV6, EBV, HBV, and HCV
\>6 months - community acquired respiratory tract infection
48
Inflammatory responses to infection:
Suppurative inflammation:
1. This is a reaction caused by?
2. Characterized by?
3. Difference between S. pneumoniae and S. aureus (and g-) pneumonia?
Inflammatory responses to infection:
Suppurative inflammation:
1. Reaction is caused by pyogenic microbes
2. Characterized by increased vas. perm. and PMN
3. S. pneumonia - spares alveolar walls so the lesions resolve completely. S. aureus leaves scars because it destroys the walls
49
Mononuclear and granulomatous inflammation:
1. What do spirochetes provoke? (in terms of cell)
2. Granulomatous inflammation is usually induced by what kind of bugs? Examples? Characteristics?
Mononuclear and granulomatous inflammation:
1. Spirochetes provoke lymphocytes
2. Induced by hard to eradicate bugs such as mycobacterium, histoplasma, and coccidioides; characterized by giant cells and areas of necrosis
50
Cytopathic-cytoproliferative inflammation:
1. This is usually virus mediated cell __ or \_\_\_.
2. Necrotizing inflammation: toxins that cause severe necrosis without? Examples
3. Chronic inflammation and scarring - examples?
Cytopathic-cytoproliferative inflammation:
1. Cell necrosis or proliferation
2. Necrotizing inflammation: minimal infiltrate: C perfringens, and E. histolytica
3. Scarring: HBV associated cirrhosis, Schistosoma eggs that calcifu, and calcified granulomas with Mycobacterium
51
This is a bladder infection with numerous calcified eggs: what caused this?
Schistosoma haematobium
52
Acute viral infections:
Examples?
Acute viral infections:
Measles, Mumps, Poliovirus, West Nile Virus, and Hemorrhagic fevers
53
Acute viral infections:
Measles:
1. This is a paramyxovirus: genome? Includes what other diseases?
2. Mechanism of transmission?
Acute viral infections:
Measles:
1. ssRNA; mumps, RSV, HPIV, and metapneumovirus
2. Aerosols
54
Acute viral infections:
Measles:
Measles replicates in the ___ \_\_\_ and then spreads to ____ \_\_\_. It binds to ___ (expressed on all nucleated cells) and signaling ____ \_\_\_ molecule (expressed on ___ cells). It is then shed into the \_\_\_.
Acute viral infections:
Measles:
Measles replicates in the _respiratory tract_ and then spreads to _reticuloendothelial tissue_. It binds to _CD46_ (expressed on all nucleated cells) and signaling _lymphocytic activation_ molecule (expressed on _T_ cells). It is then shed into the _blood_.
55
Acute viral infections:
Measles:
Histological characteristic feature? Where is this seen?
Acute viral infections:
Measles:
Multinucleated giant cells known as _Warthin-Finkeldey_ cells. They are in reticuloendothelial tissue, lungs, and sputum
56
Acute viral infections:
Measles:
1. What does the rash result from?
2. What is characteristically found in the mouth? This is a result from?
Acute viral infections:
Measles:
1. Rash results from vasculitis
2. Koplik spots in the mouth result from epithelial necrosis and a neutrophil exudate
57
Acute viral infections:
Measles:
1. What does the reticuloendothelial tissue typically show?
2. What are other symptoms?
Acute viral infections:
Measles:
1. Reticuloendotheilal tissue shows follicular hyperplasia, large germinal centers, and multinucleated giant cells
2. Cough, coryza, conjunctivitis, and photophobia
58
Acute viral infection:
Mumps:
1. Mode of transmission?
2. Where does it replicate?
Acute viral infection:
Mumps:
1. Aerosols
2. Replicates in T cells in draining lymph nodes
59
Acute viral infection:
Mumps:
1. It sheds into the ____ and infects the ___ \_\_\_.
2. Incubation period?
Acute viral infection:
Mumps:
1. Shed into the blood and infects the salivary glands
2. 16-18 day incubation period
60
Acute viral infection:
Mumps:
1. What are the symptoms?
2. Complications: 25% of postpubertal males? 50% of all?
Acute viral infection:
Mumps:
1. fever, HA, maliase, swelling of the parotids and submandibular glands
2. 25% of pospubertal males develop orchitis; 50% have transient meningitis
61
This multinucleated cell is in what disease?
What is it also known as?
Measles
This cell is a Warthin-Finkeldy cell
62
Acute viral infection:
Mumps:
Mumps can also affect the ____ with destructive lesions, parenchymal and ____ necrosis
Acute viral infection:
Mumps:
Mumps can also affect the _pancreas_ with destructive lesions, paranchymal and _fat_ necrosis (slide 633)
63
Acute viral infection:
Poliovirus:
1. This belongs to what class of virus? Genome?
2. Definition of poliomyelitis?
Acute viral infection:
Poliovirus:
1. Enterovirus with ssRNA
2. Acute febrile disease with neuronal damage potentially yielding paralysis
64
Acute viral infection:
Poliovirus:
1. Transmission? Disseminates to?
2. Asymptomatic percent of patients?
Acute viral infection:
Poliovirus:
1. Fecal/oral transmission; disseminates to the CNS
2. 90/95% of patients are asymptomatic
65
Acute viral infection:
Poliovirus:
1. Minor illness: percent and symptoms?
2. Major illness: percent and symptoms?
Acute viral infection:
Poliovirus:
1. Minor: 4-8%; fever, HA, pharyngitis, nausea, vomitting, and abdominal pain. Lasts 1-4 days
2. Major: 1%; fever, HA, pharyngitis, nausea, vomitting, abdominal pain, nauchal rigidity, back pain, muscle pain, and spasms (with CSF pleocytosis)
66
Acute viral infection:
Poliovirus:
Paralytic disease - percent and symptoms? Time of symptoms?
Acute viral infection:
Poliovirus:
.01% become paralyzed with continued CNS necrosis and inflammation. Symptoms appear 3-4 days after the resolution of the minor illness
(minor/major: fever, HA, pharyngitis, N/V, ab/back pain, nauchal rigidity, muscle pain and spasms)
67
Acute viral infection:
Poliovirus:
1. Spinal form: replication is where? May involve?
2. Bulbar form: replication where? May involve? Why is this serious?
Acute viral infection:
Poliovirus:
1. Spinal - SC motor neurons; may involve paralysis of the limbs
2. Bulbar - replication in Brain stem; may involve paralysis of any muscles innervated by the cranial nerves; dangerous because it may involve respiration and involve death
68
Acute viral infection:
West nile virus:
1. Class of virus? Transmission?
2. Incubation period?
Acute viral infection:
Poliovirus:
1. Flavivirus; arthropods but also transfusion/transplant/transplacentally
2. 2-14 day incubation period
69
Acute viral infection:
West Nile Virus:
1. Percent of asymptomatic patients?
2. 20% have? and 50% of these also present with?
Acute viral infection:
West Nile Virus:
1. 80% asymptomatic
2. 20% have fever, HA, and fatigue for 3-6 days; 50% of these also have a rash on the trunk, lymphadenopathy, and arthralgia
70
Acute viral infection:
West Nile Virus:
Less than one percent develop meningitis/encephalitis
1. 25-35% develop?
2. Encephalitis or meningioencephalitis: percent and symptoms?
Acute viral infection:
West Nile Virus:
1. Self-limiting aseptic meningitis
2. 60-75%; fever, HA, stiff neck, altered CNS function, seizures, and change in mental status
71
Acute viral infection:
Hemorrhagic Fevers:
1. Mode of transmission?
2. Different classes of viruses?
Acute viral infection:
Hemorrhagic Fevers:
1. Arthropod bites
2. Arenavirus, Filovirus, Bunyaviruses, and Flaviviruses
72
Acute viral infection:
Hemorrhagic Fevers:
1. Arenavirus example?
2. Filovirus examples?
Acute viral infection:
Hemorrhagic Fevers:
1. Arenavirus = lassa virus
2. Filovirus = marburg and ebola virus
73
Acute viral infection:
Hemorrhagic Fevers:
1. Bunyavirus example?
2. Flavivirus examples?
Acute viral infection:
Hemorrhagic Fevers:
1. Bunyavirus = hantavirus
2. Flavivirus = yellow fever and dengue fever
74
Acute viral infection:
Hemorrhagic Fevers:
1. Hemorrhage is associated with?
2. Shock is associated with?
Acute viral infection:
Hemorrhagic Fevers:
1. Hemorrhage is associated with thrombocytopenia and/or endotheilal cell lysis
2. Shock is associated with elevated cytokines and DIC
75
Acute viral infection:
Dengue Fever Virus:
1. This disease is ___ \_\_\_\_
2. Mode of transmission? Replicates where?
Acute viral infection:
Dengue Fever Virus:
1. This disease is _self limiting_
2. Transmitted by arthropods; replicates in reticuloendothelial tissue
76
Acute viral infection:
Dengue Fever Virus:
1. What are the initial symptoms?
2. What are the symptoms related to?
Acute viral infection:
Dengue Fever Virus:
1. fever, myalgia, joint/bone pain, N/V
2. Symptoms are related to high concentrations of proinflammatory cytokines (TNF)
77
Acute viral infection:
Dengue Fever Virus:
1. What presents 3 days after the onset of fever?
2. There is also generalized lymphadenopathy and \_\_\_\_.
Acute viral infection:
Dengue Fever Virus:
1. Rash after 3 days
2. General leukopenia
78
Acute viral infection:
Dengue Fever Virus:
1. What are the nonspecific immune responses?
2. What is generated later?
Acute viral infection:
Dengue Fever Virus:
1. IFN and NK cell activity
2. Later is the production of antibodies
79
Acute viral infection:
Dengue Fever Virus:
DV produces a capillary leak syndrome:
1. What is the primary cellular target?
2. What ultimately causes the leak?
Acute viral infection:
Dengue Fever Virus:
1. Primary cell target is monocytes
2. Cytokines induce endothelial cells to induce plasma leakage
80
Acute viral infection:
Dengue hemorrhagic fever/shock:
1. Initial presentation?
2. What occurs after 3-4 days of fever? What can this cause?
Acute viral infection:
Dengue hemorrhagic fever/shock:
1. Initial presentation: same as self limited disease - fever, myalgia, joint/bone pain, N/V
2. There is then increased vascular permeability, thrombocytopenia, DIC, and hemorrhage; this can cause hypovolumic shock, circulatory failure, or death
81
Chronic/Latent viral infection:
Examples?
Chronic/Latent viral infection:
Herpes virus and CMV
82
Chronic/Latent viral infection:
Alphaherpesvirinae:
1. Type of infection? Where?
2. What viruses?
Chronic/Latent viral infection:
Alphaherpesvirinae:
1. Latent virus in the neurons
2. HSV1, HSV2, and VZV
83
Chronic/Latent viral infection:
Betaherpesvirinae:
1. Type of infection?
2. Type of viruses?
Chronic/Latent viral infection:
Betaherpesvirinae:
1. Latent
2. HHV6/7 (Roseolovirus) and CMV
84
Chronic/Latent viral infection:
Gammaherpesvirinae:
1. Type of infection? Where?
2. Type of viruses?
Chronic/Latent viral infection:
Gammaherpesvirinae:
1. Latent in lymphoid cells
2. HHV8 (Rhadinovirus), and EBV
85
Chronic/Latent viral infection:
HSV:
1. Mode of transmission?
2. Primary infection involves? What do the infected cells form?
Chronic/Latent viral infection:
HSV:
1. Intimate contact
2. Primary infection, may be asymptomatic, involves a vesicular lesion with dermal inflammation; Infected cells form multinucleated giant cells with intranuclear inclusions
86
Chronic/Latent viral infection:
HSV:
1. Latent infection by HSV-1 occurs where?
2. Latent infection by HSV-2 occurs where?
Chronic/Latent viral infection:
HSV:
1. HSV-1: trigeminal ganglia
2. HSV-2: sacral ganglia
87
Chronic/Latent viral infection:
HSV:
Examples of Primary HSV infections?
Examples of Latent HSV infections
Chronic/Latent viral infection:
HSV:
Primary = gingivostomatitis, genital herpes, meningioencephalitis, keratoconjunctivitis
Latent = Herpes labialis (cold sore) and genital infection
88
Chronic/Latent viral infection:
Gingivostomatitis:
1. Virus? Incubation period?
2. Initial presentation?
Chronic/Latent viral infection:
Gingivostomatitis:
1. HSV; 4-6 day incubation
2. Fever, sore gums, and sore mouth are the initial presentations
89
Chronic/Latent viral infection:
Gingivostomatitis:
1. What occurs within 3 days of oral pain?
2. How long can symptoms last?
Chronic/Latent viral infection:
Gingivostomatitis:
1. Gingivitis with ulcers and perioral lesions as well as cervical lymphadenopathy
2. 2 weeks
90
Chronic/Latent viral infection:
Genital Herpes:
1. Most cases are caused by what? The rest are from?
2. Incubation period? Initial symptoms?
Chronic/Latent viral infection:
Genital Herpes:
1. Most = HSV-2; 10-20% are caused by HSV-1
2. 2-7 day incubation period; fever, malaise, dysuria, and eruption of painful, pruritic vesicles, as well as urethral discharge
91
Chronic/Latent viral infection:
Genital Herpes:
1. In addition to normal symptoms, 5-30% also develop?
2. What occurs with the vesicles in men?
Chronic/Latent viral infection:
Genital Herpes:
1. 5-30% also develop inguinal adenopathy and aseptic meningitis
2. Men have vesicles that rupture and crust over
92
Chronic/Latent viral infection:
Genital Herpes:
1. What happens to women?
2. How long does this last? What virus recurrs 80-90% of the time? 55% of the time?
Chronic/Latent viral infection:
Genital Herpes:
1. In women, the labia, vagina, urethra, and cervix are involved. The vesicles rupture, ulcerate, and have a watery discharge
2. Symptoms last around 2 weeks; 80/90% recurr when primary infection is HSV-2; 55% recurr when primary infection is HSV-1
93
Chronic/Latent viral infection:
Meningioencephalitis:
1. HSV-1 causes?
2. HSV-2 causes?
3. In neonates, both HSV1 and HSV2 cause?
Chronic/Latent viral infection:
Meningioencephalitis:
1. HSV1 = encephalitis
2. HSV2 = meningitis
3. Neonates, both cause encephalitis
94
Chronic/Latent viral infection:
Meningioencephalitis:
1. In viral encephalitis: there is a ____ infiltrate and ___ proliferation in the \_\_\_, cortex, and white matter
2. Herpes specific encephalitis: where are the focal areas of necrosis?
Chronic/Latent viral infection:
Meningioencephalitis:
1. In viral encephalitis: there is a _lymphocytic_ infiltrate and proliferation in the _meninges_, cortex, and white matter
2. Herpes specific encephalitis: focal areas of necrosis in the orbitofrontal, temporal cortex and limbic system
95
Chronic/Latent viral infection:
Meningioencephalitis:
1. General meningioencephalitis symptoms?
2. Herpes specific symptoms?
Chronic/Latent viral infection:
Meningioencephalitis:
1. General meningioencephalitis symptoms: fever, HA, N/V, stiff neck, cerebral edema, seizures, and confusion
2. Herpes specific: loss of smell and memory, speech deficits, behavior changes, and hallucinations
96
Chronic/Latent viral infection:
Meningioencephalitis:
1. What occurs in 2/3 of those that recover?
2. Viral meningitis (nothing herpes specific) presents with?
Chronic/Latent viral infection:
Meningioencephalitis:
1. 2/3 that recover develop _neurologic sequelae_
2. Meningitis: HA, fever, photophobia, N/V, stiff neck, nauchal rigidity, and myalgias (slide 642)
97
Chronic/Latent viral infection:
Keratoconjunctivitis:
Presentation?
Chronic/Latent viral infection:
Keratoconjunctivitis:
Often unilateral with acute onset of pain, conjunctivitis with a discharge, and blurred vision
98
Chronic/Latent viral infection:
HSV stromal keratitis:
Has an extensive ____ infiltrate with \_\_\_\_\_, possibly resulting in scarring and \_\_\_\_
Chronic/Latent viral infection:
HSV stromal keratitis:
Has extensive _mononuclear_ infiltrate with _neovascularization_ resulting in scarring and _blindness_
99
Examples of HSV recurrent infections?
Herpes labialis and genital infection
100
Herpes labialis:
1. What is this?
2. Presentation?
Herpes labialis:
1. Cold sore
2. Pain, burning, and itching followed by a papule that develops into a vesicle that crusts
101
Genital infection:
Recurrences are more common with?
Genital infection:
More common with HSV-2
102
Chronic/Latent viral infection:
CMV:
1. Where do latent infections occur?
2. Most common routes of transmission?
Chronic/Latent viral infection:
CMV:
1. Latent infections: mononuclear cells, kidney, and heart
2. Transmission: congenital, perinatal, oral, sexual, from blood, and from transplanted tissue
103
Chronic/Latent viral infection:
CMV:
1. CMV can prevent _____ expression
2. The congenital infection is known as?
Chronic/Latent viral infection:
CMV:
1. CMV can prevent _MHC-1_ expression
2. Congenital infection: _cytomegalic inclusion disease_
104
Chronic/Latent viral infection:
Cytomegalic inclusion disease:
1. Most ___ disease and ___ organs are infected.
2. How does it present at birth?
3. Those that survive usually have?
Chronic/Latent viral infection:
Cytomegalic inclusion disease:
1. Most _serious_ disease and _several_ organs are infected
2. Presents: jaundice, hepatosplenomegaly, petechial rash, seizures, and respiratory distress
3. Those that survive have permanent CNS damage
105
Chronic/Latent viral infection:
Perinatal infection:
1. 20% of pregnant women are colonized and 50% of neonates become \_\_\_\_\_.
2. Most always ____ or may have a self-limited ___ like syndrome. There also may be subtle developmental deficits in ___ and \_\_\_.
Chronic/Latent viral infection:
Perinatal infection:
1. 20% of pregnant women are colonized and 50% of neonates become _carriers_
2. Most always _asymptomatic_ or may have a self limited _sepsis_ like syndrome. There also may be subtle developmental deficits in _hearing_ and _intelligence_
106
Chronic/Latent viral infection:
Mononucleosis:
1. __ causes 20% of all mono.
2. What are heterophile antibodies?
Chronic/Latent viral infection:
Mononucleosis:
1. CMV causes 20%
2. Heterophile antibodies - recognize antigens on RBCs from other species
107
Chronic/Latent viral infection:
Mononucleosis:
1. CMV mono is heterophile \_\_\_, while EBV mono is \_\_\_.
2. Presentation?
Chronic/Latent viral infection:
Mononucleosis:
1. CMV = heterophile negative; EBV = heterophile positive
2. Presents with lymphocytosis, _fever_, fatigue, _mild hepatitis_, and myocarditis. Sometimes presents with a rash
108
Chronic/Latent viral infection:
CMV hepatitis:
1. Is associated with what?
2. Presentation?
Chronic/Latent viral infection:
CMV hepatitis:
1. Is associated with CMV mono
2. Presentation: self-limited jaundice, hepatomegaly, and elevated liver enzymes in the blood
109
What is this multinucleated giant cell associated with?
(it has intranuclear inclusions)
HSV
110
What disease is this? What virus?
This is gingivostomatitis; HSV
111
CMV infection: what is the arrow pointing to - more specifically what is the major characteristic of CMV
Major characteristic: Owl's eye inclusion
112
CMV infection in immunocompromised host:
1. Most severe disease?
2. 3 others that are common?
CMV infection in immunocompromised host:
1. Most severe: pneumonia
2. Chorioretinitis, Colitis/esophagitis, and CNS infection
113
CMV infection in immunocompromised host:
1. Pneumonia occurs in what kind of patients?
2. Colitis/esophagitis presentation?
3. CNS infection presentation?
CMV infection in immunocompromised host:
1. Pneumonia occurs in bone marrow transplant patients
2. C/E presentation: painful ulcerations, difficulty swallowing, and watery or bloody diarrhea
3. CNS presentation: polyradiculopathy (spinal nerve root) with ascending weakness, loss of deep tendon reflexes, and loss of bowel/bladder control
114
Chronic/Latent viral infections:
VZV:
1. 5 childhood exanthems (rashes)?
2. Transmission?
3. Primary infection?
Chronic/Latent viral infections:
VZV:
1. Varicella, rubella, measles, roseola, and parvovirus B19
2. Transmitted by respiratory tract secretions or vesicle fluid
3. Primary infection is chickenpox: varicella
115
Chronic/Latent viral infections:
VZV:
1. Primary infection is established in the ___ \_\_ --\> regional nodes --\> blood --\> infects?
2. Shed again --\> incubation of ____ days --\> acute onset of?
Chronic/Latent viral infections:
VZV:
1. Primary infection in the _respiratory tract_ --\> nodes and blood --\> infects _liver, spleen, and other reticuloendothelial tissue_
2. Shed again --\> 1_0/12_ day incubation --\> acute onset of fever, HA and sore throat
116
Chronic/Latent viral infections:
VZV:
1. Where does the rash appear first? Progression?
2. Where is the latent infection established?
Chronic/Latent viral infections:
VZV:
1. Appears on head and scalp first then the trunk and extremities
2. Latent infection is established in neurons usually at the site of the most concentrated rash
117
Chronic/Latent viral infections:
VZV:
Complications in children:
1. Secondary bacterial infection by?
2. What may happen in children treated with aspirin?
Chronic/Latent viral infections:
VZV:
Complications in children:
1. Secondary bacterial infection: S. pyogenes
2. Asprin - cause Reye's syndrome
118
Chronic/Latent viral infections:
VZV:
1. Complications in children: What are some rare symptoms?
2. Infection in immunocompromised patients may result in?
Chronic/Latent viral infections:
VZV:
1. Rare: ataxia, vomiting, altered speech, fever, vertigo, and tremors
2. Immunocompromised: hemorrhagic skin lesions and disseminated disease (high fatality rate)
119
Chronic/Latent viral infections:
VZV:
1. Recurrent infection is?
2. Where do you see the rash? Presentation?
Chronic/Latent viral infections:
VZV:
1. Recurrent: Zoster or Shingles
2. The rash seldom crosses the midline and is usually confined to a specific dermatome; presents with pain and neuralgia at the eruption site
120
Chronic productive viral infections:
What is unique about these infections?
Examples?
Chronic productive viral infections:
These are infections that the immune system may not be able to eliminate.
HIV, HBV, HCV, HDV
121
Chronic productive viral infections:
HBV:
1. Envelope? Genome?
2. What are the 4 Antigens that can be detected?
Chronic productive viral infections:
HBV:
1. Enveloped; circular ss AND ds DNA
2. 4 Antigens: _s_ (surface), _c_ (core), _e_ (core protein) and the _dane particle_ (intact virus)
122
Chronic productive viral infections:
HBV:
Transmission?
Chronic productive viral infections:
HBV:
Transmitted by blood, sex, and direct contact
123
Chronic productive viral infections:
HBV Acute Hepatitis:
1. Incubation period?
2. Most of the damage is ___ mediated with extensive ___ necrosis.
Chronic productive viral infections:
HBV Acute Hepatitis:
1. Incubation: 4-26 weeks
2. Most of the damage is _CMI_ mediated with extensive _portal_ necrosis
124
Chronic productive viral infections:
HBV Chronic Hepatitis:
1. Continuous inflammation leads to ____ and then ___ of the liver.
2. Continuous inflammation also predisposes to?
Chronic productive viral infections:
HBV Chronic Hepatitis:
1. Continuous inflammation leads to _fibrosis_ and then _cirrhosis_ of the liver.
2. Predisposes to _hepatocellular carcinoma_
125
Chronic productive viral infections:
HBV Chronic persistant Hepatitis Presentation?
Chronic active Abs? Symptoms?
Chronic productive viral infections:
Chronic persistant: no jaundice or other symptoms
Chronic active: low or no anti-s and c Ab; relentless progression with persistant symptoms
126
Transforming viral infections:
Examples?
Transforming viral infections:
EBV, HBV, HTLV-1, and HPV
127
Transforming viral infections:
EBV:
1. Mode of transmission?
2. The virus can bind to ___ on B-cells, ___ and ___ epithelial cells
3. Immune evasion may be partly mediated by the production of an IL-\_\_\_ like protein that ___ \_\_\_ activity
Transforming viral infections:
EBV:
1. Sexual contact
2. The virus can bind to _CD21_ on B cells, _nasopharyngeal_ and _cervical_ epithelial cells
3. Immune evasion: IL-_10_ like protein that _inhibits Th1_ activity
128
Transforming viral infections:
EBV:
1. EBV infects B cells --\> induces B cell ____ with the expression of ___ nuclear Ag, latent \_\_\_, and latent ____ proteins.
2. t8:14 translocation involving the ___ gene
3. ____ activates signaling pathways that ___ \_\_ cell activation
Transforming viral infections:
EBV:
1. EBV infects B cells --\> induces B cell _proliferation_ with the expression of _EB_ nuclear Ag, _latent proteins_, and _latent membrane proteins_
2. t8:14 translocation involving the _c-myc_ gene
3. _LMP-1_ activates signaling pathways that _mimic B_ cell activation
129
Transforming viral infections:
EBV:
1. ___ stimulates transcription of the cyclin ___ gene
2. The ____ (\_\_) pathway occurs in epithelial cells and/or __ cells with the expression of the ___ Ag, viral ___ Ag, and \_\_\_\_\_, resulting in infectious viral particles, T cell activation, and the appearance of ____ cells which are activated \_\_\_.
Transforming viral infections:
EBV:
1. _EBNA-2_ stimulates the transcription of the _cyclin D gene_
2. The _productive (lytic)_ pathway occurs in epithelial cells and/or _B_ cells with the expression of the _early_ Ag, _viral capsid Ag, and EBNA's_, resulting in infectious particles, T cell activation, and the appearance of _Downey_ cells which are activated _Tc_
130
Transforming viral infections:
EBV:
1. __ cell proliferation accounts for the characteristic _____ and splenomegaly
2. Incubation period?
3. Initial symptoms?
Transforming viral infections:
EBV:
1. _T_ cell proliferation accounts for the characteristic _lymphadenopathy_ and splenomegaly
2. Incubation: 1-8 weeks
3. Acute onset of fever, pharyngitis, lymphadenopathy, hepatosplenomegaly, and fatigue
131
Transforming viral infections:
EBV:
1. Virtually all have ____ Abs and lymphocytosis
2. What symptoms may persist for months?
3. Complications: 80% have? 50% have?
Transforming viral infections:
EBV:
1. Virtually all have _heterophile_ Abs and lymphocytosis
2. Long lasting symptoms: fatigue, lymphadenopathy, hepatosplenomegaly, and viral secretion
3. 80% have mild hepatitis with elevated liver enzymes; 50% have mild thrombocytopenia
132
Transforming viral infections:
HPV:
1. Genome? Enveloped?
2. The productive infection forms?
3. The latent/transforming infection forms?
Transforming viral infections:
HPV:
1. Circular dsDNA genome; non-enveloped
2. Productive - warts
3. Latent - cervical cancer
133
Transforming viral infections:
HPV:
1. In the latent infection, what happens with the genome? What does this lead to?
2. In the integrated state what genes are transcribed that inhibit p53?
3. Mode of transmission?
Transforming viral infections:
HPV:
1. In the latent infection the genome is integrated into the host genome and may activate oncogenes to inhibit apoptosis and promote cell proliferation
2. E6 and E7 inhibit p53
3. Direct contact or inanimate objects (skin must be compromised)
134
Transforming viral infections:
HPV:
1. What is the virus very resistant to?
2. Where does skin hyperplasia initially occur?
Transforming viral infections:
HPV:
1. Resistant to environmental stress
2. Hyperplasia in the stratum spinosum
135
Bacterial Infections - Gram Positive:
Name 3.
Bacterial Infections - Gram Positive:
a. Staphylococcus aureus
b. Staphylococcus epidermidis
c. Staphylococcus saprophyticus
136
Bacterial Infections - Gram Positive:
Staph Aureus:
1. This is the only one that produces \_\_\_\_.
2. \_\_\_\_\_, __ acid, and lipotechioic acid induce ____ production
3. Role of Protein A?
Bacterial Infections - Gram Positive:
Staph Aureus:
1. This is the only one that produces _coagulase!_
2. _Peptidoglycan_, _techoic_ acid, and lipotechioic acid induce _cytokine_ production
3. Protein A: binds Fc of IgG preventing opsonization
137
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Produces a number of adhesion molecules such as clumping factor that binds?
2. Some strains produce a _capsule/biofilm_: function?
3. Function of coagulase?
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Clumping factor binds fibrinogen, collagen BP, and fibronectin
2. Capsule: inhibits chemotaxis and phagocytosis and facilitates adherence to tissue and/or artificial joints
3. Coagulase: clots plasma
138
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Beta lactamase function?
2. Staphylococcal compliment inhibitor blocks?
3. Chemotaxis inhibitory protein blocks the receptors for?
Bacterial Infections - Gram Positive:
Staph Aureus:
1. B-lactamase: provides beta-lactam resistance
2. SCI blocks formation of C3b on the bacterial surface
3. CIP blocks receptors for C5a and formyl-peptides, thus blocking the activation of phagocytes
139
Bacterial Infections - Gram Positive:
Staph Aureus:
Cytolytic toxins:
1. Alpha toxin: causes? How?
2. Beta toxin is ____ that is cytolytic and causes \_\_\_
3. What is cytolytic for phagocytes?
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Alpha toxin: causes necrosis by forming a pore in PM
2 Beta toxin is _sphingomyelinase_ that is cytolytic and causes _necrosis_
3. _Leukocidin_ is cytolytic for phagocytes
140
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Super antigens activate __ cells and induce ___ pdtn
2. Enterotoxins: resistant to? Associated with?
3. Pyrogenic exotoxin: C is also known as?
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Super antigens activate _T_ cells and induce _cytokine_ pdtn
2. Enterotoxins: resistant to acid and heat; associated with food poisoning
3. Pyrogenic exotoxin C is also known as Toxic Shock Symdrome Toxin-1 (TSST-1)
141
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Exfoliatins are _____ exotoxins that cause? Associated with?
2. Regardless of the infection, it is pyogenic (except \_\_\_\_) and ____ inflammation is the pathologic finding
Bacterial Infections - Gram Positive:
Staph Aureus:
1. Exfoliatins are _epidermolytic_ exotoxins that cause the separation of the epidermis from the dermis; this is associated with scalded skin syndrome and impetigo
2. Regardless of the infection, it is pyogenic (except _impetigo_) and _suppurative inflammation_ is the pathologic finding
142
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Folliculitis_: is an infection of ___ \_\_\_ involving the formation of a small abscess with ___ inflammation
2. _Furuncle_: this is a _____ infection involving a ___ \_\_\_, usually following folliculitis, the lesion is usually painful and ____ \_\_\_\_\_.
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Folliculitis_: is an infection of _hair follicles_ involving the formation of a small abscess with _minor_ inflammation
2. _Furuncle_: this is a _subcutaneous_ infection involving a _hair follicle_, usually following folliculitis, the lesion is usually painful and _drains spontaneously_
143
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Carbuncle_: fusion of multiple ____ that drain through? It is often accompanied by?
2. _Cellulitis_: this is a common \_\_\_, rapidly spreading ____ infection that may have originated from \_\_\_, a furuncle or a \_\_\_\_. Orbital cellulitis may originate from an infection of the ____ \_\_\_ with pain, \_\_\_\_, edema, and fever
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Carbuncle_: fusion of multiple _furuncles_ that drain through several openings; often accompanied by a fever
2. _Cellulitis_: this is a common _acute_, rapidly spreading _subcutaneous_ infection that may have originated from _trauma_, a furuncle, or a _carbuncle_. Orbital cellulitis may originate from an infection of the _paranasal sinuses_ with pain, _erythema_, edema, and fever
144
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Necrotizing fasciitis_: this usually develops from ____ and is a ___ infection involving ___ and fascia and causes \_\_\_.
2. _impetigo_: occurs in? Presentation?
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Necrotizing fasciitis_: this usually develops from _cellulitis_ and is a _deep_ infection involving _muscle_ and fascia and causes _necrosis_
2. _Impetigo_: occurs in neonates and young children with rigid or flaccid fluid filled bullae - older lesions break down and crust
145
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Impetigo_: represents the localized effect of the ___ (\_\_\_\_) toxin causing granular cells of the epidermis to?
2. _Scalded Skin Syndrome_: occurs in? Mediated by _____ toxin. Symptoms?
3. _Scalded Skin Syndrome_: has a positive Nikolsky sign - what is this?
Bacterial Infections - Gram Positive:
Staph Aureus:
1. _Impetigo_ represents the localized effect of the _epidermolytic (exfoliative)_ toxin: epidermis separation
2. _SSS_: occurs in young children; Mediated by _epidermolytic_ toxin; Symptoms: starts with a fever and diffuse rash followed by the development of flaccid bullae
3. + Nikolsky sign: epidermis easily separates with slight pressure
146
Bacteremia/Septicemia:
1. Top 4 bacterial causes?
2. Presentation?
Bacteremia/Septicemia:
1. Top 4 causes: S. aureus, E. coli, S. Epidermidis, and Enterococcus
2. Presentation: fever, chills, rigors followed by tachycardia, tachypnea, shock and death
147
Bacteremia/Septicemia:
1. Systemic inflammatory response syndrome (SIRS): presentation? No evidence of?
2. Sepsis = ?
3. Severe sepsis = ?
4. Septic shock = ?
Bacteremia/Septicemia:
1. SIRS: fever, elevated WBC, elevated HR/respiratory rate. NO evidence of infection
2. Sepsis = SIRS + infection
3. Severe sepsis = Sepsis + signs of organ dysfunction
4. Septic shock = severe sepsis + hypotensive shock and multiple organ dysfunction
148
Bacteremia/Septicemia:
1. Pathology is associated with what kind of injury?
2. What occurs in the brain?
3. Heart?
4. Kidneys?
5. Lungs?
Bacteremia/Septicemia:
1. Hypoxic injury
2. Ischemic encephalopathy
3. Heart = coagulation necrosis and hemorrhage
4. Kidneys = acute tubular necrosis --\> failure
5. Lungs = diffuse alveolar damage and edema
149
Endocarditis:
1. Main cause of infective endocaditis?
2. Presentation?
Endocarditis:
1. Main cause = Staphylococcus
2. Presentation: ever, chills, bleeding, murmur, and embolism
150
Pneumonia:
1. _____ causes \<10% of CAP.
2. Often follows the \_\_\_\_
3. _____ necrosis with ___ formation or the formation of a _____ (thin walled cyst)
4. Presentation?
Pneumonia
1. _S. aureus_ causes \<10% of CAP
2. Often follows the _flu_
3. _Hemorrhagic_ necrosis with _abscess_ formation or the formation of a _pneumatocele_ (cyst)
4. Presentation: acute onset of fever, dyspnea, tachypnea (increased resp. rate), and production of mucopurulent sputum
151
Aute Osteomyelitis and acute septic arthritis:
1. Majority is caused by?
2. Osteomyelitis presentation?
3. Septic arthritis involves an infection of the ____ space with synovial \_\_\_\_\_, _____ degradation, effusion (with ____ necrosis), and bone \_\_\_\_\_.
4. Septic arthritis presentation?
Aute Osteomyelitis and acute septic arthritis:
1. Majority: _S. aureus_
2. Osteomyelitis: bone destruction, pain, swelling, and fever
3. Septic arthritis involves an infection of the _synovial_ space with synovial _hypertrophy_, _cartilage_ degradation, effusion (with _pressure_ necrosis), and bone _resorption_
4. Septic arthritis: local inflammation, pain, and swelling usually of a SINGLE joint
152
Food poisoning:
1. ______ (toxin) food poisoining is caused by the ingesion of preformed ____ \_\_\_\_\_. The toxin is __ and acid stable.
2. Mechanism: ___ induced inflammation, _____ cell degranulation, and the production of ___ and \_\_\_.
3. Symptoms?
Food poisoning:
1. _S. aureus_ caused by ingestion of preformed _staph enterotoxin_ that is _heat_ and acid stable.
2. Mechanism: _superantigen_ induced inflammation, _mast_ cell degranulation, and the production of _PGE2_ and _LTB4_
3. Symptoms: N/V, cramps, and diarrhea
153
Staphylococcal Toxic Shock:
1. Mediated by TSST-1 from what bacteria?
2. TSST-1: what does it induce?
3. Presentation?
4. There may be?
Staphylococcal Toxic Shock
1. TSST-1: from _s. aureus_
2. Induces T cell activation and cytokine release
3. Presentation: acute onset of fever, rash, myalgia, hyperemia, and GI symptoms
4. There may be shock, renal failure, and CNS disturbances
154
Streptococcus:
1. Oxygen requirements?
2. Catalase?
3. Shape?
Streptococcus:
1. Faculative anaerobe
2. Catalase negative
3. Oval in pairs or chains
155
Strep. Pyogenes:
Virulence factors:
1. Role of M-proteins?
2. Role of streptolysin S?
3. Role of streptolysin O?
Strep. Pyogenes:
Virulence:
1. M-proteins = antiphagocytic
2. Streptolysin S = O2 stable hemolysin
3. Streptolysin O = (SLO) O2 labile hemolysin that lyses RBCs, leukocytes, and mycardial cells by forming a transmembrane pore: also induces TNFalpha from mast cells
156
Strep. Pyogenes:
1. Has pyrogenic ______ (these are ____ antigens; ____ is associated with scarlet fever and strep toxic shock)
2. Characterized by diffuse _____ \_\_\_\_\_ with ___ destruction to host tissue
Strep. Pyogenes:
1. Has pyrogenic _exotoxins_ (these are _super_ antigens; _SPEA_ is associated with scarlet fever and strep TSS)
2. Characterized by diffuse _interstitial infiltrates_ with _minimal_ destruction to the host tissue
157
Strep. Pyogenes:
Pharyngitis:
1. Most common bacterial infection of?
2. Most common transmission?
3. Incubation period?
Strep. Pyogenes:
Pharyngitis:
1. Most common bacterial infection of childhood
2. Aerosol transmission
3. Incubation = 2-4 days
158
Strep. Pyogenes:
Pharyngitis:
1. Symptoms?
2. Which nodes are enlarged?
3. What else is enlarged? May be covered with?
Strep. Pyogenes:
Pharyngitis:
1. Fever, pharyngitis (no cough) and maliase along with erythema and edema of posterior pharynx
2. Cervical nodes at angles of mandible are enlarged
3. Tonsils are also enlarged and hyperemic; may be covered with an exudate
159
Strep. Pyogenes:
Scarlet fever:
1. Pharyngitis caused by \_\_\_\_\_.
2. PResentation?
Strep. Pyogenes:
Scarlet fever:
1. Caused by _SPEA_
2. Presentation: pharyngitis and diffuse erythematous rash that begins on the chest and then the extremities (palms, soles, and area around the mouth is spared) --\> desquamation follows the rash
160
Strep. Pyogenes:
Cellulitis:
1. 2 Most common causes?
2. Involves diffuse infection of?
3. Presentation?
Strep. Pyogenes:
Cellulitis:
1. S. aureus and S. pyogenes
2. Involved diffuse infection of skin and subcutaneous tissue
3. Presentation: pain, fever, chills, leukocytosis, and inflammation at the site with swelling and erythema
161
Strep. Pyogenes:
Erysipela:
1. Acute _____ infection.
2. Where is it commonly found?
3. Associated with?
4. Presentation?
Strep. Pyogenes:
Erysipela:
1. Acute _skin_ infection
2. Commonly found on face and extremities
3. Associated with facial infection or pharyngitis
4. Presentation: pain, fever, chills, leukocytosis, inflammation: lesions form distinct raised borders and bullae may also develop
162
Strep. Pyogenes:
Necrotizing fasciitis:
1. Associated with?
2. What does this affect? Often following?
3. Symptoms?
Strep. Pyogenes:
Necrotizing fasciitis:
1. Associated with TSS
2. Deep infection of muslce and fascia following cellulitis, surgery, or minor trauma
3. Skin becomes purplish with hemorrhagic bullae (skin begins to slough) most have bacteremia, high fever, and extreme pain at site of infection
163
Strep. Pyogenes:
Strep impetigo:
1. Mode of transmission?
2. Starts as erythematus ___ that develops into a ____ and then a \_\_\_\_.
Strep Pyogenes:
Impetigo:
1. Transmission = direct contact
2. Starts as erythematous _papule_ that develops into a _vesicle_ and then a _pustule_ that breaks down and crusts
164
Nonsuppurative complications associated with S pyogenes:
Name 2.
Nonsuppurative complications associated with S pyogenes:
a. Nephritis
b. Rheumatic fever
165
Nonsuppurative complications associated with S pyogenes:
1. Nephritis: post infectious _____ \_\_\_\_\_ GN that follows \_\_\_\_
2. RF: occurs after infection with any ___ associated with pharyngitis
Nonsuppurative complications associated with S pyogenes:
1. Nephritis: post infectious _acute proliferative_ GN that follows _pharyngitis_
2. RF: occurs after infection with any _M-type_
166
Strep Agalactiae:
1. Colonizes where?
2. Neonatal infection: 2 types?
Strep Agalactiae:
1. Colonizes in oral cavity, lower GI tract, and vagina
2. Neonatal: early onset infection and late onset
167
Strep Agalactiae:
Early neonatal infection:
1. More common when?
2. Most common presentations?
3. Regardless of the focus of infection, most have _____ \_\_\_\_ presenting with?
Strep Agalactiae:
Early neonatal infection:
1. More common when there are complications or premature
2. 60% septicemia, 30% pneumonia, and 10% meningitis
3. Most have _respiratory distress_ presenting with tachypnea, cyanosis, and grunting
168
Strep Agalactiae:
Late neonatal infection:
1. When does it present?
2. Presentation?
Strep Agalactiae:
Late neonatal infection:
1. Presents more than 7 days after birth
2. 60% septicemia and/or meningitis (35%)
169
Strep Agalactiae:
Adult infection:
Most common in who?
Strep Agalactiae:
Adult infection:
Most common in pregnant women, the elderly, or those with underlying disease (diabetes most common)
170
Strep Agalactiae:
Adult infection:
1. Elderly and those with underlying disease: most common infections are?
2. Pregnant women: common infections?
Strep Agalactiae:
Adult infection:
1. Elderly/disease: bacteremia/septicemia, skin/soft tissue infection, and UTI
2. Pregnant: UTI, bacteremia/septicemia, and chorioamnionitis
171
S. pneumoniae:
1. What are the 2 most important virulence factors and their actions?
2. This is the most common bacterial cause of what 3 things?
S. pneumoniae:
1. Virulence factors: capsule (antiphagocytic) and pneumolysin O (hemolysin that is cytotoxic and causes alveolar edema and hemorrhage)
2. Most common cause of community-acquired pneumonia (CAP), otitis media, and bacterial meningitis
172
S. pneumoniae:
Pneumonia:
1. First colonization of ____ followed by aspiration where?
2. Invades what cells? Moves from alveolus to alveolus through?
2. Hallmark is inflammatory infiltrate composed of ____ followed later by \_\_\_\_\_\_\_.
S. pneumoniae:
Pneumonia:
1. First colonization of _nasopharynx_ then _lower RT_
2. Invades _type II pneumocytes_. Moves from alveolus to alveolus through _pores of Cohn_
2. Hallmark is inflammatory infiltrate composed of _neutrophils_ followed later by _macrophages_
173
S. pneumoniae:
Pneumonia:
1. Pathologically there is ____ effusion, consolidation from \_\_\_\_, and eventually \_\_\_\_.
2. Presentation?
S. pneumoniae:
Pneumonia:
1. Pathologically there is _alveolar_ effusion, consolidation from _edema_, and eventually hemorrhage
2. Presentation: fever, shaking chills, severe chest pain, and a cough productive of blood tinged sputum
174
S. pneumoniae:
Invasive disease:
1. What predisposes to invasive disease?
2. Sustained bacteremia may result in?
3. Purulent meningitis presents with at least ___ of the 4 symptoms which are?
S. pneumoniae:
Invasive disease:
1. Predisposition: vaccination status, chronic disease, diabetes, alcohol abuse, asplenia, and immunosuppression
2. Sustained bacteremia --\> meningitis
3. Purulent meningitis: 2/4 symptoms: fever, HA, stiff neck, and altered mental status
175
S. pneumoniae:
Acute otitis media:
1. Definition?
2. Presentation?
3. Most common cause?
4. Other causes of S. pneumoniae?
S. pneumoniae:
Acute otitis media:
1. Definition: presence of fluid in the middle ear accompanied by acute signs/symptoms of ME inflammation
2. Presentation: pain (w/ or w/o fever), swollen and red tympanic membrane (w/ or w/o discharge), restless sleep, vertigo, and hearing loss
3. H. Influenzae causes 50%
4. Causes acute sinusitis and acute conjunctivitis
176
Corynebacterium diphtheriae:
1. Gram?
2. Shape? Cell walls similar to \_\_\_\_\_, how?
3. Oxygen requirement?
4. Look on tellurite agar?
Corynebacterium diphtheriae:
1. Gram +
2. Rod with cell walls similar to Mycobacterium with arabinogalactan and short-chain mycolic acids
3. Strict aerobe
4. Forms black colonies on tellurite agar
177
Corynebacterium diphtheriae:
Diphtheria:
1. Disease manifestations are mediated by? This toxin is produced when? MOA?
2. Transmission? Incubation?
Corynebacterium diphtheriae:
Diphtheria:
1. Manifestations mediated by A-B exotoxin on a lysogenic bacteriophage only produced when iron is limiting; B subunt binds to cellular receptors and the A is taken up, inactivates EF-2, and inhibits protein synthesis
2. Aerosole transmission to URT; 2-5 days incubation
178
Corynebacterium diphtheriae:
Diphtheria:
1. Initial manifestation? Followed by?
2. Toxin disseminates to what 2 main organ systems?
3. 75% develop _______ symptoms with?
4. 66% develop _____ manifestations presenting as?
Corynebacterium diphtheriae:
Diphtheria:
1. Pharyngitis with an adherent pseudomembrane --\> fever, lymphadenopathy, splenomegaly, and difficulty swallowing
2. Heart and CNS
3. 75% develop _neurologic_ symptoms; paralysis of soft palate and peripheral neuritis
4. 66% = cardiac; myocarditis (w/ arrhythmias)
179
Listeria monocytogenes:
1. Gram?
2. Faculative _____ and faulative ____ pathogen.
3. Mode of transmission?
Listeria monocytogenes:
1. Gram +
2. Faculative _psychrophile_ (grows in extreme cold) and faculative _intracellular_ pathogen
3. Contaminates food --\> ingestion
180
Listeria monocytogenes:
1. How does it escape immune detection and spread between cells?
2. Infections?
Listeria monocytogenes:
1. Forms actin tails and pushes against the host membrane to form projections that are then ingested by neighboring cells
2. Pregnancy: septicemia, neonatal infection, and adult meningitis
181
Listeria monocytogenes:
1. Pregnancy: septicemia presenting with?
2. Neonatal early onset: How is it acquired? Associated with?
3. Neonatal late onset: when does it occur? Common presentation?
4. Adult meningitis: symptoms? What could occur thats rare with other bacteria?
Listeria monocytogenes:
1. Pregnancy: septicemia - fever, Ha, myalgia, arthralgiea
2. Neonatale early: from inhalation of infected amniotic fluid; associated with premature birth, stillborn, or miscarriage
3. Neonatal late: during birth or up to 2 weeks after; meningitis
4. Adult meningitis: fever, N/V, seizures, and movement disorders; _RARE: infection of brain parenchyma_
182
Bacillus anthracis:
Virulence factors:
1. ____ factor taken up by cells and causes increased intracellular ____ (causes altered ion flux and ____ resulting in \_\_\_\_\_)
2. Protective Ag - ______ factor inhibits ___ kinase signaling pathways and induces apoptosis and necrosis
Bacillus anthracis:
Virulence factors:
1. _Edema_ factor taken up by cells and causes increased intracellular _cAMP_ ( causes altered ion flux and _hypersecretion_ resulting in _edema_)
2. Protective Ag - _Lethal_ factor inhibits _MAP_ kinase signaling pathways
183
Bacillus anthracis:
1. The major pathalogic consequences of the toxins are increased _____ \_\_\_\_\_ and _____ (DIC)
2. 3 different types of anthrax and route of transmission?
Bacillus anthracis:
1. The consequences are increased _vascular permeability_ and _thrombosis_ (DIC)
2. Intestinal (ingestion), inhalation (endospores inhaled), cutaneous (inoculation of skin)
184
Bacillus anthracis:
Intestinal anthrax:
1. Incubation period?
2. Presentation?
3. Very high _____ rate.
Bacillus anthracis:
Intestinal:
1. 2-5 day incubation
2. Mesenteric lymphadenitis (ab pain), toxemia (fever, chills, shock), and N/V, with bloody diarrhea (GI necrosis)
3. Very high _fatality_ rate
185
Bacillus anthracis:
Inhalation anthrax:
1. Incubation period?
2. Initial symptoms?
3. Later stages involve?
Bacillus anthracis:
Inhalation:
1. 4-6 days incubation
2. Nonspecific and "flu-like" initial symptoms
3. Later stages involve toxemia (fever, chills, shosk) and worsening pulmonary involvement with effusion, necrossis, and hemorrhage resulting in dyspnea leading to respiratory failure and death
186
Bacillus anthracis:
Cutaneous anthrax:
1. Incubation period?
2. Signs?
Bacillus anthracis:
Cutaneous:
1. 1-12 day incubation period
2. Papule with regional lymphadenopathy --\> pustule with bluish-black fluid that then breaks down and forms a painless crustedeschar
187
Nocardia:
1. These are partially \_\_\_\_-\_\_\_
2. Oxygen requirements?
3. Infections are exogenous, \_\_\_\_\_, and do NOT produce \_\_\_\_\_
4. What is found in the lesions?
Nocardia:
1. These are partially _acid-fast_
2. Strict aerobes
3. Exogenous, _suppurative_, and do not produce _granulomas_
4. Sulfer granules
188
Nocardia Asteroides:
1. Causes ____ \_\_\_ infections in the immunocompromised that disseminates where?
2. Lesions characterized how?
3. Most common CNS manifestation?
Nocardia Asteroides:
1. Causes _respiratory tract_ infections in _immunocompromised_ that disseminates to the CNS
2. Lesions characterized by _necrosis and abscess formation with draining sinuses_
3. Brain abscesses are the most common CNS manifestation
189
Nocardia Brasiliensis:
1. Where does this occur (part of the world)?
2. Disease is known as?
3. Presentation?
Nocardia Brasiliensis:
1. This occurs in central and south america
2. Known as _madura foot_
3. Swelling, pain, acscesses, and draining sinuses
190
Nisseria meningitidis and nisseria gonorrhoeae:
1. Gram?
2. These require specific nurition - thus they are \_\_\_\_.
3. Express OPA proteins to enhance?
4. What do they have in the outer membrane?
Nisseria meningitidis and nisseria gonorrhoeae:
1. Gram -
2. They are fastidious
3. OPA proteins enhance adherence and invasion
4. Have LOS in the outer membrane that is proinflammatory
191
Nisseria Meningitidis:
1. Produce a capsule that is antiphagocytic how?
2. Capsule serotypes that are antiphagocytic?
3. ___ is released in the form of outer membrane blebs. What does this induce?
Nisseria Meningitidis:
1. Antiphagocytic by inhibiting complement activation
2. Serotypes A, B, C, X, Y, and W135
3. _LOS_ is released in the form of outer membrane blebs that induce necrosis, DIC, and IL-1 and TNF release
192
Nisseria Meningitidis:
1. Second most common overall cause of?
2. Most common cause of _____ \_\_\_\_ in older kids and young adults.
3. Mode of transmission?
4. What occurs in the absence of immunity?
Nisseria Meningitidis:
1. Second most common overall cause of _bacterial meningitis_
2. Most common cause of _purulent meningitis_ in young adults and older kids
3. Inhaled
4. Absence of immunity - capsule synthesis stops, bugs are internalized by RT epithelial cells --\> released into subepithelial tissue --\> blood
193
Nisseria Meningitidis:
Meningococcemia:
1. Pathology is associated with ___ and ___ that induce endotheilal necrosis, \_\_\_\_, DIC, and \_\_\_\_\_
2. Presentation?
3. Severe/acute onset form involves?
Nisseria Meningitidis:
Meningococcemia:
1. Path is associated with _LOS_ and _PG_ that induce necrosis, _bleeding_, DIC, and _thrombocytopenia_
2. fever, HA, N/V, leukocytosis, and petichiae/ecchymoses (_unusual with other causes of sepsis_\_
3. Fulminant form: DIC, hemorrhage, shock, and myocardial dysfunction/CV collapse to cause death
194
Nisseria Meningitidis:
Meningitis:
1. Presentation?
2. What is less common in N. meningitidis in comparison to other causes of purulent meningitis?
Nisseria Meningitidis:
Meningitis:
1. Sudden onset of fever, HA, N/V, inability to concentrate, and myalgias with rapid progression --\> may cause cerebral edema and coma
2. Seizures are less common
195
Nisseria Gonorrhoeae:
1. Pili bind to ____ and penetrate (mediated by ___ proteins) and grow intracellularly --\> pass into the ____ tissue and induce \_\_\_\_\_\_.
2. Incubation period?
Nisseria Gonorrhoeae:
1. Pili bind to _CD46_ and penetrate (mediated by _OPA_ proteins) and grow intracellularly --\> pass into the _subepithelial tissue_ and induce _inflammation_
2. 1-10 day incubation
196
Nisseria Gonorrhoeae:
1. Genital infection in men presentation? Most common complication?
2. Genetial infection in women presentation? If left untreated how does it present?
Nisseria Gonorrhoeae:
1. Men: _urethritis_ with dysuria and a copious _purulent exudate_; most common complication is _epididymitis_ with unilateral testicular pain and swelling
2. Women: _cervicitis with purulent vaginal discharge_ as well as _urethritis with dysuria_; Untreated, 10-40% develop pelvic inflammatory disease (PID) with salpingitis, endometritis, tuboovarian abscesses, and/or pelvic peritonitis
197
Bordetella pertussis:
1. Also known as?
2. Gram?
3. Shape?
4. Oxygen requirement?
Bordetella pertussis:
1. Whooping cough
2. Gram -
3. Bacilli
4. Aerobe
198
Bordetella pertussis:
Virulence factors:
1. _Pertussis toxin_ - an ___ toxin that causes increased inctracellular ___ resulting in increased \_\_\_\_\_, ____ sensitization, lymphocytosis, \_\_\_\_, and necrosis.
2. LPS Lipid A role?
3. LPS Lipid X role?
Bordetella pertussis:
1. _Pertussis toxin_ - an _A/B_ toxin that causes increased intracellular _cAMP_ resulting in increased _secretions_, _histamine_ sensitization, lymphocytosis, _edema_, and necrosis
2. Lipid A: proinflammatory
3. Lipid X: proinflammatory and pyrogenic
199
Bordetella pertussis:
1. Role of invasive adenylate cyclase?
2. Mode of transmission?
3. initial manifestation? Progresses with prominent ___ necrosis and inflammation, pathology now includes ____ and \_\_\_\_.
Bordetella pertussis:
1. IAC - increases cAMP in phagocytes that then inhibit phagocytic activity
2. Aerosol transmission
3. _Peribronchitis and peribronchiolitis_, progresses with _subepithelial_ necrosis and inflammation, pathology now includes _endobronchitis and endobronchiolitis_
200
Bordetella pertussis:
1. Presents with the ___ stage after 10 day incupation characterized by ___ and \_\_\_.
2. Late stage also has ___ with mostly lymphocytes
Bordetella pertussis:
1. Presents with the _catarrhal_ stage characterized by _rhinorrhea_ and _fever_
2. Late stage also has _leukocytosis with mostly lymphocytes_
201
Bordetella pertussis:
1. The catarrhal stage is followed by the ____ \_\_\_\_ stage characterized by?
2. What is the last stage? What does it present with?
Bordetella pertussis:
1. Catarrhal followed by _paroxysmal cough_ stage characterized by paroxysmal cough, inspiratory whoops, and vommiting lasting around 3 weeks
2. Convalescent stage with decreasing cough intensity that lasts a month or more
202
Pseudomonas aeruginosa:
1. Gram?
2. Oxygen requirement?
3. Virulence factors?
Pseudomonas aeruginosa:
1. Gram -
2. Aerobe
3. _LPS, capsule/glycocalyx/biofilm, heat-labile hemolysin, exotoxins A and S, and antibiotic resistance_
203
Pseudomonas aeruginosa:
Virulence factors:
1. Capsule/glycocalyx/Biofilm function?
2. Exotoxins A and S function?
3. Type ____ secretion. What is this?
Pseudomonas aeruginosa:
Virulence
1. These resist phagocytosis, opsonization, and antibiotics
2. Exotoxins A and S inhibit protein synthesis
3. Type _III_ secretion - injection of toxins directly into host cells causing disruption of cellular processes
204
Pseudomonas aeruginosa:
1. Major cause of what nosocomial infections?
2. Important cause of pneumonia in what patients?
3. Important cause of sepsis and symptoms are like other Gram - except for the necrotic lesions of _______ \_\_\_\_\_\_\_\_.
Pseudomonas aeruginosa:
1. Nosocomial RTI --\> _necrotizing pneumonia_
2. Pneumonia in CF patients
3. Necrotic lesions of _ecythema gangrenosum_
205
Pseudomonas aeruginosa:
1. What other things can it cause?
Pseudomonas aeruginosa:
1. External otitis, keratitis, nosocomial UTI, _wound and burn infections_, and generalized folliculitis (often associated with whirlpools, pools, and hottubs)
206
Yersinia pestis:
1. Secretion?
2. What products mediate host cell adherance?
3. ____ gene products are cytotoxic
4. Function of V and W Ags?
Yersinia pestis:
1. Type III secretion
2. yadA gene products mediate cell adherance
3. _Yop_ gene products are cytotoxic
4. V and W Ags are immunosuppressive and necessary for intracellular growth
207
Yersinia pestis:
1. Mode of transmission?
2. 3 clinical syndromes?
Yersinia pestis:
1. Flea bite
2. Bubonic plague, pneumonic plague, and septicemic plague
208
Yersinia pestis:
Bubonic plague:
1. Incubation?
2. Symptoms?
Yersinia pestis:
Bubonic plague:
1. 2-10 day incubation
2. High fever, chills, HA, weakness, and painful lymphadenopathy in the region of the flea bite
209
Yersinia pestis:
1. Pneumonic plague involves a rapidly progressive?
2. Septicemic plague: what occurs?
Yersinia pestis:
1. Rapidly progressive hemorrhagic and necrotizing pneumonia
2. Septicemic plague: endotoxemis and shock, DIC, thrombi, and vascular collapse
210
Haemophilus ducreyi:
1. The disease is _____ characterized by?
2. Mode of transmission?
3. Papule develops --\> _____ (more painful in ___ than \_\_\_\_). Regional _____ occurs and the ___ often rupture forming a draining ___ tract
Haemophilus ducreyi:
1. The disease is _chancroid_ characterized by genital ulcers and inguinal lyphadenitis
2. Sex
3. Papule develops --\> _ulcerates_ (more painful in _men_ than _women_) Regional _lymphadenitis_ occurs and the _nodes_ often rupture forming a draining _sinus_ tract
211
Mycobacteria Tuberculosis:
1. Gram?
2. What are the cell wall components? Function?
3. Where does it grow?
4. What response is needed to eliminate the infection?
Mycobacteria Tuberculosis:
1. Gram -
2. Arabinogalactan, cord factor, and lipoarabinomannan - proinflammatory, toxic, inhibit chemotaxis, and inhibit the fusion of lysosomes with phagosomes in unactivated phagocytes
3. Grows in unactivated macrophages and T II pneumocytes
4. Need TH1 to eliminate the infection
212
Mycobacteria Tuberculosis:
Primary pulmonary TB:
1. Transmission?
2. Pathology?
3. Most individuals are ___ or have mild ____ with ___ symptoms. The lesions heal with?
Mycobacteria Tuberculosis:
Primary pulmonary TB:
1. Aerosol
2. TH1 sensitization develops and inflammatory consolidation occurs via epithelioid granulomas that undergo central caseous necrosis
3. Most individuals are _asymptomatic_ or have mild _pneumonitis_ with _flu-like_ symptoms. Heal with fibrosis and calcification
213
Mycobacteria Tuberculosis:
Progressive primary TB:
1. When does this occur?
2. Presentation?
3. There are usually expanding areas of? with?
Mycobacteria Tuberculosis:
Progressive primary TB:
1. This occurs when the primary infection isnt contained
2. Fever, productive cough, and chest pain
3. Expanding areas of caseating necrosis with irregular cavity formation
214
Mycobacteria Tuberculosis:
Progressive primary TB:
1. There is erosion of? Causes?
2. Healing?
Mycobacteria Tuberculosis:
Progressive primary TB:
1. Erosion of blood vessels resulting in hemoptysis
2. Heal with fibrosis
215
Mycobacteria Tuberculosis:
Secondary TB:
1. Who gets secondary TB?
2. The lesions are localized where?
3. Symptoms?
Mycobacteria Tuberculosis:
Secondary TB:
1. Arises in a previously infected and sensitized person
2. Lesions localized to the apex of the upper lobes
3. Symptoms: remittent low grade fever, night sweats, wt. loss, hemoptysis, and cavity formation
216
Mycobacteria Tuberculosis:
What is miliary TB?
Mycobacteria Tuberculosis:
Miliary TB is when it disseminates viea the blood to the rest of the body
217
Mycobacterium avium-intracellulare:
1. Causes a ____ infection and disseminated disease in ____ patients, usually when ___ counts are very low.
2. Pathologic hallmark?
Mycobacterium avium-intracellulare:
1. Causes a _pulmonary_ infection and disseminated disease in _AIDS_ patients, usually when _CD4_ counts are very low
2. Pathologic hallmark = _acid-fast bacilli in macrophages_
218
Mycobacterium Leprae:
1. Where does this grow?
2. What inhibits immunity and causes anergy?
3. Induces ____ expression on ___ cells that then bind to M. leprae lipopeptides which then induces ___ cell \_\_\_.
Mycobacterium Leprae:
1. Grows in macrophages and Schwann cells
2. Phenolic glycolipid capsule and lipoarabinomannan
3. Induces _TLR_ expression on _schwann_ cells that then induce _schwann_ cell _apoptosis_
219
Mycobacterium Leprae:
1. Invasion of schwann cells also causes?
2. What mediates tissue damage early in the infection?
Mycobacterium Leprae:
1. Rapid demyelination of peripheral nerves
2. CMI mediates early tissue damage
220
Mycobacterium Leprae:
Leprosy:
1. Definition?
2. What are the 4 forms?
Mycobacterium Leprae:
Leprosy:
1. Definition: chronic disease of the skin, peripheral nerves, and mucosa of the upper respiratory tract
2. 4 forms: _indeterminant, tuberculoid, borderline, lepromatous_
221
Mycobacterium Leprae:
Leprosy:
1. Indeterminant involves?
2. Tuberculoid involves?
3. Borderline involves?
4. Lepromatous involves?
Mycobacterium Leprae:
Leprosy:
1. Indeterminant = early lesions of hypopigmented macules
2. Tuberculoid = one or a few hypopigmented, anesthetic lesions and sin and muscle atrophy
3. Borderline = Skin lesions of both tuberculoid and lepromatous leprosy
4. Lepromatous = bilateral and symmetrical papules/nodules
222
Mycobacterium Leprae:
Leprosy:
1. Mode of transmission? Incubation period?
2. Begins as ___ leprosy with invasion of peripheral \_\_\_\_. There is transition to ___ and then ____ associated with disseminated ____ \_\_\_\_ ( ___ activity is now suppressed and ___ is activated), hypergammaglobulenimia, and cutaneous papules and nodules
Mycobacterium Leprae:
Leprosy:
1. Contact; 2-5 year incubation
2. Begins as _tuberculoid_ leprosy with invasion of peripheral _nerves_. There is transition to _borderline_ and then _lepromatous_ associated with disseminated _peripheral neuropathy_ ( _TH1_ activity is now suppressed and _TH2_ activated)
223
Mycobacterium Leprae:
Leprosy:
1. What else is usually heavily infected?
2. May also present with ___ \_\_\_ ___ from cutaneous deposition of immune complexes.
Mycobacterium Leprae:
Leprosy:
1. Respiratory tract is usually heavily infected
2. May also present with _erythema nodosum leprosum_ from cutaneous deposition of IC
224
Treponema Pallidum:
1. Also known as?
2. Gram?
3. Tissue damage is caused by?
4. Mode of transmission?
Treponema Pallidum:
1. Syphilis
2. Gram -
3. Tissue damage caused by the inflammatory response
4. Sexual contact, transplacental, kissing, or close contact with an active lesion
225
Treponema Pallidum:
1. Incubation period is proportional to?
2. Syndromes? (5)
Treponema Pallidum:
1. Incubation period proportional to size of the inoculum
2. Syndromes: primary, secondary, latent, late, and congenital
226
Treponema Pallidum:
Primary syphilis:
1. Characterized by?
Latent syphilis:
2. Manifestation?
3. Length of this stage?
Treponema Pallidum:
Primary syphilis:
1. Characterized by chancre (inflammatory lesion with plasma cells, macrophages, lymphocytes) at site of entry
Latent
2. No clinical manifestation
3. Can last 10 years
227
Treponema Pallidum:
Secondary syphilis:
1. Characterized by?
2. When does it occur?
3. What occurs to skin?
4. What occurs to mucous membranes?
Treponema Pallidum:
Secondary syphilis:
1. Characterized by disseminated disease and extensive spirochetemia
2. 2-8 weeks after primary lesion
3. skin: macular, maculopapular, papular, and/or pustular lesions
4. Mucous membrane: ulcer/erosions
228
Treponema Pallidum:
Secondary syphilis:
1. In warm, moist areas papules coalesce to form highly ____ plaques known as ____ \_\_\_.
2. It also disseminates to the \_\_\_\_\_.
3. Systemic manifestations?
Treponema Pallidum:
Secondary syphilis:
1. Form highly _infectious_ plaques = _condylomata lata_
2. Disseminates to the _CNS_
3. Systemic: fever, HA, sore throat, arthralgias, lyphadenoapthy, anorexia, and weight loss
229
Treponema Pallidum:
Late/Tertiary syphilis:
1. _Meningiovascular neurosyphilis_: involves ____ \_\_\_\_ (inflammation of the ___ of an artery resulting in \_\_\_\_) affecting small blood vessels of? Leads to?
2. _Parenchymatous neurosyphilis_: involves actual destruction of ___ cells. Where? Presentation?
Treponema Pallidum:
Late/Tertiary syphilis:
1. _Meningiovascular neurosyhpilis_: involves _endarteritis obliterans_ (inflammation of the _intima_ of an artery resulting in _occlusion_) affects small BV of meninges, brain, and SC leading to multiple areas of infarction
2. _parenchymatous_: destruction of _nerve_ cells in the cortex and posterior columns/roots of the SC: paresis (change in personality, intellect etc) and tabes dorsalis (pain, ataxia)
230
Treponema Pallidum:
Congenital syphilis:
1. Early Presentation?
2. Late presentation?
Treponema Pallidum:
Congenital syphilis:
1. Early: like secondary except rash is often vesicular or bullous and the liver (fibrosis), CNS, bone, and lung (fibrosis) are involved.
2. Late: CNS (deafness), interstitial keratitis, and bone development issues associated with periostitis and osteochondritis and _hutchinson teeth_ (small, notched incisors)
231
Relapsing fever:
1. ____ causes the form endemic in s. ameria where lice are the vectors.
2. What is responsible for the one in western us? vectors?
Relapsing fever
1. _B. recurrentis_ in s. america with lice vector
2. Western us = _B. hermsii_ with a _tick_ vector
232
Borrelia hermsii:
1. Incubation period?
2. Initial symptoms?
3. Initial symptoms are followed by? Then?
Borrelia hermsii:
1. 2-14 day incubation
2. Septicemia with fever, chills, HA, myalgia, and hepatosplenomegaly
3. Followed by a latent period and then a relapse of symptoms (bc bugs modify their outer membrane Ag): 3 relapses are common!
233
Borrelia burgdorferi:
1. Also known as?
2. Vector? Time?
Borrelia burgdorferi:
1. AKA: lyme disease
2. Deer tick - must be attached for more than 24 hrs
234
Borrelia burgdorferi (Lyme disease):
Early localized disease:
1. Incubation?
2. Symptoms?
3. Pathologically characterized by ___ and \_\_\_\_-\_\_\_\_ infiltrate (the adaptive response is \_\_\_/\_\_\_\_ cell)
4. Like borreila hermsii it modifies?
Borrelia burgdorferi (Lyme disease):
Early localized disease:
1. 3-30 days
2. Rash at the site of the bite, fever, chills, myalgias, lymphadenopathy and fatigue.
3. _Edema_ and a _lymphocytic-plasma_ cell infilatrate (adaptive response is _TH2/B_ cell)
4. Modifies its surface antigens
235
Borrelia burgdorferi (Lyme disease):
Early disseminated disease:
1. Occurs ____ \_\_\_ after the tick bite.
2. Presentation?
Late disease:
3. When does this occur?
4. Involves?
Borrelia burgdorferi (Lyme disease):
Early disseminated disease:
1. Occurs _3-5 weeks_ after the bite
2. Presntation: secondary skin lesions, facial nerve palsy, meningitis, and rarely carditis
Late:
3. weeks to months after infection
4. Arthritis of large joints and rarely CNS
236
Anaerobes:
1. Most infections are ____ and they are characterized by ____ formation with a foul ____ \_\_\_\_\_.
2. Non spore forming gram + cocci?
3. Non-spore forming gram + rods?
4. Gram - rods?
Anaerobes:
1. Most infections are _endogenous_ and they are characterized by _abscess_ formation with a foul _smelling exudate_
2. G+ cocci: peptostreptococcus and streptococcus
3. G+ rods: Eubacterium, propionibacterium, bifidobacterium and lactobacillus
4. G- rods: bacteroides fragilis, prevotella, porphyromonas, fusobacterium
237
Peptostreptococcus and Streptococcus:
1. These are non-\_\_\_ forming gram ____ \_\_\_.
2. Oxygen requirements?
3. 4 main infections?
Peptostreptococcus and Streptococcus:
1. These are non_-spore_ forming _gram + cocci_
2. Anaerobes
3. _brain abscess, aspiration pneumonia, intra-abdominal infections, and femal pelvic infections_
238
Bacteroides fragilis:
1. Gram ___ \_\_\_. Oxygen requirement?
2. Causes 60% of all _________ infections with ___ etiology and 70% of all _____ \_\_\_\_.
3. Certain strains also produce community acquired \_\_\_\_
Bacteroides fragilis:
1. Gram _- rod_. Anaerobe
2. Causes 60% of all _intra-abdominal infections_ with _anaerobic_ eitiology and 70% of all _anaerobic bacteremias_
3. Also produce _community acquired gastroenteritis_
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Clostridium Perfringens:
1. Oxygen? Gram? Shape? Spores?
2. 3 Exotoxins?
3. Major infections (2)?
Clostridium Perfringens:
1. Anaerobic; Gram +; Rod; Spore-forming
2. Alpha-toxin, beta-toxin, and theta-toxin
3. Cellulitis and myonecrosis (gas gangrene)
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Clostridium Perfringens:
1. Function of _alpha toxin?_
2. Function of beta toxin?
3. Function of theta toxin?
4. ___ toxin causing partial hemolysis and the __ toxin causing complete
Clostridium Perfringens:
1. _Alpha toxin_ - lyses cells causing necrosis, hepatic toxicity, and myocardial dysfunction
2. Beta-toxin: necrosis and hypertension seen with enteritis necroticans
3. Theta toxin: pore forming hemolysin that also lyses endothelial cells
4. alpha = partial; theta = complete
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Clostridium Perfringens:
Cellulitis:
1. Characterized by?
2. Amount of necrosis is ____ to the amount of inflammatory ____ and ____ present
Clostridium Perfringens:
Cellulitis:
1. Characterized by a foul odor and rapid tissue destruction
2. Amount of necrosis is _disproportionate_ to the amount of inflammatory _infiltrat__e_ and _bugs_ present
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Clostridium Perfringens:
Myonecrosis (gas gangrene)
1. Acute onset of?
2. Extensive ___ exudate with sparse ____ cells, extensive \_\_\_\_\_, vascular damage, and \_\_\_\_\_.
3. Color of skin?
Clostridium Perfringens:
Myonecrosis:
1. Acute onset of pain followed by rapid and extensive muscle necrosis involving tissue not damaged by the trauma
2. Extensive _fluid_ exudate with sparse _inflammatory_ cells, extensive _hemolysis_, vascular damage, and _thrombosis_
3. Changes from red --\> brown --\> green-black with visible gas
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Clostridium tetani:
Produces a ___ sensitive ____ that blocks the release of ____ neurotransmitters by degrading \_\_\_\_; this causes unregulated synaptic activity and ____ \_\_\_\_
Clostridium tetani:
Produces a _heat_ sensitive _neurotoxin_ that blocks the release of _inhibitory_ neurotransmitters by degrading _synaptobrevin_; this causes unregulated synaptic activity and _spastic paralysis_
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Clostridium Botulinum:
1. Produces a ___ sensitive ___ that localizes at ____ synapses where it inhibits the release of ____ resulting in ___ or autonomic dysfunction.
2. Usually the first evidence is? Followed by?
Clostridium Botulinum:
1. Produces a _heat_ sensitive _neurotoxin_ that localizes at _cholinergic_ synapses where it inhibits the release of _ACh_ resultign in _paralysis_ or autonomic dysfunction
2. First: bilateral cranial nerve dysfunction: dry mouth, blurred vision, diplopia, and difficulty swallowing and speaking followed by symmetric descending weakness and paralysis
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Clostridium Difficile:
1. Produces an enterotoxin (toxin \_\_: induces cytokine release and fluid ___ and necrosis) and a cytotoxin (toxin \_\_\_: causes ____ depolymerization and cell death)
2. Syndromes include?
3. Presentation?
Clostridium Difficile:
1. Produces an enterotoxin ( toxin _A_: induces cytokine release and fluid _secretion_ and necrosis) and a cytotoxin (toxin _B_: causes _actin_ depolymerization and cell death)
2. Syndromes include self limited diarrhea and pseudomembranous entercolitis
3. Presentation: ever, abdominal pain, and profuse bloody diarrhea
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Obligate intracellular bacteria:
Examples?
Obligate intracellular bacteria:
a. Chlamydia
b. Chlamydophila
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Chlamydia trachomatis:
Causes what 3 infections?
Chlamydia trachomatis:
a. Lymphogranuloma venerum
b. Trachoma
c. Oculogenital
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Chlamydia trachomatis:
Lymphogranuloma venerum:
1. Serotypes:
2. Most characteristic?
3. Presentation?
Chlamydia trachomatis:
Lymphogranuloma venerum:
1. Serotypes L1, 2, and 3
2. Inguinal lymphadenopathy
3. Presentation: painful node that ruptures forming draining sinuses, healing by fibrosis
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Chlamydia trachomatis:
Trachoma:
1. Serotypes?
2. Beings as acute ____ \_\_\_\_ followed by _____ proliferation and as the infection resolves there is ___ and scarring of the ___ and \_\_\_\_. Eyelashes grow \_\_\_\_\_.
3. Follicules composed of aggregates of?
Chlamydia trachomatis:
Trachoma:
1. Serotypes A, B, Ba, and C
2. Begins as acute _follicular conjunctivitis_ followed by _epithelial_ proliferation and as the infection resolves there is _fibrosis_ and scarring of the _conjunctiva_ and _cornea_. Eyelashes grow _inward_.
3. Follicules composed of aggregates of _lymphocytes_ and _macrophages_
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Chlamydia trachomatis:
Oculogenital:
1. Serotypes?
2. Men?
3. Women?
Chlamydia trachomatis:
Oculogenital:
1. Serotypes D-K
2. Men: conjunctivitis, urethritis with dysuria, and purulent discharge
3. Women: conjunctivitis, cervicitis with urethritis, dysuria, and purulent discharge
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Rickettsial infections:
Name 3.
Rickettsial infections:
a. Ehrlichia chaffeensis (human monocytis ehrlichiosis)
b. Anaplamsa phagocytophilum (human granulocytis anaplamosis)
c. Rickettsia rickettsii (rocky mountain spotted fever)
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Ehrlichia chaffeensis: _human monocytic ehrlichiosis_:
1. Cell cycles is associated with?
2. Mode of transmission?
3. Bugs enter blood and lymphatics and then ________ tissue where they infect ____ and \_\_\_\_
Ehrlichia chaffeensis: human monocytic ehrlichiosis:
1. Cell cycle is associated with infectious elementary bodies similar to Chlamydia
2. Lone star tick
3. Bugs enter blood and lymphatics and then _reticuloendothelial_ tissue where they infect _monocytes_ and _macrophages_
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Ehrlichia chaffeensis: human monocytic ehrlichiosis:
1. Presentation?
2. Some also have?
Ehrlichia chaffeensis: human monocytic ehrlichiosis:
1. Presentation: fever, HA, myalgia, chills, N/V, diarrhea, and abdominal pain
2. Some also have petechial rash or CSF lymphocytosis with neurological manifestations (confusion to coma)
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Anaplasma phagocytophilum: _human granulocytic anaplasmosis_:
1. Transmission?
2. Bugs enter the blood and disseminate where?
Anaplasma phagocytophilum: human granulocytic anaplasmosis:
1. Deer ticks
2. Enter blood and disseminate to _bone marrow_ and the _spleen_
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Anaplasma phagocytophilum: human granulocytic anaplasmosis:
1. In bone marrow it infects? Results in?
2. Presentation?
Anaplasma phagocytophilum: human granulocytic anaplasmosis:
1. Bone marrow it infects myeloid and monocytic progenitor cells resulting in a reduced CMI
2. Presentation: fever, HA, myalgia. 50% present with N/V and CNS manifestations
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Rickettsia rickettsii: _Rocky mountain spotted fever_:
1. Transmission?
2. Results in ____ lesions (with necrosis and \_\_\_\_\_)
Rickettsia rickettsii: Rocky mountain spotted fever:
1. Wood or dog tick
2. Vascular lesions (necrosis and _thrombosis_)
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Rickettsia rickettsii: Rocky mountain spotted fever:
1. Major effect of endothelial injury?
2. Presentation?
Rickettsia rickettsii: Rocky mountain spotted fever:
1. Effect of endothelial injury is increased vascular permeability (edema) hypovolemia, hypotension, and shock
2. Presentation: fever, HA, myalgias, after 2-6 days a rash starts on wrists, palms, and ankles and then becomes generalized
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Fungal infections:
Name several.
Fungal infections:
a. Candida albicans
b. Cryptococcus neoformans
c. Aspergillus
d. Mucormycosis
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Candida albicans:
1. Can grow as ____ or \_\_\_\_.
2. Cutaneous/mucous membrane infections?
Candida albicans:
1. Can grow as _yeast__s_ or _filaments_
2. Cutaneous/mucous membrane infections: _oral candidiasis, genital candidiasis, and generalized intertriginous candiasis_
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Candida albicans:
1. Oral candiasis: aka? Main presentation?
2. Genital candidiasis: presentation?
3. Generalized intertriginous candidiasis: lesions are?
Candida albicans:
1. Oral candidiasis: thrush; mucosal pseudomembrane
2. Genital candidiasis: mucosal pseudomembrane, purulent discharge and burning and itching
3. Generalized intertriginous candidiasis: lesions are erythematous, dry, and scaly (may be pruritic)
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Candida albicans:
Systemic candida infections? (8)
Candida albicans:
Systemic infections: esophagitis, GI candidiasis, Fungemia, bronchopulmonary candidiasis, urinary tract, endocarditis, hepatosplenic candidiasis, and CNS candidiasis
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Candida albicans:
Esophagitis:
a. Common in who?
b. Presentation?
Candida albicans:
Esophagitis:
1. Common in AIDS and hematologic malignancies
2. Pseudomembranes, ulcerations, and pain on swallowing
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Candida albicans:
GI candidiasis:
1. Common in?
2. Presentation?
Candida albicans:
GI:
1. Common in hematologic malignancies
2. Numerous gastic lesions and GI bleeding
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Candida albicans:
1. _Fungemia_: presentation?
2. _Bronchopulmonary_: presentation?
3. _Urinary tract_: presentation?
Candida albicans:
1. _Fungemia_: fever, shock, DIC, renal failure, and skin lesions
2. _Bronchopulmonary_: fever, and productive bloody cough
3. _Urinary tract_: cystitis from catheterization or pyelonephritis from fungemia
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Candida albicans:
1. _Endocarditis_: from? Presentation?
2. _Hepatosplenic candidiasis_: presentation?
3. _CNS candidiasis_: occurs in who? Presentation?
Candida albicans:
1. _Endocarditis_: from fungemia with fever, emboli, and large vegetations
2. _Hepatosplenic candidiasis_: fever, elevated liver enzymes, and hepatosplenomegaly
3. _CNS_: Occurs in low birth weight neonates and hematologic malignanciesl presents with meningioencephalitis
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Cryptococcus neoformans:
1. Capsule serotype A =?
2. Capsule serotype D = ?
3. Capsule serotypes B and C = ?
Cryptococcus neoformans:
1. Serotype A = C. neoformans var grubii
2. Serotype D = C. neoformans var neoformans
3. Serotypes B and C = C. neoformans var gattii
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Cryptococcus neoformans:
1. This is the only pathogenic fungus that has what virulence factor? Function?
2. Role of melanin?
3. Pathogenesis: mode of transmission? disseminates where?
Cryptococcus neoformans:
1. Only fungus with a _capsule_ = immunosuppressive by blocking T cell activation and inhibiting phagocytosis
2. Melanin: protects the yeast from oxidative damage
3. Inhalation and dissemination to skin and CNS
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Cryptococcus neoformans:
3 infections?
Cryptococcus neoformans:
a. Acute pulmonary cryptococcosis
b. Skin lesions
c. CNS infection
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Cryptococcus neoformans:
1. _Acute pulmonary cryptococcosis_ - presentation?
2. _Skin lesions_: presentation?
3. _CNS infection_: who? Results in?
Cryptococcus neoformans:
1. _Acute pulmonary cryptococcosis_: often asymptomatic but may have fever, cough, chest pain, and dyspnea
2. _Skin lesions_: vary from pustules to ulcerations
3. _CNS_: in immunocompromised; results in incurable meningioencephalitis
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Aspergillus:
1. What causes 90% of infections? 10%?
2. Mode of transmission?
3. Induction of ____ response may limit infection
4. Infections?
Aspergillus:
1. 90% = _aspergillus fumigatus_ 10% = _aspergillus flavus_
2. Inhalation of conidia
3. Induction of _Th1_ response may limit infection
4. Allergic bronchopulmonary aspergillosis, aspergilloma, invasive sinusitis, and invasive pulmonary aspergillosis
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Aspergillus:
1. _Allergic bronchopulmonary aspergillosis_: this is ____ exacerbated by type ___ and ____ reactions to aspergillus fumagatus. Presentation?
2. _Aspergilloma_: this is a fungus ____ in the ___ with no mucosal invasion. Presentation?
Aspergillus:
1. _Allergic bronchopulmonary aspergillosis_: this is _asthma_ exacerbated by type _I_ and _III_ reactions. Episodic wheezing, cough, and dyspnea
2. _Aspergilloma_ this is a fungus _ball_ in the _sinuses_ with no mucosal invasion. Presents with sinus congestion, pain, cough, hemoptysis, wheezing, and dyspnea
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Aspergillus:
1. _Invasive sinusitis_: occurs in who? And involves a very aggressive infection that \_\_\_\_\_\_\_\_\_\_\_\_\_\_
2. _Invasive pulmonary aspergillosis_: underlying conditions that predispose? Characterization?
Aspergillus:
1. _Invasive sinusitis_: occurs in _immunocompromised_ with infection that _disseminates_
2. _Invasive pulmonary aspergillosis_: underlying conditions: neutropenia, chemo, corticosteroid therapy, transplants, and immunodeficiency; characterized by _rapidly progressing infection with necrosis and vascular invasion by the hyphae_
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Mucormycosis:
1. Disease is limited to?
2. Major genera? (4)
Mucormycosis:
1. Disease is limited to immunocompromised, diabetics, and those with severe trauma
2. Genera: Rhizopus, Rhizomucor, Absidia, and Mucor
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Mucormycosis:
1. Mode of transmission? Hyphae invade ___ and ___ causing _____ and necrosis.
2. Major syndromes?
Mucormycosis:
1. Inhalation; hyphae invade _tissue_ and _blood_ causing _thrombosis_ and necrosis
2. Syndromes: rhinocerebral mucormycosis, pulmonary mucormycosis, and cutaneous mucormycosis
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Mucormycosis:
1. _Rhinocerebral_: occurs in who? Presentation?
2. _Pulmonary_: occurs in who? Causes a highly ____ \_\_\_\_ presenting with?
3. _Cutaneous_:how does one get it
Mucormycosis:
1. _Rhinocerebral_: occurs in _diabetics_; _facial pain_, edema, HA, fever, and orbital cellulitis
2. _Pulmonary_: in immunocompromised (esp those with neutropenia); causes a highly _necrotic pneumonia_ presenting with fever, dyspnea, cough, and hemoptysis
3. _Cutaneous_: with traumatic inoculation of spores
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