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unit 9 Flashcards

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1
Q

crust rash

A

dried fluids from a lesion on the skin surface

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2
Q

papule rash

A

small raised skin lesions

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3
Q

bulla rash

A

fluid-filled skin lesion larger than 1 cm

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4
Q

pustule rash

A

raised, pus-filled skin lesions

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5
Q

vesicle rash

A

small fluid-filled lesions smaller than 1 cm

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6
Q

ulcer rash

A

break in the skin

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7
Q

macule rash

A

flat discoloured lesion

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8
Q

wheal rash

A

swollen, inflamed skin that itches and burns

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9
Q

different diseases caused by s. aureus

A

folliculitis, furuncles, carbuncles, scalded skin syndrome, impetigo

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10
Q

features of folliculitis

A

signs: bumps, pimples that itch, red/pus-fill

virulence factors: leukocidins which kill WBCs

transmission: opportunistic infections (sweat, skin injury, ingrown hairs, tight clothing, shaving)
entry: parenteral
detection: skin inspection
treatments: self-limiting, topical antibiotics

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11
Q

features of furuncles

A

signs: larger lesions

VF: leukocidins kill WBC

transmission: direct contact, opportunistic infection
entry: parenteral
detection: skin inspection
treatments: self-limiting, topical

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12
Q

features of carbuncles

A

signs: deeper lesions

VF: leukocidins kill WBC

transmission: direct contact, opportunistic infection
entry: parenteral
detection: skin inspection, culture swabs to verify ID
treatments: lesions drained; antibiotics

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13
Q

features of scalded skin syndrome

A

signs: skin redness and peeling, affects mainly newborns

VF: exotoxins leading to sign and symptoms

transmission: opportunistic infection
entry: parenteral
detection: blood tests, culture swabs
treatments: IV antibiotics

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14
Q

features of impetigo

A

signs: formation of vesicles, pustules, bullae around the nose and mouth; later these rupture and form crusts

VF: none

transmission: direct contact; opportunistic infection
entry: parenteral
detection: visual inspection
treatments: topical or oral antibiotics

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15
Q

which disease has an co-infection and what is it

A

impetigo s. aureus w/ s. pyogenes

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16
Q

what disease is caused by s. pyogenes

A

necrotizing fasciitis

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17
Q

features of necrotizing fasciitis

A

signs: rapid death in connective tissue

VF: capsule, M-protein - both to avoid phagocytosis, bacterial protease to destroy host tissues, exoenzymes: streptolysin, hyaluronidase, streptokinase

transmission: opportunistic infection
entry: parenteral, sometimes unknown
detection: visual inspection, culture swab for ID
treatment: debridement (removal of infected tissue), amputation, IV antibiotics

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18
Q

etiology and features of acne

A

cutibacterium acnes; (gram-positive, aerotolerant)

signs: papules, pustules
transmission: clogged pores leading to comedones (whiteheads & blackheads; non-inflammatory); this leads to infection by c. acnes & digests lipids in sebum and secretes free fatty acids leading to lesions
entry: opportunistic infection

detection: visual
treatments: topical agents, antibiotics (erythromycin), acne creams, hormones, phototherapy & laser therapy to reduce oil build-up

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19
Q

herpes simplex virus - type 1

A

cold sores

signs: blisters around the lip region; eventually break open and crust, infection is latent and recurs upon stress or environmental conditions
transmission: direct contact during active infection
entry: skin
detection: visual infection; lab testing
treatments: topical meds to manage symptoms

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20
Q

herpes simplex virus - type 2

A

genital herpes

signs: blisters around genitals; eventually break open and crust, infection is latent and recurs upon stress or environmental conditions
transmission: direct contact during active infection
entry: skin
detection: visual infection; lab testing
treatments: antiviral meds to manage infection

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21
Q

different diseases of candidiasis

A

cutaneous, vaginal, thrush

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22
Q

cutaneous candidiasis features

A

etiology: candida spp.
signs: red, itchy rash on skin folds, nails
transmission: opportunistic infection
entry: skin
detection: visual
treatment: n/a

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23
Q

vaginal candidiasis features

A

etiology: candida spp.
signs: vaginal itching, thick yellow/white discharge, odor
transmission: opportunistic infection, following treatments that disrupt normal flora, sexual transmission
entry: skin
detection: visual
treatments: anti-fungal creams

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24
Q

thrush candidiasis features

A

etiology: candida spp
signs: white patches in the mouth, possible bleeding
transmission: opportunistic infection
entry: skin
detection: visual
treatments: n/a

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25
Q

describe the protective features of respiratory system

A

mucus traps microbes and prevents them from colonizing, ciliary escalator dislodges, and propels mucus and trapped microbes out of the epiglottis, alveolar macrophages stay in lower respiratory, IgA antibodies

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26
Q

typical members of pathogenic organisms in upper respiratory

A

streptococcus, haemophilus, neisseria

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27
Q

strep throat features

A

etiology: streptococcus pyogenes (gram-positive)
signs: high fever, dark swollen tonsils, petechaie (red bumps) rash on soft/hard palate, swollen lymph nodes

VF: hyaluronidase, collagenase, streptokinase, streptolysins
complications: acute rheumatic fever and acute glomerulonephritis

transmission: direct contact or droplet transmission through coughing and sneezing
entry: mucus membranes
detection: immunoassay followed up by culture swab for ID
treatments: antibiotics

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28
Q

bacterial pneumonia: streptococcus pneunomiae

A

gram-positive

signs: lung infections, leading to inflammation in the alveoli, painful breathing

VF: capsule to prevent phagocytosis, contains other factors to promote disease progression

transmission: direct contact; droplet transmission
entry: mucus membrane

detection: culture swabs for ID
treatments: antibiotics

vaccine: yes - conjugate vaccine

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29
Q

bacterial pneumonia: haemophilus influenza

A

gram-negative

signs: lung infections, leading to inflammation in the alveoli, painful breathing

VF: capsule to prevent phagocytosis

transmission: direct contact; droplet transmission
entry: mucus membrane
detection: culture swabs for ID
vaccine: yes - conjugate vaccine

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30
Q

bacterial pneumonia: mycoplasma pneumoniae

A

no cell walls, disease tends to be more mild

signs: lung infections, leading to inflammation in the alveoli, painful breathing

VF: n/a

transmission: direct contact; droplet transmission
entry: mucus membrane
detection: culture swabs for ID
vaccine: no

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31
Q

diseases of the respiratory system

A

bacterial causes: strep throat, bacterial pneumonia, tuberculosis, pertussis - whooping cough, viral causes: common cold, influenza, viral pneumonia, measles, chickpox

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32
Q

tuberculosis etiology

A

mycobacterium tuberculosis (gram-positive)

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33
Q

tuberculosis features

A

signs: chronic cough, chest pain, coughing up blood/sputum

VF & pathogenesis: waxy mycolic acid protects against digestion after phagocytosis, an inflammatory response is initiated and more macrophages are recruited, small lesions called tubercle are formed, eventually these tubercules rupture allowing the bacteria to spread, most lesions will heal to form calcified Ghon complexes, complications: chronic disease (can last months to years) and many drug resistant strains are present

transmission: direct contact; droplet
entry: mucus membranes
treatments: antibiotics
vaccine: yes - attenuated vaccine

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34
Q

etiology of pertussis

A

bordetella pertussis (gram-negative)

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35
Q

signs of pertussis

A

long period of severe coughing leading to a “whoop” sound during cough

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36
Q

three stages of whooping cough

A

cararrhal - which is relatively mild
paryxosymal - which leads to uncontrollable coughing spasm
convalescence - which is a long recovery period where patients experience a chronic cough

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37
Q

VF & pathogenesis for pertussis

A

uses an adhesion for adherence, A-B extoxins called the pertussis toxin known to enhance inflammatory responses, cytotoxins that damages ciliated epithelial cells leading to increased mucus production

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38
Q

pertussis: entry, detection, treatments, vaccine

A

droplet, mucus membrane, culture swab for ID, self-limiting & antibiotics, yes toxoid vaccine

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39
Q

common cold features

A

etiology: rhinoviruses, coronaviruses, adenoviruses - these viruses tend to replicate in conditions slightly lower than body temp
signs: runny nose, sore throat, coughing, no fever
pathogenesis: irritation of mucosa leading to an inflammatory response
transmission: direct; droplet
entry: mucus membrane
treatments: self-limiting

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40
Q

features of influenza

A

eti: influenza virus
signs: fever, chills, bodyaches

VF & pathogenesis: 2 spike proteins - hemagglutinin (H) used for viral entry & neuraminidase (N) used for viral exit

transmission: direct contact; droplet
entry: mucus membrane
treatments: self-limiting; antivirals in more severe cases
vaccine: seasonal flu vaccine - inactivated

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41
Q

antigenic drift

A

result of point mutations causing slight changes in the spike proteins - requires new vaccines to be developed every year

42
Q

antigenic shift

A

result of large changes due to gene reassortment - can occur when a host is infected with multiple influenza viruses - leads to formation of new influenza viruses

43
Q

viral pneumonia features

A

eti: adenoviruses, influenza viruses, parainfluenza viruses, respiratory syncytial viruses
signs: range from mild cold-like symptoms to severe pneumonia, depending on the causative virus

44
Q

measles features

A

eti: measles virus

signs & pathogenesis: virus
enters the respiratory system, then spreads to the bloodstream (viremia) and eventually forms a characteristic macular rash on the skin, the rash starts first on the face and later spreads to the extremities, other signs includes high fever & Koplik’s spots

transmission: direct contact, droplet, airborne
entry: mucus membranes
detection: based on signs, presence of Koplik’s spots
treatments: self-limiting, supportive care to manage symptoms
vaccine: live attenuated vaccine

45
Q

chickpox features

A

eti: varicella-zoster virus

signs & pathogenesis: after exposure, the virus spreads through the bloodstream & eventually leads to a pustular rash on face, which later progresses to the trunk, eventually the lesions burst forming crusts, the virus moves along the sensory nerves to the dorsal ganglia in the spinal cord

transmission: direct, droplet
entry: mucus membranes
detection: based on signs
treatments: self-limiting, supportive care
vaccine: attenuated vaccine

46
Q

connection between chickpox and shingles

A

virus can become reactivated due to stress, aging

virus then moves along the sensory nerves resulting in painful lesions

shingles itself is not contagious, but a non-exposed person can develop chickpox as a primary infection if in contact with a person with shingles

shingles can be treated with antivirals

vaccine available - same vaccine as chickpox

47
Q

bacteremia

A

presence of bacteria in the blood

48
Q

septicemia

A

bacteria reproducing in the blood

49
Q

viremia

A

presence of viruses in the blood

50
Q

toxemia

A

presence of toxins in the blood

51
Q

systemic inflammatory response syndrome (SIRS)

A

inflammation so severe that it damages host tissues and organs more than the actual infection

can lead to sepsis: excessive production of excess cytokines leading to damaging inflammation

52
Q

ischemia

A

reduced blood flow to tissues

53
Q

necrosis

A

tissue death

54
Q

lymphangitis

A

inflammation of the lymphatic vessels

55
Q

diseases of the circulatory system

A

toxic shock syndrome, gas gangrene, infectious mononucleosis, burkitt lymphoma, hantavirus pulmonary syndrome, AIDS, lymphatic filariasis

56
Q

toxic shock syndrome features

A

eti: staphylococcus aureus (gram-positive)
signs: vomiting, diarrhea, fever, hypotension & erythematous rash

VF: production of TSST-1 (superantigen exotoxin), leads to excessive release of cytokines leads to drop in blood pressure and formation of blood clots

transmission: occurs through localized or systemic wounds
entry: parenteral
detection: clinical signs, serologic tests, toxin detection
treatments: debridement of infected tissues, vasopressors to increase blood pressure and antibiotics

57
Q

gas gangrene causative organism

A

clostridium perfingens (gram-positive, endospore-forming)

58
Q

gas gangrene features

A

signs, VF, pathogenesis: pathogen is obligate anaerobe, so toxins produced are there to decrease oxygen levels in local environments, several toxins leads to ischemia and necrosis, gas produced through fermentation

transmission: trauma wounds, damage to blood vessel
entry: parenteral
detection: rapid spread of myonecrosis, pain, gas pockets
treatments: debridement, amputation, hyperbaric oxygen therapy, antibiotics

59
Q

infectious mononucleosis and burkitt lymphoma causative organism

A

epstein-barr virsu

60
Q

infectious mononucleosis features

A

signs & pathogenesis: leads to pharyngitis, fever, fatigue continuing from months

transmission: direct contact
entry: mucus membranes
detection: serological tests
treatment: self-limiting

61
Q

burkitt lymphoma features

A

signs: rapidly growing tumours, more prevalent in children & Africa

transmission & entry: n/a

detection: biopsy
treatments: chemo

62
Q

hantavirus pulmonary syndrome features

A

eti: hantavirus

signs &pathogensis: starts off with flu symptoms, progresses to pulmonary edema and hypotension

transmission: airborne: zoonotic
entry: mucus membranes
detection: n/a
treatments: supportive care with limited antivirals

63
Q

lymphatic filariasis

A

eti: wuchererua bancrofti (nematode)

signs & pathogenesis: targets & blocks lymphatic vessels, leads to edema & fibrosis, causing extreme swelling

transmission: vector biological (mosquitoes transfer larvae)
entry: parenteral
treatment: prevention = sanitation, mosquito control & anti-helminthic medication

64
Q

peptic ulcers causative organism

A

helicobacter pylori

65
Q

peptic ulcer features

A

signs: nausea, lack of appetite, bloating, burping, weight loss, dark stools
transmission: direct contact or contaminated water
entry: mucus membranes
detection: breath test, radiolabeled urea, biopsy
treatments: antibiotics

66
Q

VF & pathogensis of peptic ulcers

A

bacterium tolerates acidic environment of stomach, VF includes production of urease, which can lead to the production of ammonia which neutralizes the stomach acids, the infection damages the lining & can lead to stomach perforation and increased risk of stomach cancer

67
Q

staphylococcal food poisoning features

A

VF & pathogenesis: typically only intoxication, produces heat-stable enterotoxins which act as a superantigen

transmission: vehicle” consumption of raw meat, dairy productions, salty foods
entry: mucus membranes
detection: not typical
treatment: oral rehydration therapy

68
Q

shigellosis etiology

A

shigella spp. (gram negative)

69
Q

shigellosis features

A

signs: cramps, fever, watery diarrhea

VF & pathogensis: organism is invasive & moves to neighbouring cells, shiga toxin produced leads to hemorrhaging, complications: ulceration of mucosa, dehydration, rectal bleeding, HUS

transmission: direct contact & vehicle transmission (fecal-oral)
entry: mucus membranes
detection: stool sample
treatments: antibiotics

70
Q

salmonellosis etiology

A

salmonella spp. (gram-negative)

71
Q

salmonellosis features

A

VF & pathogensis: invasive, no movement to other cells, can persist in macrophages, can enter bloodstream & persist in body, making person carrier, can be infection or intoxication

transmission: vehicle transmission - consumption of contaminated food
entry: mucus membrane
detection: stool sample & serotyping
treatments: oral rehydration therapy, antibiotics in severe

72
Q

EPEC (enteropathogenic E. coli)

A

gram negative

signs & VF: leads to vomiting & diarrhea, “travelers diarrhea”, can lead to severe dehydration

transmission: vehicle transmission
entry: mucus membranes
detection: n/a
treatments: oral rehydration, antibiotics

73
Q

EHEC (enterohemorrhagic e. coli)

A

gram negative

signs & VF: more severe, produces shiga-like toxin

transmission: vehicle transmission
entry: mucus membranes
detection: presence of toxin in food or stool
treatments: oral rehydration - NO antibiotics (endotoxin produced)

74
Q

cholera features

A

eti: vibrio cholera (gram-negative)
signs: severe diarrhea (rice water stools)

VF: motile produces A-B exotoxins, leads to activation of chloride channels which leads to loss of ions followed by water

transmission: vehicle transmission - fecal oral
entry: mucus membranes
detection: stool sample
treatments: oral rehydration, antibiotics

75
Q

c. difficile features

A

eti: clostridioides difficile (gram positive, endospore forming

VF: produces 2 toxins leads to diarrhea, dehydration, loss of appetite & abdominal pain

transmission: healthcare-associated infection, opportunistic infection
entry: mucus membranes
detection: stool sample
treatments: oral rehydration, fecal transplants

76
Q

Giardiasis

A

etiL Giardia lamblia (protozoan)

Signs: Diarrhea, nausea, stomach cramps, gas, dehydration (lasts 2-6 weeks);

VF: Protist attaches to the intestinal mucosa using an adhesive disk, which blocks the absorption of nutrients
complications: development of chronic infections that are resistant to treatment

transmission: vehicle transmission (ingestion of contaminated food or water (especially during camping
season) , Direct contact

entry: mucus membranes

Detection: stool sample examination looking for cysts and trophozoites

Treatments Anti-protozoan medication

Prevention: filtration of water to remove cysts (boiling water is not effective)

77
Q

meningitis

A

inflammation of the meninges

78
Q

encephalitis

A

inflammation of the brain tissue

79
Q

bacterial meningitis: neisseria meningitidis (gram-negative) VF:

A 
Produces endotoxin, factors
for attachment, capsule
to avoid phagocytosis, and
produces enzymes to avoid
the immune system
Leads to a characteristic
petechial rash
Children and young adults
more susceptible (before
vaccine or booster)
Complications: rapid
progression leading to
sepsis, multiple organ
failure and death
80
Q

bacterial meningitis: Streptococcus pneumoniae (gram-positive) VF:

A 
Also contains several
virulence factors for
attachment and triggering
inflammation; has a
capsule

Children prior to receiving
the vaccine are more
susceptible

Complications: can lead to
septicemia

81
Q

bacterial meningitis: Haemophilus influenzae

(gram-negative) VF:

A 
Also contains several
virulence factors to trigger
inflammation, adherence,
invasion, as well as a
capsule
82
Q

transmission of bacterial meningitis

A

Pathogens gain access to bloodstream after trauma, production of toxins, or spread
from respiratory tract (direct contact or droplet transmission)

In the bloodstream, the presence of pathogens leads to inflammation, which makes the CNS more susceptible to infection

83
Q

entry, treatments, vaccine for bacterial meningitis

A

mucus membranes, antibiotics, conjugate vaccine

84
Q

detection of neisseria men.

A

gram-staining of CFS ( negative w/ coffee bean morphology)

85
Q

detection of streptococcus pneumoniae

A

gram-staining CFS

86
Q

cryptococcosis (fungal meningitis) eti:

A

Cryptococcus neoformans

87
Q

Cryptococcosis (fungal meningitis) features

A

Virulence factors; pathogenesis; signs/symptoms: has a thick capsule used to prevent phagocytosis

Transmission: vehicle transmission where the pathogen is found in soil and
aerosolized pigeon droppings

entry: mucus membranes (respiratory system)

Detection: urine sample

Treatments: Anti-fungal drugs

88
Q

Amoebic meningitis eti:

A

Naegleria fowleri (protozoan)

89
Q

Amoebic meningitis features

A

virulence factors; pathogenesis;
signs: parasite in trophozoite form will enter through the nasal passages and ultimately makes its way to the CNS

transmission: submersion of head while swimming in freshwater
entry: mucus membranes (nose)
detection: Direct observation of cerebrospinal fluid

Treatments Anti-protozoan drug coupled with therapeutic hypothermia (works only if infection is caught early)

90
Q

Tetanus eti:

A

Clostridium tetani (gram-positive, obligate anaerobe, endospore-forming

91
Q

tetanus feaures:

A

signs, virulence
factors; pathogenesis: produces an exotoxin called tetanospasmin, which prevents the release of the neurotransmitter GABA, which is necessary for muscle relaxation

transmission: direct contact through wounds, vector biological transmission through animal bites
entry: parenteral
treatments: assisted breathing, wound debridement, antibiotic therapy, anti-toxins

Vaccine Toxoid vaccine

92
Q

localized & generalized tetanus

A

• localized tetanus affects only the muscle groups at the site of injury, leading
to muscle spasms in that area
• generalized tetanus is spread throughout the body, leading to lockjaw,
uncontrollable and sudden muscle spasms (characteristic arched back), and
eventually progressing to the respiratory system (leading to death)

93
Q

Botulism eti

A

Clostridium botulinum (gram-positive, obligate anaerobe, endospore-forming

94
Q

Botulism VF:

A

Produces an exotoxin called botulism toxin, this exotoxin prevents the release of the neurotransmitter acetylcholine which prevents muscle contraction (progressive flaccid paralysis)

signs and symptoms start with blurred vision, dropping eyelids, abdominal cramps, nausea,
vomiting, diarrhea; in more severe cases, the respiratory system is affecting leading to death

Medical usage of toxin: used to treat various medical conditions such as cerebral palsy,
multiple sclerosis, Parkinson’s disease; also used for cosmetic purposes to remove wrinkles,
prevent excessive sweating

95
Q

Botulism features

A

transmission; entry
foodborne botulism: foodborne vehicle transmission (honey, improper canning
procedures, etc.); mucus membranes (GI system) – occurs in infants or
immunocompromised adults

inhalation botulism: airborne vehicle transmission; mucus membranes (respiratory
system)

iatrogenic botulism: direct contact transmission, parenteral (rare event after
therapeutic or cosmetic use of toxin)

Treatments Anti-toxins

96
Q

Rabies

A

Eti: Rabies virus
Signs: furious rabies, where the individual shows signs and symptoms such as agitation,
hydrophobia, and excessive salivation
paralytic rabies, where the muscles progressively become paralyzed leading to coma

Pathogenesis: after entering the body, the incubation period can be quite long, ranging over
weeks - years, as the virus replicates, it moves along the neuron, once it reaches the brain, it disrupts normal neurotransmitter function (e.g., acetylcholine, GABA, glycine), eventually the virus can move out to other tissues such as salivary glands and nasal cavity

transmission: vector biological transmission through animal bites
entry: parenteral

Treatments: vaccines (inactivated vaccine) due to slow progression of pathogen, antibodies are also administered

97
Q

Cystitis (urinary tract infection)

A

Eti: various, including E. coli, Proteus vulgaris, Pseudomonas aeruginosa, Klebsiella pneumonaie

Signs and
symptoms: Dysuria (painful urination), pyuria (pus in urine), hematuria (blood in urine),
bladder pain

Pathogenesis: can progress to pyelonephritis if not treated

transmission: Non-communicable: typically a result of fecal contamination, irritants from radiation
treatment, or hygiene sprays

Detection Urine culture

Treatments Antibiotics

98
Q

Kidney infections

A

Etiology Same as cystitis

Signs and
symptoms: Back pain (kidney area), fever, nausea/vomiting
Pathogenesis Can progress to pyelonephritis if not treated

transmission:
Non-communicable: spread from cystitis, or from a bacterial infection in the bloodstream

Detection Urine culture and urine testing

Treatments Antibiotics

99
Q

Gonorrhea

A

Etiology Neisseria gonorrhoeae (gram-negative bacterium)

Signs:
Typically asymptomatic but if present:
• Males: burning during urination and discharge
• Females: pelvic pain and discharge

VF: contains a variety of virulence factors which includes fimbriae and production of
endotoxins

Complications: can spread throughout the body leading to bacteremia and affect different
organs; in females, can spread to the endometrium and fallopian tubes leading to PID

transmission:
Direct contact  (sexual contact)
entry: mucus membranes (urogenital system)

Detection Culture swabs from infected areas

Treatments Antibiotics (with increased strains that are antibiotic-resistant)

100
Q

Syphilis stages

A
  • Primary stage: Formation of a painless lesion called a chancre
  • Secondary stage: Characterized by a skin rash that takes on many forms

o After the secondary stage, the bacterium can enter a latent phase

• Tertiary stage: Formation of granulomatous lesions called gummas

o These can cause severe tissue damage in locations such as the cardiovascular or the nervous system

101
Q

Syphilis

A

Etiology Treponema pallidum (gram-negative spirochete

signs, VF: most of the tissue damage is caused by the production of lipoproteins by the bacterium, allowing it to cause damaging inflammation to enhance further invasion

transmission: direct contact (sexual contact)
entry: mucus membranes (urogenital system)

Detection Microscopy or culture swabs from lesions

Treatments Antibiotics

102
Q

Human Papillomas

A

Etiology: Human Papillomavirus (non-enveloped DNA virus)

signs, VF: some serotypes lead to genital warts – irregular, soft, pink growths, Some serotypes can lead to cancer such as oropharyngeal, cervical, anal, vaginal, vulvar, penile

transmission: direct contact (sexual contact)
entry: mucus membranes (urogenital system)

Detection Testing is done only for women – pap smears (looking for cells with enlarged nuclei – koilocytes)

Treatments Self-limiting:
Genital warts – removal or use of topical medications (interferons)

Cancers – biopsy for confirmation and then chemotherapy

Vaccine Subunit vaccines for serotypes that cause cancer (Gardasil and Cervarix) for both boys and
girls

Biology 2401 (30 decks)

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