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Pathology > Chapter 8 - Infectious Diseases > Flashcards

Chapter 8 - Infectious Diseases Flashcards

1
Q

Categories of infectious agents?

A

a. prions
b. viruses
c. bacteria
d. fungi
e. parasites

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2
Q

Prions:

  1. Pathology involves ____ encephalopathies ___ inflammation.
  2. The normal prion protien is associated with?
A

GERD:

  1. Pathology involves spongiform encephalopathies withoutinflammation.
  2. The normal prion protein is associated with neuronal development and prevention of cell death.
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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

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4
Q

Prions:

Genetic prion disease?

Infectious?

A

Prions:

Genetic: Cruetzfeldt-Jakob

Infectious: iatrogenic CJD, Kuru, and new variant CJD

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5
Q

Prions:

The human form of Bovine spongiform encephalopathy (BSE) is called?

A

Prions:

BSE human form = new variant CJD

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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

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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

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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

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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

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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

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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

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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

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13
Q

STD:

The common sexually transmitted viruses?

A

STD:

HIV, HTLV1, HBV, HDV, HCV, HSV, and CMV (all with V, most with H)

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14
Q

STD:

Sexually transmitted bacteria?

A

STD:

C. trachomatis, N. gonorrhoeae, H. ducreyi, mycoplasma, and ureaplasma

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15
Q

STD:

C. trachomatis and N. Gonorrhoeae cause?

A

STD:

Cause urethritis, epidiymitis, cervicitis, and PID

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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

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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

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18
Q

STD:

Sexually transmitted fungi? Causes?

Sexually transmitted parasite? Causes?

A

STD:

Fungus: C. Albicans - vaginitis

Parasite: Trichomonas vaginalis - urethritis and vaginitis

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19
Q

Trophism:

What disseminates to the skin?

What disseminates to the brain?

A

Trophism:

Skin - chickenpox, yaws

Brain - poliomyelitis

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20
Q

Trophism:

What infects the lungs?

What infects the kidneys?

A

Trophism:

Lungs - measles and rubella

Kidney - hematogenous pyelonephritis

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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

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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)

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23
Q

Virus-mediated tropism/cell injury:

Injury/death:

  1. Virus replication resulting in cell ___
  2. Inhibition of _____ synthesis
  3. Insertion of viral proteins into the host ___. What does this cause?
A

Virus-mediated tropism/cell injury:

Injury/death:

  1. Virus replication resulting in cell lysis
  2. Inhibition of macromolecular synthesis
  3. Insertion of viral proteins into the host membrane. This disrupts integrity, promotes cell fusion, and loss of cellf function.
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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**

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25
Q

Bacteria-mediated tropism/cell injury:

Effective intracellular growth may involve inhibition of ____ ____ fusion, escaping from the ___, blocking the host ___ ____ pathways, and rearranging ___.

A

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.

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26
Q

Bacteria-mediated tropism/cell injury:

Intrinsic toxins?

All of these are ____ and can induce cellular ___.

A

Bacteria-mediated tropism/cell injury:

Intrinsic toxins - LPS, LTA, PG, TA, and LOS

All of these are proinflammatory and can induce cellular_ necrosis_

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27
Q

Bacteria-mediated tropism/cell injury:

Examples of secreted exotoxins?

Some are superantigens: what do they do?

A

Bacteria-mediated tropism/cell injury:

Exotoxins - cholera, enterotoxin, Ef/LF from B. anthracis, tetanus, proteases, and hemolysins

Superantigens non-selectively activate T cells

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28
Q

What is this bacterial infection that is associated with skeletal muscle necrosis?

A

V. vulnificus

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29
Q

What is this bacteria associated with adrenal hemorrhage and necrosis? (also known as Waterhouse-Friedrickson syndrome)

A

N. meningitidis

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30
Q

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?
A

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
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31
Q

This is c. albicans forming microabscess in the __.

A

lung

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32
Q

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?

A

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

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33
Q

This shows septate hyphae with acute angle branching: what is it?

A

This is aspergillus

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34
Q

This is showing broad, aseptate hyphae with right angle branching as well as invasions of vasculature and the airways. What is this?

A

This is mucormycosis

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35
Q

This is blastomyces dermatitidis: with thick walled ____ and neutrophilic infiltrate and broad based ___.

A

Thick walled yeast and neutrophilic infiltrate and broad based buds

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36
Q

What is this?

What is in the spherule?

A

This is coccidioides immitis

There are endospores in the spherule

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37
Q

Immune evasion by infectious agents:

There is replication in inaccessible sites to the host immune response: Where is this?

Agents change or shed ____.

A

Immune evasion by infectious agents:

Inaccessible - lumen of intestine and keratinized epithelium

Agents change or shed antigens

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38
Q

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
A

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
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39
Q

Immune evasion by infectious agents:

Form “shields” of?

Types of intracellular growth?

A

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

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40
Q

Immune evasion by infectious agents:

What inhibits protease activity?

What blocks MHC synthesis?

What blocks TAP transport?

A

Immune evasion by infectious agents:

Inhibits protease: EBV, CMV

Blocks MHC synthesis: Adenovirus, CMV

Blocks TAP transport: HSV

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41
Q

Mechanisms of antigenic variation:

For given type give example:

  1. High mutation rate?
  2. Genetic reassortment?
A

Mechanisms of antigenic variation:

For given type give example:

  1. High mutation rate - HIV, influenza
  2. Reassortment - influenza, rotavirus
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42
Q

Mechanisms of antigenic variation:

For given type give example:

  1. Genetic rearrangement/recombination?
  2. Diverse serotypes?
A

Mechanisms of antigenic variation:

For given type give example:

  1. Recombination - Borrelia, Neisseria, Plasmodium
  2. Serotypes - rhinoviruses, S. pneumoniae
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43
Q

Infection in the immunosuppressed host:

Hypogammaglobulinemia:

  1. Recurrent sinopulmonary infections and/or otitis due to?
  2. Gastroenteritis caused by? (3)
  3. 2 other infections?
A

Infection in the immunosuppressed host:

Hypogammaglobulinemia:

  1. Sinopulmonary - S. pneumoniae and H. influenzae
  2. GE - giardia, rotavirus, and cryptosporidium
  3. Enterovirus and P. aeruginosa
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44
Q

Infection in the immunosuppressed host:

T cell defects (SCID, DiGeorge):

Name some disease in which the host is suceptible to getting.

A

Infection in the immunosuppressed host:

T cell defects:

Candida, pneumocystis, viral pneumonia, aspergillosis, slamonellosis, and CMV

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45
Q

Infection in the immunosuppressed host:

Complement deficiencies:

Infections by?

A

Infection in the immunosuppressed host:

Complement:

Infections by Nisseria, s. pneumoniae, and h. influenzae

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46
Q

Infection in the immunosuppressed host:

Phagocyte or chemotactic deficiencies:

Susceptible to?

A

Infection in the immunosuppressed host:

Phagocyte:

Susceptible to s. aureus, Gram- bacilli, and aspergillus

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47
Q

Infection in the immunosuppressed host:

Transplant:

Within one month, what is the greatest risk for with an allograft?

1-6 months after?

>6 months?

A

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

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48
Q

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?
A

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
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49
Q

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?
A

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
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50
Q

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?
A

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
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51
Q

This is a bladder infection with numerous calcified eggs: what caused this?

A

Schistosoma haematobium

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52
Q

Acute viral infections:

Examples?

A

Acute viral infections:

Measles, Mumps, Poliovirus, West Nile Virus, and Hemorrhagic fevers

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53
Q

Acute viral infections:

Measles:

  1. This is a paramyxovirus: genome? Includes what other diseases?
  2. Mechanism of transmission?
A

Acute viral infections:

Measles:

  1. ssRNA; mumps, RSV, HPIV, and metapneumovirus
  2. Aerosols
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54
Q

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 ___.

A

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.

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55
Q

Acute viral infections:

Measles:

Histological characteristic feature? Where is this seen?

A

Acute viral infections:

Measles:

Multinucleated giant cells known as Warthin-Finkeldey cells. They are in reticuloendothelial tissue, lungs, and sputum

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56
Q

Acute viral infections:

Measles:

  1. What does the rash result from?
  2. What is characteristically found in the mouth? This is a result from?
A

Acute viral infections:

Measles:

  1. Rash results from vasculitis
  2. Koplik spots in the mouth result from epithelial necrosis and a neutrophil exudate
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57
Q

Acute viral infections:

Measles:

  1. What does the reticuloendothelial tissue typically show?
  2. What are other symptoms?
A

Acute viral infections:

Measles:

  1. Reticuloendotheilal tissue shows follicular hyperplasia, large germinal centers, and multinucleated giant cells
  2. Cough, coryza, conjunctivitis, and photophobia
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58
Q

Acute viral infection:

Mumps:

  1. Mode of transmission?
  2. Where does it replicate?
A

Acute viral infection:

Mumps:

  1. Aerosols
  2. Replicates in T cells in draining lymph nodes
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59
Q

Acute viral infection:

Mumps:

  1. It sheds into the ____ and infects the ___ ___.
  2. Incubation period?
A

Acute viral infection:

Mumps:

  1. Shed into the blood and infects the salivary glands
  2. 16-18 day incubation period
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60
Q

Acute viral infection:

Mumps:

  1. What are the symptoms?
  2. Complications: 25% of postpubertal males? 50% of all?
A

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
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61
Q

This multinucleated cell is in what disease?

What is it also known as?

A

Measles

This cell is a Warthin-Finkeldy cell

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62
Q

Acute viral infection:

Mumps:

Mumps can also affect the ____ with destructive lesions, parenchymal and ____ necrosis

A

Acute viral infection:

Mumps:

Mumps can also affect the pancreas with destructive lesions, paranchymal and fat necrosis (slide 633)

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63
Q

Acute viral infection:

Poliovirus:

  1. This belongs to what class of virus? Genome?
  2. Definition of poliomyelitis?
A

Acute viral infection:

Poliovirus:

  1. Enterovirus with ssRNA
  2. Acute febrile disease with neuronal damage potentially yielding paralysis
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64
Q

Acute viral infection:

Poliovirus:

  1. Transmission? Disseminates to?
  2. Asymptomatic percent of patients?
A

Acute viral infection:

Poliovirus:

  1. Fecal/oral transmission; disseminates to the CNS
  2. 90/95% of patients are asymptomatic
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65
Q

Acute viral infection:

Poliovirus:

  1. Minor illness: percent and symptoms?
  2. Major illness: percent and symptoms?
A

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)
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66
Q

Acute viral infection:

Poliovirus:

Paralytic disease - percent and symptoms? Time of symptoms?

A

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)

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67
Q

Acute viral infection:

Poliovirus:

  1. Spinal form: replication is where? May involve?
  2. Bulbar form: replication where? May involve? Why is this serious?
A

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
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68
Q

Acute viral infection:

West nile virus:

  1. Class of virus? Transmission?
  2. Incubation period?
A

Acute viral infection:

Poliovirus:

  1. Flavivirus; arthropods but also transfusion/transplant/transplacentally
  2. 2-14 day incubation period
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69
Q

Acute viral infection:

West Nile Virus:

  1. Percent of asymptomatic patients?
  2. 20% have? and 50% of these also present with?
A

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
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70
Q

Acute viral infection:

West Nile Virus:

Less than one percent develop meningitis/encephalitis

  1. 25-35% develop?
  2. Encephalitis or meningioencephalitis: percent and symptoms?
A

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
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71
Q

Acute viral infection:

Hemorrhagic Fevers:

  1. Mode of transmission?
  2. Different classes of viruses?
A

Acute viral infection:

Hemorrhagic Fevers:

  1. Arthropod bites
  2. Arenavirus, Filovirus, Bunyaviruses, and Flaviviruses
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72
Q

Acute viral infection:

Hemorrhagic Fevers:

  1. Arenavirus example?
  2. Filovirus examples?
A

Acute viral infection:

Hemorrhagic Fevers:

  1. Arenavirus = lassa virus
  2. Filovirus = marburg and ebola virus
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73
Q

Acute viral infection:

Hemorrhagic Fevers:

  1. Bunyavirus example?
  2. Flavivirus examples?
A

Acute viral infection:

Hemorrhagic Fevers:

  1. Bunyavirus = hantavirus
  2. Flavivirus = yellow fever and dengue fever
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74
Q

Acute viral infection:

Hemorrhagic Fevers:

  1. Hemorrhage is associated with?
  2. Shock is associated with?
A

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
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75
Q

Acute viral infection:

Dengue Fever Virus:

  1. This disease is ___ ____
  2. Mode of transmission? Replicates where?
A

Acute viral infection:

Dengue Fever Virus:

  1. This disease is self limiting
  2. Transmitted by arthropods; replicates in reticuloendothelial tissue
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76
Q

Acute viral infection:

Dengue Fever Virus:

  1. What are the initial symptoms?
  2. What are the symptoms related to?
A

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)
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77
Q

Acute viral infection:

Dengue Fever Virus:

  1. What presents 3 days after the onset of fever?
  2. There is also generalized lymphadenopathy and ____.
A

Acute viral infection:

Dengue Fever Virus:

  1. Rash after 3 days
  2. General leukopenia
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78
Q

Acute viral infection:

Dengue Fever Virus:

  1. What are the nonspecific immune responses?
  2. What is generated later?
A

Acute viral infection:

Dengue Fever Virus:

  1. IFN and NK cell activity
  2. Later is the production of antibodies
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79
Q

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?
A

Acute viral infection:

Dengue Fever Virus:

  1. Primary cell target is monocytes
  2. Cytokines induce endothelial cells to induce plasma leakage
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80
Q

Acute viral infection:

Dengue hemorrhagic fever/shock:

  1. Initial presentation?
  2. What occurs after 3-4 days of fever? What can this cause?
A

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
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81
Q

Chronic/Latent viral infection:

Examples?

A

Chronic/Latent viral infection:

Herpes virus and CMV

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82
Q

Chronic/Latent viral infection:

Alphaherpesvirinae:

  1. Type of infection? Where?
  2. What viruses?
A

Chronic/Latent viral infection:

Alphaherpesvirinae:

  1. Latent virus in the neurons
  2. HSV1, HSV2, and VZV
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83
Q

Chronic/Latent viral infection:

Betaherpesvirinae:

  1. Type of infection?
  2. Type of viruses?
A

Chronic/Latent viral infection:

Betaherpesvirinae:

  1. Latent
  2. HHV6/7 (Roseolovirus) and CMV
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84
Q

Chronic/Latent viral infection:

Gammaherpesvirinae:

  1. Type of infection? Where?
  2. Type of viruses?
A

Chronic/Latent viral infection:

Gammaherpesvirinae:

  1. Latent in lymphoid cells
  2. HHV8 (Rhadinovirus), and EBV
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85
Q

Chronic/Latent viral infection:

HSV:

  1. Mode of transmission?
  2. Primary infection involves? What do the infected cells form?
A

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
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86
Q

Chronic/Latent viral infection:

HSV:

  1. Latent infection by HSV-1 occurs where?
  2. Latent infection by HSV-2 occurs where?
A

Chronic/Latent viral infection:

HSV:

  1. HSV-1: trigeminal ganglia
  2. HSV-2: sacral ganglia
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87
Q

Chronic/Latent viral infection:

HSV:

Examples of Primary HSV infections?

Examples of Latent HSV infections

A

Chronic/Latent viral infection:

HSV:

Primary = gingivostomatitis, genital herpes, meningioencephalitis, keratoconjunctivitis

Latent = Herpes labialis (cold sore) and genital infection

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88
Q

Chronic/Latent viral infection:

Gingivostomatitis:

  1. Virus? Incubation period?
  2. Initial presentation?
A

Chronic/Latent viral infection:

Gingivostomatitis:

  1. HSV; 4-6 day incubation
  2. Fever, sore gums, and sore mouth are the initial presentations
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89
Q

Chronic/Latent viral infection:

Gingivostomatitis:

  1. What occurs within 3 days of oral pain?
  2. How long can symptoms last?
A

Chronic/Latent viral infection:

Gingivostomatitis:

  1. Gingivitis with ulcers and perioral lesions as well as cervical lymphadenopathy
  2. 2 weeks
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90
Q

Chronic/Latent viral infection:

Genital Herpes:

  1. Most cases are caused by what? The rest are from?
  2. Incubation period? Initial symptoms?
A

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
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91
Q

Chronic/Latent viral infection:

Genital Herpes:

  1. In addition to normal symptoms, 5-30% also develop?
  2. What occurs with the vesicles in men?
A

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
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92
Q

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?
A

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
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93
Q

Chronic/Latent viral infection:

Meningioencephalitis:

  1. HSV-1 causes?
  2. HSV-2 causes?
  3. In neonates, both HSV1 and HSV2 cause?
A

Chronic/Latent viral infection:

Meningioencephalitis:

  1. HSV1 = encephalitis
  2. HSV2 = meningitis
  3. Neonates, both cause encephalitis
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94
Q

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?
A

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
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95
Q

Chronic/Latent viral infection:

Meningioencephalitis:

  1. General meningioencephalitis symptoms?
  2. Herpes specific symptoms?
A

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
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96
Q

Chronic/Latent viral infection:

Meningioencephalitis:

  1. What occurs in 2/3 of those that recover?
  2. Viral meningitis (nothing herpes specific) presents with?
A

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)
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97
Q

Chronic/Latent viral infection:

Keratoconjunctivitis:

Presentation?

A

Chronic/Latent viral infection:

Keratoconjunctivitis:

Often unilateral with acute onset of pain, conjunctivitis with a discharge, and blurred vision

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98
Q

Chronic/Latent viral infection:

HSV stromal keratitis:

Has an extensive ____ infiltrate with _____, possibly resulting in scarring and ____

A

Chronic/Latent viral infection:

HSV stromal keratitis:

Has extensive mononuclear infiltrate with neovascularization resulting in scarring and blindness

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99
Q

Examples of HSV recurrent infections?

A

Herpes labialis and genital infection

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100
Q

Herpes labialis:

  1. What is this?
  2. Presentation?
A

Herpes labialis:

  1. Cold sore
  2. Pain, burning, and itching followed by a papule that develops into a vesicle that crusts
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101
Q

Genital infection:

Recurrences are more common with?

A

Genital infection:

More common with HSV-2

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102
Q

Chronic/Latent viral infection:

CMV:

  1. Where do latent infections occur?
  2. Most common routes of transmission?
A

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
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103
Q

Chronic/Latent viral infection:

CMV:

  1. CMV can prevent _____ expression
  2. The congenital infection is known as?
A

Chronic/Latent viral infection:

CMV:

  1. CMV can prevent MHC-1 expression
  2. Congenital infection: cytomegalic inclusion disease
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104
Q

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?
A

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
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105
Q

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 ___.
A

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
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106
Q

Chronic/Latent viral infection:

Mononucleosis:

  1. __ causes 20% of all mono.
  2. What are heterophile antibodies?
A

Chronic/Latent viral infection:

Mononucleosis:

  1. CMV causes 20%
  2. Heterophile antibodies - recognize antigens on RBCs from other species
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107
Q

Chronic/Latent viral infection:

Mononucleosis:

  1. CMV mono is heterophile ___, while EBV mono is ___.
  2. Presentation?
A

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
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108
Q

Chronic/Latent viral infection:

CMV hepatitis:

  1. Is associated with what?
  2. Presentation?
A

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
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109
Q

What is this multinucleated giant cell associated with?

(it has intranuclear inclusions)

A

HSV

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110
Q

What disease is this? What virus?

A

This is gingivostomatitis; HSV

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111
Q

CMV infection: what is the arrow pointing to - more specifically what is the major characteristic of CMV

A

Major characteristic: Owl’s eye inclusion

112
Q

CMV infection in immunocompromised host:

  1. Most severe disease?
  2. 3 others that are common?
A

CMV infection in immunocompromised host:

  1. Most severe: pneumonia
  2. Chorioretinitis, Colitis/esophagitis, and CNS infection
113
Q

CMV infection in immunocompromised host:

  1. Pneumonia occurs in what kind of patients?
  2. Colitis/esophagitis presentation?
  3. CNS infection presentation?
A

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
Q

Chronic/Latent viral infections:

VZV:

  1. 5 childhood exanthems (rashes)?
  2. Transmission?
  3. Primary infection?
A

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
Q

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?
A

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 –> 10/12 day incubation –> acute onset of fever, HA and sore throat
116
Q

Chronic/Latent viral infections:

VZV:

  1. Where does the rash appear first? Progression?
  2. Where is the latent infection established?
A

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
Q

Chronic/Latent viral infections:

VZV:

Complications in children:

  1. Secondary bacterial infection by?
  2. What may happen in children treated with aspirin?
A

Chronic/Latent viral infections:

VZV:

Complications in children:

  1. Secondary bacterial infection: S. pyogenes
  2. Asprin - cause Reye’s syndrome
118
Q

Chronic/Latent viral infections:

VZV:

  1. Complications in children: What are some rare symptoms?
  2. Infection in immunocompromised patients may result in?
A

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
Q

Chronic/Latent viral infections:

VZV:

  1. Recurrent infection is?
  2. Where do you see the rash? Presentation?
A

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
Q

Chronic productive viral infections:

What is unique about these infections?

Examples?

A

Chronic productive viral infections:

These are infections that the immune system may not be able to eliminate.

HIV, HBV, HCV, HDV

121
Q

Chronic productive viral infections:

HBV:

  1. Envelope? Genome?
  2. What are the 4 Antigens that can be detected?
A

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
Q

Chronic productive viral infections:

HBV:

Transmission?

A

Chronic productive viral infections:

HBV:

Transmitted by blood, sex, and direct contact

123
Q

Chronic productive viral infections:

HBV Acute Hepatitis:

  1. Incubation period?
  2. Most of the damage is ___ mediated with extensive ___ necrosis.
A

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
Q

Chronic productive viral infections:

HBV Chronic Hepatitis:

  1. Continuous inflammation leads to ____ and then ___ of the liver.
  2. Continuous inflammation also predisposes to?
A

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
Q

Chronic productive viral infections:

HBV Chronic persistant Hepatitis Presentation?

Chronic active Abs? Symptoms?

A

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
Q

Transforming viral infections:

Examples?

A

Transforming viral infections:

EBV, HBV, HTLV-1, and HPV

127
Q

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
A

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
Q

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
A

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
Q

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 ___.
A

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
Q

Transforming viral infections:

EBV:

  1. __ cell proliferation accounts for the characteristic _____ and splenomegaly
  2. Incubation period?
  3. Initial symptoms?
A

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
Q

Transforming viral infections:

EBV:

  1. Virtually all have ____ Abs and lymphocytosis
  2. What symptoms may persist for months?
  3. Complications: 80% have? 50% have?
A

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
Q

Transforming viral infections:

HPV:

  1. Genome? Enveloped?
  2. The productive infection forms?
  3. The latent/transforming infection forms?
A

Transforming viral infections:

HPV:

  1. Circular dsDNA genome; non-enveloped
  2. Productive - warts
  3. Latent - cervical cancer
133
Q

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?
A

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
Q

Transforming viral infections:

HPV:

  1. What is the virus very resistant to?
  2. Where does skin hyperplasia initially occur?
A

Transforming viral infections:

HPV:

  1. Resistant to environmental stress
  2. Hyperplasia in the stratum spinosum
135
Q

Bacterial Infections - Gram Positive:

Name 3.

A

Bacterial Infections - Gram Positive:

a. Staphylococcus aureus
b. Staphylococcus epidermidis
c. Staphylococcus saprophyticus

136
Q

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?
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
Q

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?
A

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
Q

Bacterial Infections - Gram Positive:

Staph Aureus:

  1. Beta lactamase function?
  2. Staphylococcal compliment inhibitor blocks?
  3. Chemotaxis inhibitory protein blocks the receptors for?
A

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
Q

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?
A

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

  1. Leukocidin is cytolytic for phagocytes
140
Q

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?
A

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
Q

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
A

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
Q

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 ____ _____.
A

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
Q

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
A

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
Q

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?
A

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
Q

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?
A

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
    • Nikolsky sign: epidermis easily separates with slight pressure
146
Q

Bacteremia/Septicemia:

  1. Top 4 bacterial causes?
  2. Presentation?
A

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
Q

Bacteremia/Septicemia:

  1. Systemic inflammatory response syndrome (SIRS): presentation? No evidence of?
  2. Sepsis = ?
  3. Severe sepsis = ?
  4. Septic shock = ?
A

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
Q

Bacteremia/Septicemia:

  1. Pathology is associated with what kind of injury?
  2. What occurs in the brain?
  3. Heart?
  4. Kidneys?
  5. Lungs?
A

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
Q

Endocarditis:

  1. Main cause of infective endocaditis?
  2. Presentation?
A

Endocarditis:

  1. Main cause = Staphylococcus
  2. Presentation: ever, chills, bleeding, murmur, and embolism
150
Q

Pneumonia:

  1. _____ causes <10% of CAP.
  2. Often follows the ____
  3. _____ necrosis with ___ formation or the formation of a _____ (thin walled cyst)
  4. Presentation?
A

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
Q

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?
A

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
Q

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?
A

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
Q

Staphylococcal Toxic Shock:

  1. Mediated by TSST-1 from what bacteria?
  2. TSST-1: what does it induce?
  3. Presentation?
  4. There may be?
A

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
Q

Streptococcus:

  1. Oxygen requirements?
  2. Catalase?
  3. Shape?
A

Streptococcus:

  1. Faculative anaerobe
  2. Catalase negative
  3. Oval in pairs or chains
155
Q

Strep. Pyogenes:

Virulence factors:

  1. Role of M-proteins?
  2. Role of streptolysin S?
  3. Role of streptolysin O?
A

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
Q

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
A

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
Q

Strep. Pyogenes:

Pharyngitis:

  1. Most common bacterial infection of?
  2. Most common transmission?
  3. Incubation period?
A

Strep. Pyogenes:

Pharyngitis:

  1. Most common bacterial infection of childhood
  2. Aerosol transmission
  3. Incubation = 2-4 days
158
Q

Strep. Pyogenes:

Pharyngitis:

  1. Symptoms?
  2. Which nodes are enlarged?
  3. What else is enlarged? May be covered with?
A

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
Q

Strep. Pyogenes:

Scarlet fever:

  1. Pharyngitis caused by _____.
  2. PResentation?
A

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
Q

Strep. Pyogenes:

Cellulitis:

  1. 2 Most common causes?
  2. Involves diffuse infection of?
  3. Presentation?
A

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
Q

Strep. Pyogenes:

Erysipela:

  1. Acute _____ infection.
  2. Where is it commonly found?
  3. Associated with?
  4. Presentation?
A

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
Q

Strep. Pyogenes:

Necrotizing fasciitis:

  1. Associated with?
  2. What does this affect? Often following?
  3. Symptoms?
A

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
Q

Strep. Pyogenes:

Strep impetigo:

  1. Mode of transmission?
  2. Starts as erythematus ___ that develops into a ____ and then a ____.
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
Q

Nonsuppurative complications associated with S pyogenes:

Name 2.

A

Nonsuppurative complications associated with S pyogenes:

a. Nephritis
b. Rheumatic fever

165
Q

Nonsuppurative complications associated with S pyogenes:

  1. Nephritis: post infectious _____ _____ GN that follows ____
  2. RF: occurs after infection with any ___ associated with pharyngitis
A

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
Q

Strep Agalactiae:

  1. Colonizes where?
  2. Neonatal infection: 2 types?
A

Strep Agalactiae:

  1. Colonizes in oral cavity, lower GI tract, and vagina
  2. Neonatal: early onset infection and late onset
167
Q

Strep Agalactiae:

Early neonatal infection:

  1. More common when?
  2. Most common presentations?
  3. Regardless of the focus of infection, most have _____ ____ presenting with?
A

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
Q

Strep Agalactiae:

Late neonatal infection:

  1. When does it present?
  2. Presentation?
A

Strep Agalactiae:

Late neonatal infection:

  1. Presents more than 7 days after birth
  2. 60% septicemia and/or meningitis (35%)
169
Q

Strep Agalactiae:

Adult infection:

Most common in who?

A

Strep Agalactiae:

Adult infection:

Most common in pregnant women, the elderly, or those with underlying disease (diabetes most common)

170
Q

Strep Agalactiae:

Adult infection:

  1. Elderly and those with underlying disease: most common infections are?
  2. Pregnant women: common infections?
A

Strep Agalactiae:

Adult infection:

  1. Elderly/disease: bacteremia/septicemia, skin/soft tissue infection, and UTI
  2. Pregnant: UTI, bacteremia/septicemia, and chorioamnionitis
171
Q

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?
A

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
Q

S. pneumoniae:

Pneumonia:

  1. First colonization of ____ followed by aspiration where?
  2. Invades what cells? Moves from alveolus to alveolus through?
  3. Hallmark is inflammatory infiltrate composed of ____ followed later by _______.
A

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
  3. Hallmark is inflammatory infiltrate composed of neutrophils followed later by macrophages
173
Q

S. pneumoniae:

Pneumonia:

  1. Pathologically there is ____ effusion, consolidation from ____, and eventually ____.
  2. Presentation?
A

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
Q

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?
A

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
Q

S. pneumoniae:

Acute otitis media:

  1. Definition?
  2. Presentation?
  3. Most common cause?
  4. Other causes of S. pneumoniae?
A

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
Q

Corynebacterium diphtheriae:

  1. Gram?
  2. Shape? Cell walls similar to _____, how?
  3. Oxygen requirement?
  4. Look on tellurite agar?
A

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
Q

Corynebacterium diphtheriae:

Diphtheria:

  1. Disease manifestations are mediated by? This toxin is produced when? MOA?
  2. Transmission? Incubation?
A

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
Q

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?
A

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
Q

Listeria monocytogenes:

  1. Gram?
  2. Faculative _____ and faulative ____ pathogen.
  3. Mode of transmission?
A

Listeria monocytogenes:

  1. Gram +
  2. Faculative psychrophile (grows in extreme cold) and faculative intracellular pathogen
  3. Contaminates food –> ingestion
180
Q

Listeria monocytogenes:

  1. How does it escape immune detection and spread between cells?
  2. Infections?
A

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
Q

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?
A

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
Q

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
A

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
Q

Bacillus anthracis:

  1. The major pathalogic consequences of the toxins are increased _____ _____ and _____ (DIC)
  2. 3 different types of anthrax and route of transmission?
A

Bacillus anthracis:

  1. The consequences are increased vascular permeability and thrombosis (DIC)
  2. Intestinal (ingestion), inhalation (endospores inhaled), cutaneous (inoculation of skin)
184
Q

Bacillus anthracis:

Intestinal anthrax:

  1. Incubation period?
  2. Presentation?
  3. Very high _____ rate.
A

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
Q

Bacillus anthracis:

Inhalation anthrax:

  1. Incubation period?
  2. Initial symptoms?
  3. Later stages involve?
A

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
Q

Bacillus anthracis:

Cutaneous anthrax:

  1. Incubation period?
  2. Signs?
A

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
Q

Nocardia:

  1. These are partially ____-___
  2. Oxygen requirements?
  3. Infections are exogenous, _____, and do NOT produce _____
  4. What is found in the lesions?
A

Nocardia:

  1. These are partially acid-fast
  2. Strict aerobes
  3. Exogenous, suppurative, and do not produce granulomas
  4. Sulfer granules
188
Q

Nocardia Asteroides:

  1. Causes ____ ___ infections in the immunocompromised that disseminates where?
  2. Lesions characterized how?
  3. Most common CNS manifestation?
A

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
Q

Nocardia Brasiliensis:

  1. Where does this occur (part of the world)?
  2. Disease is known as?
  3. Presentation?
A

Nocardia Brasiliensis:

  1. This occurs in central and south america
  2. Known as madura foot
  3. Swelling, pain, acscesses, and draining sinuses
190
Q

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?
A

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
Q

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?
A

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
Q

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?
A

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
Q

Nisseria Meningitidis:

Meningococcemia:

  1. Pathology is associated with ___ and ___ that induce endotheilal necrosis, ____, DIC, and _____
  2. Presentation?
  3. Severe/acute onset form involves?
A

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
Q

Nisseria Meningitidis:

Meningitis:

  1. Presentation?
  2. What is less common in N. meningitidis in comparison to other causes of purulent meningitis?
A

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
Q

Nisseria Gonorrhoeae:

  1. Pili bind to ____ and penetrate (mediated by ___ proteins) and grow intracellularly –> pass into the ____ tissue and induce ______.
  2. Incubation period?
A

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
Q

Nisseria Gonorrhoeae:

  1. Genital infection in men presentation? Most common complication?
  2. Genetial infection in women presentation? If left untreated how does it present?
A

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
Q

Bordetella pertussis:

  1. Also known as?
  2. Gram?
  3. Shape?
  4. Oxygen requirement?
A

Bordetella pertussis:

  1. Whooping cough
  2. Gram -
  3. Bacilli
  4. Aerobe
198
Q

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?
A

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
Q

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 ____.
A

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
Q

Bordetella pertussis:

  1. Presents with the ___ stage after 10 day incupation characterized by ___ and ___.
  2. Late stage also has ___ with mostly lymphocytes
A

Bordetella pertussis:

  1. Presents with the catarrhal stage characterized by rhinorrhea and fever
  2. Late stage also has leukocytosis with mostly lymphocytes
201
Q

Bordetella pertussis:

  1. The catarrhal stage is followed by the ____ ____ stage characterized by?
  2. What is the last stage? What does it present with?
A

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
Q

Pseudomonas aeruginosa:

  1. Gram?
  2. Oxygen requirement?
  3. Virulence factors?
A

Pseudomonas aeruginosa:

  1. Gram -
  2. Aerobe
  3. LPS, capsule/glycocalyx/biofilm, heat-labile hemolysin, exotoxins A and S, and antibiotic resistance
203
Q

Pseudomonas aeruginosa:

Virulence factors:

  1. Capsule/glycocalyx/Biofilm function?
  2. Exotoxins A and S function?
  3. Type ____ secretion. What is this?
A

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
Q

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 _______ ________.
A

Pseudomonas aeruginosa:

  1. Nosocomial RTI –> necrotizing pneumonia
  2. Pneumonia in CF patients
  3. Necrotic lesions of ecythema gangrenosum
205
Q

Pseudomonas aeruginosa:

  1. What other things can it cause?
A

Pseudomonas aeruginosa:

  1. External otitis, keratitis, nosocomial UTI, wound and burn infections, and generalized folliculitis (often associated with whirlpools, pools, and hottubs)
206
Q

Yersinia pestis:

  1. Secretion?
  2. What products mediate host cell adherance?
  3. ____ gene products are cytotoxic
  4. Function of V and W Ags?
A

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
Q

Yersinia pestis:

  1. Mode of transmission?
  2. 3 clinical syndromes?
A

Yersinia pestis:

  1. Flea bite
  2. Bubonic plague, pneumonic plague, and septicemic plague
208
Q

Yersinia pestis:

Bubonic plague:

  1. Incubation?
  2. Symptoms?
A

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
Q

Yersinia pestis:

  1. Pneumonic plague involves a rapidly progressive?
  2. Septicemic plague: what occurs?
A

Yersinia pestis:

  1. Rapidly progressive hemorrhagic and necrotizing pneumonia
  2. Septicemic plague: endotoxemis and shock, DIC, thrombi, and vascular collapse
210
Q

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
A

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
Q

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?
A

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
Q

Mycobacteria Tuberculosis:

Primary pulmonary TB:

  1. Transmission?
  2. Pathology?
  3. Most individuals are ___ or have mild ____ with ___ symptoms. The lesions heal with?
A

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
Q

Mycobacteria Tuberculosis:

Progressive primary TB:

  1. When does this occur?
  2. Presentation?
  3. There are usually expanding areas of? with?
A

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
Q

Mycobacteria Tuberculosis:

Progressive primary TB:

  1. There is erosion of? Causes?
  2. Healing?
A

Mycobacteria Tuberculosis:

Progressive primary TB:

  1. Erosion of blood vessels resulting in hemoptysis
  2. Heal with fibrosis
215
Q

Mycobacteria Tuberculosis:

Secondary TB:

  1. Who gets secondary TB?
  2. The lesions are localized where?
  3. Symptoms?
A

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
Q

Mycobacteria Tuberculosis:

What is miliary TB?

A

Mycobacteria Tuberculosis:

Miliary TB is when it disseminates viea the blood to the rest of the body

217
Q

Mycobacterium avium-intracellulare:

  1. Causes a ____ infection and disseminated disease in ____ patients, usually when ___ counts are very low.
  2. Pathologic hallmark?
A

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
Q

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 ___.
A

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
Q

Mycobacterium Leprae:

  1. Invasion of schwann cells also causes?
  2. What mediates tissue damage early in the infection?
A

Mycobacterium Leprae:

  1. Rapid demyelination of peripheral nerves
  2. CMI mediates early tissue damage
220
Q

Mycobacterium Leprae:

Leprosy:

  1. Definition?
  2. What are the 4 forms?
A

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
Q

Mycobacterium Leprae:

Leprosy:

  1. Indeterminant involves?
  2. Tuberculoid involves?
  3. Borderline involves?
  4. Lepromatous involves?
A

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
Q

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
A

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
Q

Mycobacterium Leprae:

Leprosy:

  1. What else is usually heavily infected?
  2. May also present with ___ ___ ___ from cutaneous deposition of immune complexes.
A

Mycobacterium Leprae:

Leprosy:

  1. Respiratory tract is usually heavily infected
  2. May also present with erythema nodosum leprosum from cutaneous deposition of IC
224
Q

Treponema Pallidum:

  1. Also known as?
  2. Gram?
  3. Tissue damage is caused by?
  4. Mode of transmission?
A

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
Q

Treponema Pallidum:

  1. Incubation period is proportional to?
  2. Syndromes? (5)
A

Treponema Pallidum:

  1. Incubation period proportional to size of the inoculum
  2. Syndromes: primary, secondary, latent, late, and congenital
226
Q

Treponema Pallidum:

Primary syphilis:

  1. Characterized by?

Latent syphilis:

  1. Manifestation?
  2. Length of this stage?
A

Treponema Pallidum:

Primary syphilis:

  1. Characterized by chancre (inflammatory lesion with plasma cells, macrophages, lymphocytes) at site of entry

Latent

  1. No clinical manifestation
  2. Can last 10 years
227
Q

Treponema Pallidum:

Secondary syphilis:

  1. Characterized by?
  2. When does it occur?
  3. What occurs to skin?
  4. What occurs to mucous membranes?
A

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
Q

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?
A

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
Q

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?
A

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
Q

Treponema Pallidum:

Congenital syphilis:

  1. Early Presentation?
  2. Late presentation?
A

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
Q

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?
A

Relapsing fever

  1. B. recurrentis in s. america with lice vector
  2. Western us = B. hermsii with a tick vector
232
Q

Borrelia hermsii:

  1. Incubation period?
  2. Initial symptoms?
  3. Initial symptoms are followed by? Then?
A

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
Q

Borrelia burgdorferi:

  1. Also known as?
  2. Vector? Time?
A

Borrelia burgdorferi:

  1. AKA: lyme disease
  2. Deer tick - must be attached for more than 24 hrs
234
Q

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?
A

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
Q

Borrelia burgdorferi (Lyme disease):

Early disseminated disease:

  1. Occurs ____ ___ after the tick bite.
  2. Presentation?

Late disease:

  1. When does this occur?
  2. Involves?
A

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:

  1. weeks to months after infection
  2. Arthritis of large joints and rarely CNS
236
Q

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?
A

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
Q

Peptostreptococcus and Streptococcus:

  1. These are non-___ forming gram ____ ___.
  2. Oxygen requirements?
  3. 4 main infections?
A

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
Q

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 ____
A

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
239
Q

Clostridium Perfringens:

  1. Oxygen? Gram? Shape? Spores?
  2. 3 Exotoxins?
  3. Major infections (2)?
A

Clostridium Perfringens:

  1. Anaerobic; Gram +; Rod; Spore-forming
  2. Alpha-toxin, beta-toxin, and theta-toxin
  3. Cellulitis and myonecrosis (gas gangrene)
240
Q

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
A

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
241
Q

Clostridium Perfringens:

Cellulitis:

  1. Characterized by?
  2. Amount of necrosis is ____ to the amount of inflammatory ____ and ____ present
A

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
242
Q

Clostridium Perfringens:

Myonecrosis (gas gangrene)

  1. Acute onset of?
  2. Extensive ___ exudate with sparse ____ cells, extensive _____, vascular damage, and _____.
  3. Color of skin?
A

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
243
Q

Clostridium tetani:

Produces a ___ sensitive ____ that blocks the release of ____ neurotransmitters by degrading ____; this causes unregulated synaptic activity and ____ ____

A

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

244
Q

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?
A

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
245
Q

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?
A

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
246
Q

Obligate intracellular bacteria:

Examples?

A

Obligate intracellular bacteria:

a. Chlamydia
b. Chlamydophila

247
Q

Chlamydia trachomatis:

Causes what 3 infections?

A

Chlamydia trachomatis:

a. Lymphogranuloma venerum
b. Trachoma
c. Oculogenital

248
Q

Chlamydia trachomatis:

Lymphogranuloma venerum:

  1. Serotypes:
  2. Most characteristic?
  3. Presentation?
A

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
249
Q

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?
A

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
250
Q

Chlamydia trachomatis:

Oculogenital:

  1. Serotypes?
  2. Men?
  3. Women?
A

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
251
Q

Rickettsial infections:

Name 3.

A

Rickettsial infections:

a. Ehrlichia chaffeensis (human monocytis ehrlichiosis)
b. Anaplamsa phagocytophilum (human granulocytis anaplamosis)
c. Rickettsia rickettsii (rocky mountain spotted fever)

252
Q

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 ____
A

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
253
Q

Ehrlichia chaffeensis: human monocytic ehrlichiosis:

  1. Presentation?
  2. Some also have?
A

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)
254
Q

Anaplasma phagocytophilum: human granulocytic anaplasmosis:

  1. Transmission?
  2. Bugs enter the blood and disseminate where?
A

Anaplasma phagocytophilum: human granulocytic anaplasmosis:

  1. Deer ticks
  2. Enter blood and disseminate to bone marrow and the spleen
255
Q

Anaplasma phagocytophilum: human granulocytic anaplasmosis:

  1. In bone marrow it infects? Results in?
  2. Presentation?
A

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
256
Q

Rickettsia rickettsii: Rocky mountain spotted fever:

  1. Transmission?
  2. Results in ____ lesions (with necrosis and _____)
A

Rickettsia rickettsii: Rocky mountain spotted fever:

  1. Wood or dog tick
  2. Vascular lesions (necrosis and thrombosis)
257
Q

Rickettsia rickettsii: Rocky mountain spotted fever:

  1. Major effect of endothelial injury?
  2. Presentation?
A

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
258
Q

Fungal infections:

Name several.

A

Fungal infections:

a. Candida albicans
b. Cryptococcus neoformans
c. Aspergillus
d. Mucormycosis

259
Q

Candida albicans:

  1. Can grow as ____ or ____.
  2. Cutaneous/mucous membrane infections?
A

Candida albicans:

  1. Can grow as yeast__s or filaments
  2. Cutaneous/mucous membrane infections: oral candidiasis, genital candidiasis, and generalized intertriginous candiasis
260
Q

Candida albicans:

  1. Oral candiasis: aka? Main presentation?
  2. Genital candidiasis: presentation?
  3. Generalized intertriginous candidiasis: lesions are?
A

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)
261
Q

Candida albicans:

Systemic candida infections? (8)

A

Candida albicans:

Systemic infections: esophagitis, GI candidiasis, Fungemia, bronchopulmonary candidiasis, urinary tract, endocarditis, hepatosplenic candidiasis, and CNS candidiasis

262
Q

Candida albicans:

Esophagitis:

a. Common in who?
b. Presentation?

A

Candida albicans:

Esophagitis:

  1. Common in AIDS and hematologic malignancies
  2. Pseudomembranes, ulcerations, and pain on swallowing
263
Q

Candida albicans:

GI candidiasis:

  1. Common in?
  2. Presentation?
A

Candida albicans:

GI:

  1. Common in hematologic malignancies
  2. Numerous gastic lesions and GI bleeding
264
Q

Candida albicans:

  1. Fungemia: presentation?
  2. Bronchopulmonary: presentation?
  3. Urinary tract: presentation?
A

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
265
Q

Candida albicans:

  1. Endocarditis: from? Presentation?
  2. Hepatosplenic candidiasis: presentation?
  3. CNS candidiasis: occurs in who? Presentation?
A

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
266
Q

Cryptococcus neoformans:

  1. Capsule serotype A =?
  2. Capsule serotype D = ?
  3. Capsule serotypes B and C = ?
A

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
267
Q

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?
A

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
268
Q

Cryptococcus neoformans:

3 infections?

A

Cryptococcus neoformans:

a. Acute pulmonary cryptococcosis
b. Skin lesions
c. CNS infection

269
Q

Cryptococcus neoformans:

  1. Acute pulmonary cryptococcosis - presentation?
  2. Skin lesions: presentation?
  3. CNS infection: who? Results in?
A

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
270
Q

Aspergillus:

  1. What causes 90% of infections? 10%?
  2. Mode of transmission?
  3. Induction of ____ response may limit infection
  4. Infections?
A

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
271
Q

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?
A

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
272
Q

Aspergillus:

  1. Invasive sinusitis: occurs in who? And involves a very aggressive infection that ______________
  2. Invasive pulmonary aspergillosis: underlying conditions that predispose? Characterization?
A

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
273
Q

Mucormycosis:

  1. Disease is limited to?
  2. Major genera? (4)
A

Mucormycosis:

  1. Disease is limited to immunocompromised, diabetics, and those with severe trauma
  2. Genera: Rhizopus, Rhizomucor, Absidia, and Mucor
274
Q

Mucormycosis:

  1. Mode of transmission? Hyphae invade ___ and ___ causing _____ and necrosis.
  2. Major syndromes?
A

Mucormycosis:

  1. Inhalation; hyphae invade tissue and blood causing thrombosis and necrosis
  2. Syndromes: rhinocerebral mucormycosis, pulmonary mucormycosis, and cutaneous mucormycosis
275
Q

Mucormycosis:

  1. Rhinocerebral: occurs in who? Presentation?
  2. Pulmonary: occurs in who? Causes a highly ____ ____ presenting with?
  3. Cutaneous:how does one get it
A

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
276
Q
A

Pathology (11 decks)

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