Exam 2: Week 9, Monday (Infectious Diseases, Viruses and Fungi) Flashcards

1
Q

Definition of infection:

A

Process in which an organism establishes a parasitic relationship with the host

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2
Q

immune response

  • What is it produced by?
  • What does it do? (simple)
A

•- Produced by invasion and multiplication of an organism

  • •Produces injury to the host due to toxins from microorganisms and tissue/cell death of host
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3
Q

Development of an infection depends on what three things?

A
  1. Transmission
  2. Proper environment
  3. Susceptibility of the host
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4
Q

Two outcomes of pathogen invasion:

A
  1. Colonization of organisms- microorganisms present in tissue but do not create systemic disease
    • You will be a carrier and transmitter of disease but may not have signs and symptoms
  2. Clinically apparent infection- host injury with signs and symptoms
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5
Q

What is the significance of the fact that different types of organisms (I think she means pathogens) vary in shape, size, structure, growth requirments, and ability to stay alive? (2 main)

A
  • Provides a basis for identification of organism (and therefore diagnosis)
  • Allows for development of a treatment
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6
Q

Characteristics of Viruses (4)

  • how many types?
  • what are they made from?
  • dependent or not dependent on host?
  • pharma treatment?
A

•over 400 that infect humans,

made up of RNA or DNA nucleus covered in protein

dependent on host for replication

antivirals- interfere with illness limiting time necessary for healing

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7
Q

Characteristics of Mycoplasmas (3)

What are they?

dependent or not dependent on host?

pharma treatment?

A

•Mycoplasmas-

self replicating bacteria

require host,

sensitive to some antibiotics

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8
Q

Characteristics of Bacteria (3)

What are they?

dependent or not dependent on host?

pharma treatment?

A

•Bacteria-

single-cell microorganism of many variations -

  • rod, spherical, spiral, gram positive/negative (staining), motility, tendency toward capsulation, capacity to form spores, aerobic, anaerobic;

do not require host,

specific antibiotic for type

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9
Q

Name 9 things Varieties of bacteria are based on:

A
    • rod,
  1. spherical,
  2. spiral,
  3. gram positive/negative (staining),
  4. motility,
  5. tendency toward capsulation,
  6. capacity to form spores,
  7. aerobic,
  8. anaerobic
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10
Q

What are Rickettsiae?

A

•- animal pathogen that effects humans via insect bite (tick, flea)

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11
Q

What are Chlamydia (not the specific disease)?

pharma treatment?

A

•smaller than bacteria but larger than virus,

respond to some antibiotics

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12
Q

What are protozoa?

A

•single cell or loosely bound group of cells, parasites (round and flatworms)

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13
Q

what are fungi?

Alterate name?

example?

A
  • yeasts or molds,
  • called mycoses in humans -
  • Example: athlete’s foot (medical name is Tinea pedis)
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14
Q

What is the term for fungi in humans?

A

mycoses (a disease caused by infection with a fungus, such as ringworm or thrush)

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15
Q

what is the medical term for Athlete’s Foot?

A

Tinea pedis

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16
Q

What are Prions?

examples

A

proteins without nucleic acid -

Nasty little things that are hard to treat

Examples:

  • Creutzfeldt-Jakob Disease (humans) or
  • mad cow disease (bovine
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17
Q

8 Infectious Organisms

A
  1. •Viruses- over 400 that infect humans, made up of RNA or DNA nucleus covered in protein, dependent on host for replication, antivirals- interfere with illness limiting time necessary for healing
  2. •Mycoplasmas- self replicating bacteria require host, sensitive to some antibiotics
  3. •Bacteria- do not require host, single-cell microorganism of many variations - rod, spherical, spiral, gram positive/negative (staining), motility, tendency toward capsulation, capacity to form spores, aerobic, anaerobic; specific antibiotic for type
  4. •Rickettsiae- animal pathogen effects humans via insect bite (tick, flea)
  5. •Chlamydia- smaller than bacteria but larger than virus, respond to some antibiotics
  6. •Protozoa- single cell or loosely bound group of cells, parasites (round and flatworms)
  7. •Fungi- yeasts or molds, called mycoses in humans - Tinea pedis (skin), athlete’s foot
  8. •Prions- proteins without nucleic acid - Creutzfeldt-Jakob Disease (humans) or mad cow disease (bovine)
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18
Q

How are viruses classified?

A

Classified by how they reproduce

Classified as replicating DNA or RNA

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19
Q

How do viruses interact with the body?

A

Virus invades the host cell, takes control of the cell’s metabolic function, and uses the cell’s synthesizing mechanisms to “crank out new viruses.”

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20
Q

What do viruses consist of, and why do I care?

A

•Viruses consist of genetic material and a protein shell (capsid) – no cellular components for reproduction, which is why it needs to take over a host cell

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21
Q

Explain the 4 steps of Viral Replication in the Host Cell

A
  1. adsorption – virus attaches to host cell wall
  2. penetration and uncoating – enters or fuses with cell wall, releasing its genetic material inside and removing any remaining viral coating
  3. biosynthesis – takes control of cell’s synthesizing system (DNAor RNA)
  4. maturation and release – mature virus genetic material and core cell released, sometimes killing host cell, but if not, host cell remains infected

(picture is an example of a virus taking over a bacterial host cell)

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22
Q

Blood borne Viral Pathogens: What are the three most common dangers to healthcare workers?

When are we at greatest risk?

A
  1. Hepatitis B (HBV)
  2. Hepatitis C (HCV)
  3. HIV (Human Immunodeficiency Virus)

Greatest risk during invasive procedures or digital palpation of sharps

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23
Q

What point did Dr. T make about using up extra protective equipment?

A

She never faults anybody for using up extra protective equipment. It is better to prevent infection than try to treat it after it has spread.

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24
Q

How many herpesivrus types are there?

A

8

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25
Q

List the 8 types of herpesviruses

A
  1. •Herpes simplex virus (HSV-1), Type 1, cold sores, visceral organs, mucocutaneous areas
  2. •Herpes simplex virus (HSV-2), Type 2, genital herpes
  3. •Type 3, varicella-zoster; chicken pox and shingles
  4. •Type 4, Epstein-Barr infectious mononucleosis virus (EBV)
  5. •Type 5,Cytomegalovirus (CMV)
  6. •Type 6, Roseola human herpes virus (HHV)
  7. •Type 7, Herpes serologically associated with roseola (HHV)
  8. •Type 8, Human herpes associated with Kaposi’s sarcoma (HHV)
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26
Q

HSV-1 stands for:

Causes:

A

Herpes simplex virus, type 1

Causes: Cold sores, visceral organs, mucocutaneous areas

Can cause pneumonia - cold sores in the lungs (terrible to treat)

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27
Q

What is the biggest category of viruses we will see?

A

Herpes viruses

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28
Q

What does HSV-2 stand for?

Example

A

Herpes Simplex Virus, type 2

genetal herpes

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29
Q

2 examples of herpes virus type 3 (common name, medical name)

A

Chicken Pox (Herpes Varicella)

Shingles (Herpes Zoster)

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30
Q

What does EBV stand for?

exmaple

A

Epstein-Barr virus (herpes type 4)

Mononucleosis virus

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31
Q

What does CMV stand for?

A

Cytomegalovirus (Herpes Type 5)

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32
Q

What does HHV stand for?

A

Roseola Human Herpes virus (herpes type 6)

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33
Q

What virus is serologically associated with roseola?

A

type 7

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34
Q

What virus is associated with Kaposi’s sarcoma?

A

Herpes type 8

Also a human herpes virus

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35
Q

What are the three Human Herpes Viruses?

A
  • Type 6, Roseola human herpes virus (HHV)
  • Type 7, Herpes serologically associated with roseola (HHV)
  • Type 8, Human herpes associated with Kaposi’s sarcoma (HHV)
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36
Q

Chicken Pox:

Transmission?

When is it contagious?

vaccine?

Anything else?

A

•Airborne transmission,

highly contagious from 1-2 days before onset until lesions crust over

now there is a vaccine (but it is new enough that many of us will not have recieved it)

Only get chicken pox once (then you are suceptible to Shingles)

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37
Q

Herpes Zoster

4 characteristics

2 possible symptoms

A

You are succeptible if you have had chicken pox (virus dormanat inside your nerve roots, reactivates to become Shingles)

Older people more susceptible

Now there is a vaccine, but only reccomended for older adults

Can be very painful (so much so that you do not want clothing touching you)

Symptoms:

  1. •Eruption follows dermatome
  2. •Post-herpetic neuralgia (PHN) may last throughout lifetime
    • •Pain, hyperalgesia (increased pain from a painful stimulus), allodynia (painful reaction to a non-painful stimulus) – hyperalgesia and allodynia are common in true neuropathic pain
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38
Q

Roseola characteristics:

Symptoms

usual population

A

•Roseola –

Population: most common in children, age 6 mo – 3 years;

Symptoms: fever, rash,

(very scary looking butnot usually too serious)

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39
Q

Infectious Mononucleosis Symptoms (4 particularly distinctive in bold)

A
  • Central
    • fatigue
    • malase
    • loss of appetite
    • headache
  • Throat
    • soreness
    • Reddeining
  • Respiratory: cough
  • Systemic
    • Chills
    • Fever
    • Aches
  • Gastric: Nausea
  • Spleen
    • enlargement
    • abdominal pain
  • Lymph nodes
    • swelling
  • Tonsils
    • reddening
    • swelling
    • white patches
  • Visual
    • photophobia
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40
Q

Infectious Mononucleosis characteristics:

common population

cause

incubation time

complication risk

What other disease is it associated with?

A

Used to be called the kissing disease

Often spread in athletes because of sharing drinks, etc.

Caused by Epstein Barr virus (Herpes type 4)

  • May incubate for 4-6 weeks
  • Major complications rare, but splenic rupture is most common (Kehr’s sign)
  • Association between infectious mononucleosis and subsequent development of multiple sclerosis (MS) – twice as likely – may be associated with immune response
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41
Q

Cytomegalovirus (CMV) details (5)

A
  1. •Common virus, common opportunistic infection in AIDS (check CD4 count)
  2. •Many people do not know they are infected because they show no symptoms
  3. •Once infected, body retains virus for life - usually remains dormant if you’re healthy
  4. •Active CMV: fever, pheumonia, diarrhea, ulcers in GI tract, hepatitis, encephalitis, behavioral changes, seizures, coma, visual changes or blindness
  5. •Spread through body fluids
    • very transmissible
    • some babies are born with it (see picture)
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42
Q

What is Kaposi’s Sarcoma? (3)

A
  • Herpes virus type 8
  • Highly associated with AIDS.
  • Look sort of like big sores or moles but not quite (sort of like in between the two).

From Wikipedia: Kaposi sarcoma (/kəˈpoʊsiː sɑrˈkoʊmə/; KS) is a tumor caused by infection with human herpesvirus 8 (HHV8), also known as Kaposi sarcoma-associated herpesvirus (KSHV) or KS agent. The viral cause for this cancer was discovered in 1994. (https://en.wikipedia.org/wiki/Kaposi’s_sarcoma)

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43
Q

Sexually Transmitted Infections:

two abbreviations

estimated prevelance in USA

causes

spread by

healthcare safety

A
  1. STI, STD
  2. Estimated that 56 million Americans (1 in 4) is carrying an STI other than HIV
  3. •Caused by bacteria, viruses, even parasites
  4. •Sexual contact and shared drug paraphernalia may spread diseases
  5. •Contact precautions for healthcare workers

See Table 8-7, p. 343-346 in Goodman & Fuller for table that goes through severeal STIs

See Figure 8-11, p. 345 in Goodman & Fuller – physical manifestations that indicate potential STI

44
Q

What are the three most common side effect of any drug? (remember for board exam)

A
  1. Headaches
  2. Dizziness
  3. GI Problems
45
Q

Where can you find a table of Anti-Viral Drugs?

A

Ciccone, Table 34-2

(pg 526 in 4th edition)

It is a long list of antiviral drugs (genaric name, trade name, principal indications)

It doesn’t look like something Dr. T would expect us to memorize, so I am going to make flash cards only the specific medications she included on the powerpoints.

46
Q

Name two Anti Viral Drugs used on Herpes Simplex I and II:

how are they administered?

Adverse affects?

A
  • •Acyclovir (Zovirax) and Valacyclovir (Valtrex)
  • Administered for
    • Topical and mucosal infections
    • •Can also be administered orally or by IV
      • •Valacyclovir is usually oral (better absorption)
  • •Topical adverse effects – local irritation
  • •Systemic adverse effects – headaches, dizziness, GI problems
47
Q

True/False: A lot of antiviral drugs are topical

A

True

48
Q

What is the relationship between Acyclovir and Valacyclovir?

A

Both are used to treat Herpes simplex I and II

Valacyclovir converts to acyclovir in the bloodstream – is a precursor, or “prodrug” of acyclovir

49
Q

What two antiviral drugs are good for Influenza A virus?

How effective?

When can they be given?

A
  1. Amantadine (Symmetrel) and Rimantadine (Flumadine)
  2. Used on influenza A virus – can be 70-90% effective in preventing influenza A if used prophylactically, so can be used in high-risk patients during flu season
  3. If given when flu symptoms first appear, can lessen the effects of the infection
    1. Certain strains of influenza A now showing resistance
50
Q

What point did Dr. T make about prophylactic use of antiviral drugs?

A

Many are the most effective if taken prophylactically, but we don’t want to put everyone on the such high-powered drugs for something that MIGHT happen. Therefore, we might only use the drug prophylactically on pts at high risk for contracting the virus or for whom contracting the virus could cause serious complications.

A good example is prophylactic use of Amantadine and Rimantadine for Influenza A virus.

51
Q

What is an off label use for Amatadine?

A

Amantadine also useful for motor abnormalities of Parkinson’s Disease, possibly by blocking excitatory neurotransmitters in the basal ganglia

52
Q

How are Amantadine and Rimantadine administered?

What are some adverse effects?

A
  • Both drugs are administered orally
  • Adverse effects –
  • CNS symptoms (confusion, loss of concentration, light-headedness, mood changes);
  • seizures in higher doses
53
Q

What is an anti viral drug used primarily to treat CMV in AIDS?

How is it it administered?

What are adverse affects?

A
  • •Cidofovir (Vistide) – primarily used to treat cytomegalovirus (CMV) in AIDS
  • •Administered by IV
  • Adverse Effects
  • •Renal excretion, so can be highly nephrotoxic
    • Also decreases neutrophilic leukocytes, resulting in neutropenia
      • Neutropenia signs – fever, chills, sore throat
      • Also GI side effects – nausea, diarrhea, anorexia
54
Q

True/False: CMV in AIDS is not life-threatening, so it doesn’t always need to be treated.

A

False

Must treat because Cytomegalovirus is life threatening in immunocompromised patients

55
Q

What anti-viral medication can be used to treat RNA and DNA viruses?

what is a common specific disease that it is used for (and some symptoms, common population)?

How is it administered?

Adverse effects?

A

Ribavirin (Virazole)

  • •Active against RNA and DNA viruses
  • •Respiratory syncytial virus (RSV) – causes severe pneumonia in infants, young children, elderly, immunosuppressed
  • •Administered via aerosol inhalation (mask for babies)
  • •Relatively few adverse effects

*Kids get RSV so easily, especially when kids go to day care.

*Ribavirin works best when we can administer it early before virus is in the cells

56
Q

What is Penciclovir (Denavir) primarily used for?

Method of administration?

A

•Penciclovir (Denavir) – primarily topical for Herpes simplex

57
Q

What is Docosanol (Abreva) usually used for?

How is it administered?

What is unique about its availability?

How does it work?

Adverse effects? (2)

A

•Docosanol (Abreva) – topical for Herpes simplex

  • •Available OTC
  • •Doesn’t act on the virus – acts on the host cells so that viral adsorption is inhibited. Best used as early as possible before virus can replicate
  • •Adverse effects – headaches, local irritation
58
Q

What are Interferons? (1)

three actions they perform

one more thing of significance

A

A group of proteins that exert specific antivral activity (highly specific)

They

  • Enable healthy cells to resist infection
  • Control cell differentiation, limit excess proliferation (helpful to stop cancer cells)
  • Influence the immune processes

•Initially, interferons were thought to be “the key” to viruses and cancer treatment – not the panacea that was hoped for, but still highly useful

59
Q

What table can you look at to see the types of Interferons?

A

Interferons (Ciccone, Table 34-4)

(page 534 in 4th edition; page 569 in 5th edition)

60
Q

What are the three classes of Interferons?

Which currently have corresponding pharmacological agents?

A

•Three classes, according to structure and how they affect cell receptors (Type I, alpha and beta; Type II, gamma; Type III, lambda)

  • •Only Type I and II pharmacological agents currently exist; Type III still in development
61
Q

What types of cells can produce interferons?

A

•Virtually all body cells are capable of producing interferons and can prevent the virus from attacking healthy cells

62
Q

How do Interferons work?

A
  • •Cells that are infected can produce interferons that travel to non-infected cells, bind to specific receptors on their surfaces, and signal pathways to produce antiviral proteins
    • Now even if the virus penetrates that cell containing the antiviral proteins, it cannot synthesize itself
63
Q

How are interferons effective against several forms of cancer?

A

•By limiting abnormal cell proliferation and activating the immune system, interferons are also effective in several forms of cancer

64
Q

What type of interferons are useful in hepatitis B and C?

A

Type I interferon useful in hepatitis B and C (Type III investigations in this area as well)

65
Q

How did Dr. T describe cancer treatment drugs?

A

Cancer treatment is mostly a mixture of medications that work on different mechanisms of cancer (cell) replication. May target different mechanisms of replication at alternating or different times.

66
Q

What type of Interferon is useful in MS?

How does it work?

Medication names?

Adverse effects?

How is it administered?

A
  • •Type II used in MS (book says type I [beta 1a and beta-1b - I think that is correct])
    • •modulation of autoimmune responses that initiate the pathological changes seen in exacerbating-remitting MS)
    • •Betaseron, Avonex, Rebif
  • •Adverse effects – flu-like symptoms, fatigue, loss of appetite, GI symptoms, depression (inhibits serotonin activity)
  • •Administered orally or IM
67
Q

What are three other conditions that interferons are useful for?

A

Other uses: viral warts, leukemias, lymphomas

68
Q

How do vaccines work? (4)

A
  • •Vaccines stimulate endogenous production of immune factors to kill the invading virus
  • •Does not affect the host because the vaccine virus is modified to retain antigenic properties, but not able to infect
    • •Killed vaccine – whole or partial virus that is completely inactivated
    • •Live attenuated vaccine – partially inactivated
  • •Works by creating an “imitation infection” that stimulates T-lymphocytes and antibodies
  • •Once the imitation infection is over, the immune memory cells (Both B and T) remain present
69
Q

Does a vaccine infect the host (the person) with the virus?

A

No

It does not affect the host because the vaccine virus is modified to retain antigenic properties, but not able to infect

Person may feel a small immune response because of the antigenic properties, but will not have actual disease. (this is why people think the flu shot gives them the flu)

70
Q

What are two forms of vaccine?

A
  • Killed vaccine – whole or partial virus that is completely inactivated
  • Live attenuated vaccine – partially inactivated
71
Q

Is it easier to develop a vaccine than to treat a viral infection?

Are vaccines permenantly effective?

A

•Easier to develop a vaccine than to treat a viral infection

  • – in vaccine, the virus essentially co-exists with the healthy cells, selectively inhibited by your immune system
  • – any vaccine may require booster, titers determine level of immunity in your system
72
Q

Example of a killed vaccine that requires annual booster

A

Flu shot

73
Q

Examples of live attenuated vaccines (5)

A
  1. •measles,
  2. mumps,
  3. rubella (MMR),
  4. chicken pox,
  5. nasal flu mist
74
Q

True/false: there are no vaccines for bacterial diseases

A

false: There are at least two types

  1. •Toxoid vaccines – prevent bacterial diseases that produce toxins (Example: TDaP for diphtheria and tetanus, with a subunit for pertussis)
  2. •Conjugate vaccines – for polysaccharide-coated bacteria (Examples: Hib, H.Influenza B)
75
Q

what are some miscelanneous infectious diseases?

Describe their details

A

•Prostheses and implant infections

  • •Biodegradation of older prostheses and implants
  • •Repeat surgical procedures for replacements
  • •Radiographs and needle aspirations are not always sufficient to diagnose – need to look at lab values, clinical picture, patient description of signs/symptoms

**Unfortunately fairly common.

**Infection may just be in a tiny pocket that gets missed by a needle.

**Listening to the patient is sometimes the only way you will know what is going on.

76
Q

Describe Lyme Disease

A
  • •Tick-borne spirochete bacteria
  • •Stage 1 – flu-like symptoms
  • •Stage 2, disseminated infection – may include aseptic meningitis, stiff neck, difficulty with mentation, cranial neuropathies, radiculopathies
  • •Stage 3, late persistent infections – if untreated, 6-% of infected individuals may have erosions or permanent joint abnormalities (Fig. 8-9)
  • •Post-infection syndromes resemble fibromyalgia or chronic fatigue syndrome – may be immune response, neurohormonal

Erethema migrans rash (see last test)

77
Q

What is HIV/AIDS?

A
  • Retrovirus that impairs CD4+ (T-helper lymphocytes)
  • Leads to severe immunocompromise
78
Q

Describe the two types of HIV

A

•HIV-1 more prevalent; HIV-2 less likely to progress to AIDS

79
Q

What do patients with HIV/AIDS usually die from?

A

pts usually die of multiple complications from multiple infections:

•AIDS is life-threatening, as it exposes the body to invasion by any microorganism

  • •Frequent invaders include Mycobacterium tuberculosis, fungal pneumonia, neoplastic diseases such as Kaposi sarcoma)
80
Q

What are complications from HIV/AIDS that PTs can help with?

How should we approach pt treatment?

A
  • Complications include neuromuscular involvement
    • •Peripheral neuropathies
    • •Myopathies
    • •CNS manifestations (dementia, psychological disturbances)
    • •Joint pain, back pain
  • HIV disease can be regarded as a degenerative neuromuscular disorder
    • Must develop good exercise protocols for these people so they can stay strong but not be torn down by too intense exercise.
  • Remeber HIV+ infection may not progress to AIDS for several years
81
Q

3 Anti-Viral Drugs for HIV

A

•Drugs targeted at viral replication, inhibiting necessary enzymes

  1. •HIV integrase inhibitors
  2. •HIV protease inhibitors
  3. •Reverse transcriptase inhibitors (RTIs), nucleoside reverse transcriptase inhibitors (NRTIs) and nonnucleoside reverse transcriptase inhibitors (NNRTIs)
82
Q

What is the primary goal of Anti-viral drugs for HIV?

What problems are there? (4 main)

What is critical?

A
  1. •Primary drug strategy is a combined approach of multiple drugs, called highly active antiretroviral therapy (HAART)
  2. •Problem of effectiveness
    • •No drug currently available to kill HIV
    • •Reduction of viral load not effective in about 20% of patients
    • •Compliance – side effects and understanding the regimen
    • •Viral resistance
  3. •Promotion of T-lymphocyte survival is critical to maintenance of a functional immune system
    • keep CDC over 100, can prevent AIDS for a long time
83
Q

What exercises are prohibited when working with a patient with HIV/AIDS?

A

there is nothing prohibited, but we should be mindful of exercise tolerance and cardiovascular endurance, and something they will be compliant with at home.

Treat as a degenerative neuromuscular disorder

84
Q

Four points about fungal infections

A
  1. •Over 200,000 fungi in nature; 200 species can cause human infection
  2. •Ringworm, athlete’s foot, candidiasis, vaginal yeast infections
  3. •May also see systemic diseases of lungs, CNS, any organ
  4. •Most problematic in immunocompromised patients
85
Q

Where can you find a table about Antifungal drugs?

A

Ciccone, Tables 35-1 and 2, systemic and topical antifungals

(pg. 546 and 547 in 4th edition)

86
Q

What type of infections do systemic antifungal agents treat?

A

For treatment of deep (invasive) infections – usually Candida or Cryptococcus

87
Q

7 Systemic Antifungal Agents

A
  1. Amphotericin B (Amphocin, Fungizone)
  2. Fluconazole (Diflucan)
  3. Flucytosine (Ancobon)
  4. Griseofulvin (Fulvicin, Grisactin)
  5. Itraconazole (Sporanox)
  6. Ketoconazole (Nizoral)
  7. Terbinafine (Lamisil)
88
Q

Details on Amphorectin B

  • Method of delivery
  • Negative affects
A

Amphotericin B (Amphocin, Fungizone),

  • usually via IV
  • High incidence of side effects – headache, joint and muscle pain, fever, weakness, GI upsets
89
Q

Details on Fluconazole

  • Method of delivery
  • Comparison to Amphotericin B
  • Negative affects
A

•Fluconazole (Diflucan)

  • •Can be IV or oral
  • •Better tolerated, but might not be as effective as amphotericin B
  • •Hepatotoxic, severe skins reactions (Stevens-Johnson Syndrome), headache, GI upsets
90
Q

Details on Ketoconazole

  • Method of delivery
  • Negative affects
A

Ketoconazole (Nizoral) –

  • mostly used locally, due to hepatotoxicity and impairment of testosterone and adrenocorticosteroid production
91
Q

Details on Ketoconazole:

  • Purpose
  • Method of delivery
  • Success rate
A

Terbinafine (Lamisil) –

  • systemic works better than local for athlete’s foot/nail fungus
  • fungal nails require weeks of treatment, success rate 30-60%
92
Q

What are some Local Antifungals?

what are some common adverse effects?

(three main ones, with extra details)

A
  1. Lamisil topical
  2. Jublia (effectiveness runs from 15-55% reported, 48 weeks of treatment)
  3. Azole antifungals (clotrimazole, miconazole, -zoles) – used for Candida infections (skin and membranes)
  4. Various others for cutaneous, oropharyngeal, vaginal infections

Mild adverse effects, usually local

93
Q

Where can you find a table about malaria and protozoal infections?

A

Ciccone table 35-3 and 35-4

94
Q

What was Malaria historicallyt reated with?

What is the med whose derivities are still in use today?

What are the most common adverse effects of antimalarials? (2)

A
  • Malaria historically treated with quinine since the 17th century – chloroquine developed in 1940s, derivatives of that still in use today
  • Adverse effects vary, most commonly GI effects, headache
95
Q

What is the most common protozoan?

Expalin where it comes from and what it does

A

most common is Toxoplasma gondii – found in many animals and birds, but reproduces in cats, both wild and domestic

  • •Found in cat feces
  • Causes Toxoplasmosis - Flu-like symptoms, parasites are walled off in cysts in the affected organs
96
Q

what is a helminth?

A

A parasitic worm

97
Q

what is the most common form of disease in the world?

A

Helminith

98
Q

Where can you find a table of antihelmintic medications?

A

Ciccone, Table 35-5 (page. 593 in 5th edition)

99
Q

Expalin 5 considerations for rehab patients in regards to fungal or protozoal infections.

A
  1. •Immunocompromised patients may frequently have fungal or protozoal infections, in addition to primary diagnoses
  2. •Medication compliance for long-term drugs must be encouraged
  3. •Working in underserved areas (poverty areas in US, international) will expose you to many patients with these infections
  4. •You may need to take prophylactic medicines as well
  5. •Will need to check side effects of medicines in use
100
Q

Tick bite and Ringworm:

Bacteria, Virus, or Fungi?

A

Tick Bite: Bacteria (lyme Disease)

Ringworm: Fungi

101
Q

______ are very oppurtunistic. These show up when?

A

Fungi are very oppurtunistic. These show up after things are wiped out.

102
Q

What method of administration is preferrable for anti-fungals?

A

Topical application is preferable, IV and oral can also be done.

103
Q

what is a nasty side effect that can happen with anti-microbials?

A

Stephen’s Johnson’s Syndrome

From Wikipedia: Stevens–Johnson syndrome, a form of toxic epidermal necrolysis, is a life-threatening skin condition, in which cell death causes the epidermis to separate from the dermis. The syndrome is thought to be a hypersensitivity complex that affects the skin and the mucous membranes. The most well-known causes are certain medications, but it can also be due to infections, or more rarely, cancers.[1]

104
Q

What is particularly important when treating nail fungus?

A

Treat nail fungus infections early.

Because

  • Topical must be absorbed through nail and skin, so the closer to the surface the fungi are the better (so early they are not deep yet)
  • Hard to get meds to nails systemically without toxcicity and getting filtered out (first pass effects).
105
Q

What other side effect besides local irritation can a topical antifungal have?

A

Could have head aches

(weird)

106
Q

Are protozoan infections limited to just third world settings?

A

No.

They are actually quite common in medically underserved populations in the developed world. So we may see these more than we think.

107
Q

what is the most common method(s) of delivery for a anti-fungal for a systemic infection?

A

oral or IV