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Microbiology > Diseases exam 3 > Flashcards

Diseases exam 3 Flashcards

1
Q

Diseases due to streptococcus were first described by

A

Hippocrates, in the 4th century

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2
Q

When were streptococcal diseases first separated as a disease entity?

A

The 16th century

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3
Q

Theodor Billroth

A

First description of a true streptococcal infection was by Theodor Billroth in 1874 and it was associated with wound infections and erysipelas (a skin infection)

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4
Q

How is streptococcus involved in the microbiota?

A

Many people carry the bacteria on their nasopharynx- does not cause disease in these cases. 5-15% of humans carry S. pyogenes or S. agalactiae, and 20-40% carry S. pneumoniae. This bacteria can be opportunistic pathogens and cause disease

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5
Q

Incidence of respiratory disease due to S. pyogenes

A

Peaks at 6 years of age and at 13 years of age- most common during late winter and early spring in temperate climates

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6
Q

When are skin infections due to streptococcus most common?

A

Skin infections are common among preschool age children- most prevalent in late summer and early fall in temperate climates and at all times in tropical climates

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7
Q

S. pyogenes in children

A

In children, S. pyogenes is associated with invasive disease. It may arise after the child has had varicella. It is also associated with burns or cancer. You become more susceptible to other diseases when you are sick, so skin infections like chicken pox predisposes someone to infect with streptococcus

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8
Q

When does streptococcus cause invasive disease in adults?

A

In adults, invasive disease is associated with surgical or nonsurgical wounds or underlying medical problems, like diabetes, cirrhosis, underlying peripheral vascular disease, or malignancy

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9
Q

Infectious agent of streptococcus

A

Streptococcus species are non motile, gram positive coccus bacteria, arranged in chains or pairs

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10
Q

How is streptococcus classified? (3)

A
  1. Cell morphology
  2. Hemolysis ability
  3. Serologic specificity- cell wall carbohydrates, pili associated proteins, and capsules (group B streptococci)
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11
Q

Clinically important streptococcus species (2)

A

Streptococcus pneumoniae and streptococcus pyogenes. They are both part of the nasopharynx microbiota that are usually outcompeted by other microorganisms. Some strains of streptococci show a predilection for the respiratory tract, others prefer the skin

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12
Q

How is S. pyogenes generally transmitted?

A

S. pyigenes is spread by respiratory droplets or contact with fomites. Skin infections often follow minor skin irritations, like insect bites.

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13
Q

Occasional transmission of S. pyogenes occurs due to (3)

A
  1. Reports of streptococcal disease traced to rectal carriers
  2. Food borne- from an infected person preparing the food and transferring bacteria
  3. Vector borne outbreaks- some vectors carry the bacteria between hosts
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14
Q

Streptococcus enzymes that contribute to disease (6)

A
  1. Streptokinase
  2. DNAse- breaks down DNA
  3. M protein
  4. Streptolysin
  5. Hyaluronidase
  6. Exotoxins- A, B, and C
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15
Q

M protein

A

helps the strep bacteria to adhere and is an antiphagocytic factor- prevents the immune system from destroying the bacteria

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16
Q

Streptolysin

A

a protein that causes hemolysis of red blood cells (hemolytic exotoxin)

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17
Q

Hyaluronidase

A

an enzyme that can digest host connective tissue and can cause soft tissue necrosis

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18
Q

Exotoxins- A, B, and C

A

Cause scarlet fever as well as the fever caused by infection. Scarlet fever can lead to rheumatic fever

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19
Q

How is S. pyogenes chemically similar to human cells?

A

The cytoplasmic membrane of S. pyogenes has antigens similar to those of human cardiac, skeletal, and smooth muscle, heart valve fibroblasts, and neuronal tissues, resulting in a molecular mimicry. Basically causes an autoimmune disease and damages the body’s tissues

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20
Q

Scarlet fever (scarletina)

A

S. pyogenes is also known to cause strep throat. Bacteria that caused strep throat is infected with a phage- produces an erythrogenic toxin. The phage contains a genetic code for a toxin that attacks red blood cells. The toxin causes inflammation of the skin. The tongue can also appear red. Can still be treated with antibiotics if caught early, but scarlet fever can cause problems later in life if not treated, as well as rheumatic fever

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21
Q

How does previous scarlet fever affect someone’s response to strep in the future?

A

If a person has had scarlet fever previously, they can develop the rash and symptoms due to a very small amount of the bacteria, since your immune system has produced antibodies against it. Therefore, a person can develop scarlet fever and test negative for strep because there is not enough bacteria to be detected by a test

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22
Q

Erysipelas

A

known for greater than two thousand years- is caused by hemolytic streptococci. Used to occur often after wounds and surgery. Causes skin infections

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23
Q

Pyoderma and impetigo

A

caused by Staphylococci, or streptococci alone or in combination- pus producing skin infection

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24
Q

Cellulitis

A

Extends deeper than erysipelas. The pathogen is only isolated in 25-35% of cases. Develops hours to days after the infection, more slowly than erysipelas. Does not involve the fascia or muscle. Forms a red, hot, swollen lesion that is also painful. Cellulitis is a type of non-necrotizing inflammation, but it may develop into necrotizing fasciitis

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25
Q

How is cellulitis diagnosed? (5)

A
  1. Observing symptoms
  2. Remove aspirates from the advancing edge of cellulitis
  3. Site of trauma
  4. Skin biopsies
  5. Blood
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26
Q

Necrotizing fasciitis

A

Frequently fatal mixed infection caused by anaerobes and facultative bacteria. Mostly linked to S. pyogenes- thus the term flesh eating bacteria. Radical excision of all necrotic fascia is an essential part of therapy. It is a very acute, toxic infection that causes necrosis of the surrounding tissue. Enters the fascia, muscle, and deeper tissues

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27
Q

Streptococcal toxic shock syndrome

A

Results from the destruction of tissues during necrotizing fasciitis. Can cause organ damage

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28
Q

How are streptococcal infections diagnosed? (2)

A
  1. Serology- fluorescent antibody, direct bacterial agglutination, and ELISA
  2. Bacterial culturing
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29
Q

Treatment of S. pyogenes

A

Penicillin is still the drug of choice. However, group D streptococci is resistant to most antibiotics, and group B is resistant to tetracycline

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30
Q

S. pneumoniae vaccines (2)

A
  1. Pneumococcal conjugate vaccine- PCV13
  2. Pneumococcal polysaccharide vaccine- PPSV23
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31
Q

Evolutionary history of herpes simplex virus

A

HSV-1 infected hominids before their evolutionary split from chimpanzees 6 million years ago. HSV-2 jumped from ancient chimpanzees to ancestors of modern humans. Some infect humans only and some are zoonotic

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32
Q

Herpes Latin meaning

A

To creep or crawl, described as a spreading skin lesion by Hippocrates

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33
Q

History of HSV

A

Human transmission was only recognized in 1793. HSV was widely studied in the 1920s-1930s and infects the skin and the nervous system. Varicella-Zoster virus (VZV) has been recorded for many centuries but often was confused with smallpox until the late 18th century. Epstein Barr virus (EBV)- viral particles isolated in 1964. Known for its role in Burkitt’s lymphoma, nasopharyngeal carcinoma, and B cell lymphomas. Cytomegalovirus (CMV) was only isolated recently. It is mostly asymptomatic in the immunocompetent patients- enlarged the infected cells

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34
Q

Which family is HSV part of?

A

Herpesviridae family

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35
Q

Structure of HSV

A

Large icosahedral enveloped virus. Linear dsDNA genome that encodes more than 100 genes

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36
Q

Herpes viruses (8)

A
  1. HHV-1- Herpes Simplex 1 (HSV-1)
  2. HHV-2- Herpes simplex 2 (HSV-2)
  3. HHV-3- Varicella Zoster virus (VZV)
  4. HHV-4- Epstein Barr virus (EBV)
  5. HHV-5- Cytomegalovirus (CMV)
  6. HHV-6A, HHV-6B- Roseolovirus
  7. HHV-7 Roseolovirus
  8. HHV-8- Kaposi’s sarcoma associated herpesvirus (KSHV)
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37
Q

Subfamilies of HSV (3)

A
  1. Alphaherpesvirinae
  2. Betaherpesvirinae
  3. Gammaherpesvirinae
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38
Q

Alphaherpesvirinae

A

HSV-1, HSV-2, VZV, HHV-8. Variable host range, relatively short reproductive cycle, rapid spread in culture, destruction of infected cells, and capacity to establish latent infection primary but not exclusively in ganglia

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39
Q

Betaherpesvirinae

A

CMV, HSV-6, HHV-7. Restricted host range, long reproductive cycle, infection progresses slowly in culture, latent in secretory cells, lymphoreticular cells, kidneys, and other tissues

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40
Q

Gammaherpesvirinae

A

EBV. Host range characteristic of the family or order of the natural host, infects specifically B or T cells, latent virus in lymphoid tissue, may cause lytic infections in some types of epithelioid and fibroblastic cells in lymphocyte, infection may be arrested at prelytic or lytic stage without the production of infectious progeny

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41
Q

Herpes simplex

A

Human herpesvirus 1 (HSV-1) and 2 (HSV-2). Causes cold sores or fever blisters (vesicles on lips). The virus can be latent and return under stress. Can be found on the skin or genital area. 85% of HSV-2 infections are in the genital area and 90% of HSV-1 infections are oral

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42
Q

Genital herpes

A

Similar to cold sores but in the genital area. If asymptomatic, someone can still be shedding virus at any time. Preventable by using condoms

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43
Q

Herpes gladiatorum

A

Vesicles on skin

44
Q

Herpetic whitlow

A

Vesicles on fingers

45
Q

Herpes encephalitis

A

Any viral encephalitis is difficult to treat, but herpes encephalitis is more treatable- still has a 70% fatality rate. HSV-1 can remain latent in trigeminal nerve ganglia and HSV-2 can remain latent in sacral nerve ganglia

46
Q

Treatment for herpes encephalitis

A

Acyclovir

47
Q

Symptoms of initial herpes simplex virus infection

A

Asymptomatic or vesicles (blistering rash) form under keratinized cells and fill with fluid from the cells that have been infected. The virus typically only affects keratinocytes

48
Q

HSV latency

A

More than 80% of the world’s population harbors the virus. Reactivation occurs spontaneously or can be activated by fevers, stress, UV light, hormones, menstrual cycles, any type of trauma

49
Q

Incubation period of HSV

A

4-10 days

50
Q

Genital herpes symptoms

A

Females- vesicles appear in the labia, vagina, and cervix, can also spread to the thighs. Males- tiny vesicles appear on the penis and foreskin, along with urethritis and watery discharge. In both- intense pain and itching at the site of the lesions and swollen lymph nodes in the groin

51
Q

Treatment of genital herpes

A

acyclovir, famciclovir, and valacyclovir

52
Q

Where does oral herpes reactivate?

A

Oral herpes becomes latent in the trigeminal nerve ganglion. When it is reactivated, it will often be in the same site as the initial lesion. However, the trigeminal nerve has 4 branches- around the eyes, nose, corner of the lips, and chin. Lesions can form at any of those areas

53
Q

Herpes prevention

A

Don’t share utensils or towels with someone who has reactive HSV. Avoid contact with individuals that have lesions and use condoms when having sex

54
Q

HHV-3

A

Also called varicella-zoster virus, causes chickenpox and shingles

55
Q

How does HHV-3 replicate?

A

Virus enters the upper respiratory tract or the conjunctiva and replicates at the site of entry, and spreads to surrounding lymph nodes and enters the blood. They travel to the liver, spleen, sensory organs, and other tissues where they will replicate again and infect the skin cells. The skin infection prompts the rash

56
Q

Chickenpox symptoms

A

The rash appears first on the face, trunk, or skull, then spreads over the rest of the body. Can spread in the mouth, eyelids, or genital area. The lesions are less than a quarter inch wide, which helps to differentiate chickenpox from smallpox- smallpox lesions are larger. The blister will eventually burst and crust over, forming scabs. Can be accompanied by flu like symptoms like body aches and fever

57
Q

Complications of chickenpox

A

Secondary bacterial infections especially by S. aureus, neurological disorders, encephalitis, and pneumonia. Scratching the scabs introduces bacteria

58
Q

How long does the chickenpox rash last?

A

The first lesions are considered macules, then progress to papules at 2 days, fluid filled vesicles at 4, and the crusting begins at day 6. The rash lasts for around 2 weeks total

59
Q

Prevention of HHV-3

A

A vaccine is available, two doses are better than one. It uses a live attenuated virus. People 60 years and older get the shingles vaccine

60
Q

Treatment of HHV-3

A

Treated with antihistamines, oatmeal baths or calamine lotion for the rash, and fever reducing medications. Acyclovir is only used for severe or complicated cases

61
Q

HHV-3 latency

A

The virus infects the skin, but will become latent in the nerve cell, with the latent viral DNA. Viruses move up the peripheral nerve and enter the spinal cord (dorsal root ganglion)
If someone is immunosuppressed or under stress, the virus can reactivate as shingles. When the virus is activated, it moves down the peripheral nerve- the rash forms the path of the infected nerve

62
Q

Shingles symptoms

A

Shingles produces a localized, painful, dermatomal rash
The rash is much more localized than that of chickenpox. The sensory nerve is affected, so that area is very sensitive and painful

63
Q

Shingles treatment

A

May be able to be treated with acyclovir cream

64
Q

Shingles complications

A

Complications depend on which nerves are affected- can cause blindness if near the eyes. Shingles can be very dangerous in immunocompromised patients

65
Q

Shingles diagnosis

A

Diagnosis is usually clinical, but you can do antibody testing. Without the rash, you would have to take a biopsy of the spinal cord to determine if someone has a latent virus

66
Q

HHV-4

A

Epstein Barr virus- causes mononucleosis. Most people (98%) will be infected at some point

67
Q

How is mono transmitted?

A

Transmitted by body fluids, particularly saliva droplets, blood and semen fluids, blood transfusions, and organ transfusions. Through kissing or sharing utensils

68
Q

How is mono diagnosed?

A

Diagnosis is difficult, is done by observing the symptoms or through antibody tests

69
Q

How is mono prevented?

A

There is no vaccine, and it is difficult to prevent since it’s transmitted through saliva

70
Q

Mono symptoms

A

Fatigue, headache, malaise, loss of appetite, photophobia, swelling and white patches on tonsils, sore and red throat, enlarged spleen, abdominal pain, nausea, muscle aches, cough. Symptoms typically only occur in teenagers and older, young children generally have no symptoms or very mild symptoms. Take 2-4 weeks to improve, but can take up to 2 months

71
Q

EBV latency

A

Once the virus is in the body, it stays there in a latent (inactive) state. When the virus reactivates, it can be transmitted to others. The virus doesn’t always reactivate, and when it does it doesn’t always cause symptoms. The virus infects epithelial cells in the oropharynx, then infects naive B cells. The latent mono infects memory B cells. The virus is transferred from B cells to lymphoid tissue to be activated again

72
Q

HHV-5

A

Cytomegalovirus. One of the causes of cerebral palsy, causes lower brain volume in babies

73
Q

Symptoms of cytomegalovirus

A

Causes fever, sore throat, fatigue, and swollen lymph nodes if not acquired during the congenital period

74
Q

Congenital CMV

A

Occurs if someone is infected during pregnancy. If a baby contracts it, congenital CMV symptoms include rash, yellowing of the skin and whites of the eyes, small head size, low birth weight, enlarged liver and spleen, damaged retina in the eyes, hearing loss, and seizures

75
Q

Potential long term health problems of congenital CMV (8)

A
  1. Worsening of hearing loss or development of hearing loss as an infant
  2. Development and motor delay
  3. Cerebral palsy
  4. Learning disabilities
  5. Autism
  6. Vision loss
  7. Seizures
  8. Small head size
76
Q

How can congenital CMV be prevented?

A

CMV+ pregnant women may have a C-section to prevent the baby from contracting CMV in the birth canal

77
Q

Transmission of CMV (4)

A
  1. Direct contact with body fluids from an infected person (urine, saliva, blood)
  2. From breast milk to nursing infants
  3. Through transplanted organs and blood transfusions
  4. From a woman to her unborn child, likely via the blood and through the placenta
78
Q

Prevention of CMV

A

Wash hands, don’t share food or utensils, don’t clean a baby’s pacifier with your mouth. No vaccine

79
Q

Diagnosis of CMV

A

Blood tests. Saliva and urine are preferred testing methods in children. Congenital CMV testing must occur within the first 2-3 weeks of life

80
Q

Treatment of CMV

A

ganciclovir or valganciclovir- reduce the duration of symptoms but don’t cure the virus

81
Q

HHV-6 and 7

A

The viruses have a different composition genetically. They both cause roseola infantum. It is very common in children. There is no treatment, no vaccine, and immunity is permanent

82
Q

HHV-6 and 7 transmission

A

Spreads by saliva, respiratory droplets, and touching of contaminated surfaces

83
Q

Roseola symptoms

A

Abrupt high fever (103 or 104) for 3-5 days along with swollen lymph nodes. Drop in fever- rash begins and lasts for 2 days

84
Q

Roseola complications

A

rare- thrombocytopenia and encephalitis

85
Q

HHV-8

A

Causes Kaposi’s sarcoma, a cancer that forms in the lining of blood and lymph vessels. Affects mainly immunocompromised patients. There is no means of preventing it and no vaccine

86
Q

Kaposi’s sarcoma symptoms

A

The tumors (lesions) are typically painless purplish spots on the legs, feet, or face. Lesions can also appear in the genital area, mouth, or lymph nodes. In serve Kaposi’s sarcoma, lesions may develop in the digestive tract and lungs

87
Q

Kaposi’s sarcoma diagnosis

A

Fecal occult blood test, chest X-ray, bronchoscopy, upper endoscopy, colonoscopy. Fecal occult blood test checks for blood in stool that is not visible with the naked eye, while the other procedures check for tumors

88
Q

Kaposi’s sarcoma treatment

A

Varies depending on the type of disease, number and location of lesions, effects of the lesions, and general health. Lesions can sometimes be removed, frozen, or burned
Low dose radiation
Injection of immunotherapy drugs can also be used. Chemotherapy is used if the patient has more than 25 lesions. Lesions are likely to return even when treated

89
Q

History of HIV

A

1st crossover from animals to humans is estimated to have occurred in 1908. There was little notice due to prevalence in small villages. Earliest documented case was 1959- Democratic Republic of Congo. The first infection in the US occurred in 1987

90
Q

Transmission of HIV

A

sexual contact, blood borne exposure (blood transfusion, shared needles), and perinatal transmission

91
Q

Which genus and family does HIV belong to?

A

HIV belongs to the Lentivirus genus and the retroviridae family

92
Q

HIV infectious agent

A

HIV-1 and HIV-2

93
Q

HIV structure

A

It is an enveloped virus with +ssRNA. Its virions contain 2 identical single strands of RNA, reverse transcriptase, integrase, protease, and an envelope. Envelope spikes are termed gp120

94
Q

Prevalence of HIV-1 and HIV-2

A

HIV-1 is the primary HIV found worldwide- 99% of cases. Genetically related to an SIV carried by chimpanzees- endemic to central Africa. HIV-2 is weakly contagious and not often found outside Africa. It is a mutation of a simian immunodeficiency virus (SIV). HIV 1 and 2 are both results of mutations and are zoonotic diseases

95
Q

Incubation period of HIV

A

9 months to 20 years or longer, with an average of 12 years

96
Q

Target of HIV infection

A

The HIB Gp120 spike combines with the CD4+ receptor on T cells

97
Q

Early HIV symptoms

A

fever, fatigue, swollen lymph nodes, diarrhea, weight loss, cough and shortness of breath

98
Q

Late HIV symptoms

A

Soaking night sweats, fever higher than 100 degrees, cough and shortness of breath, chronic diarrhea, persistent white spots or unusual lesions on your tongue or in your mouth, headaches, weight loss, skin rashes or bumps. These are from different organisms as patients become immunosuppressed

99
Q

Phase 1 of HIV infection

A

The stage when a person is first infected- they are contagious throughout this stage. After 2 months, the number of HIV particles in the blood peaks, then start decreasing as the viruses are incorporated into cells. The number of CD4 cells decrease initially, then recover as the immune system responds. Seroconversion occurs, causing a rapid decline in the HIV population

100
Q

Seroconversion

A

Detectable antibodies against the pathogen occur

101
Q

Phase 2 of HIV infection

A

The CD4 population decreases. HIV is present in the blood, but it is now also present in lymphoid tissue. Billions of HIV particles are generated daily by infected T cells

102
Q

Phase 3 of HIV infection

A

The number of CD4 cells eventually decreases enough that it results in clinical AIDS (drops to 200), which is when phase 3 begins. HIV levels in the blood begin to rise as the immune system breaks down. At this point, you are truly immunosuppressed

103
Q

HIV diagnosis

A

ELISA, PCR, and western blots

104
Q

HIV treatment (5)

A
  1. Reverse transcriptase inhibitors
  2. Fusion/cell entry inhibitors
  3. Integrase inhibitors
  4. Protease inhibitors
  5. Development of maturation inhibitors, tetherins (prevent release from cell)
    Treatment inhibits the virus, but you can’t really kill it
105
Q

HIV prevention

A
  1. Avoid sexual contact with infected individuals
  2. Use condoms when having sexual contact and intercourse
  3. Do not reuse syringes
    No vaccine is available

Microbiology (19 decks)

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