Micro Unit 9: Skin, Respiratory, Cardiovascular, Circulatory Diseases

Normal flora of skin

Propionibacterium, Staphylococcus

Crust

dried fluids from a lesion on the skin surface

Bulla

fluid-filled skin lesion larger than 1 cm

Vesicle

small fluid-filled lesion smaller than 1 cm

Macule

flat discoloured lesion

Papule

small raised skin lesions

Pustule

raised, pus-filled skin lesions

Ulcer

break in the skin

Wheal

swollen, inflamed skin that itches and burns
ex. from insect bite

Bacterial skin disease mode of transmission

direct contact or opportunistic infections

Bacterial skin disease detection

skin inspection; culture swab for more severe cases

Bacterial skin disease portal of entry

parenteral

Bacterial skin disease treatment

antibiotics; mild cases resolve on their own

S. aureus bacterial skin diseases

- pyodermic infections
- scalded skin syndrome
- impetigo

Pyodermic infections

lead to pustules
- different terms depending on size

Pyodermic infection virulence factors

leukocidins

Leukocidins

pyodermic infection virulence factor; kill WBC

Terms for pustules

depend on size
folliculitis > furuncles > carbuncles

Scalded skin syndrome

common in newborns; leads to skin redness and severe peeling
- treatment needs IV antibiotics

Scalded skin syndrome virulence factors

exotoxins

Impetigo

formation of vesicles, pustules, bull; later rupture and form crust
- can form all over body, but most frequently around nose and mouth

Streptococcus pyogenes bacterial skin diseases

- necrotizing fasciitis

Necrotizing fasciitiss

leads to rapid death in connective tissues
- treatment includes debridement, amputation, IV antibiotics

Necrotizing fasciitis virulence factors

- capsule, M protein
- bacterial proteases
- exoenzymes

Capsule + M protein

both used to avoid phagocytosis in necrotizing fasciitis

Bacterial proteases

destroy host tissues in necrotizing fasciitis

Exoenzymes in necrotizing fasciitis

streptolysin, hyaluronidase, streptokinase

Cutibacterium acnes skin disease

acne

Acne

opportunistic, non-communicable
> hair follicles clogged > comedones
> C. acnes consumes the sebum, secreting free fatty acids
> free fatty acids stimulate inflammation, lesions

Viral skin disease

Herpes simplex virus > herpes

Herpes

latent and recurrent viral infection; leads to painful blisters that break and crust
- 2 types

Herpes type 1

lip region; cold sores

Herpes type 2

genitalia

Herpes mode of transmission + portal of entry

direct contact during active infection; skin

Fungal skin disease

Candida albicans > candidiasis

Candidiasis

leads to:
- cutaneous candidiasis
- vaginal yeast infection
- thrush

Candidiasis mode of transmission + portal of entry

opportunistic, skin

Cutaneous candidiasis

red, itchy rash on skin folds, nails, etc
(candidiasis)

Vaginal yeast infection

vaginal itching, thick yellow/white discharge
(candidiasis)

Thrush

white patches in the mouth, possible bleeding
(candidiasis)

Normal flora of upper respiratory tract

Streptococcus, Haemophilus, Neisseria

Protective features of respiratory system

- mucus
- ciliary escalator
- alveolar macrophages
- IgA antibodies

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 system (no microbes should be here)

Infections of the nose

sinusitis, rhinitis

Infections of the throat

pharyngitis, laryngitis, tonsillitis

Infections of the ear

otitis

Infections of the lower respiratory tract

bronchitis, epiglottitis, pneumonia

Pneumonia

inflammation of alveoli leading to accumulation of fluid

Bacterial respiratory disease mode of transmisison

direct/indirect contact; air, vehicle

Streptococcus pyogenes respiratory disease

strep throat

Strep throat

leads to high fever, dark swollen tonsils, petechiae rash on soft/hard palate, swollen lymph nodes

Strep throat virulence factors

hyaluronidase, collagenase, streptokinase, streptolysins (toxins)

Bacterial pneumonia pathogens

S. pneumoniae, H. influenzae, M. pneumoniae

Bacterial pneumoniae virulence factors

capsule in S. pneumoniae and H. influenzae

S. pneumoniae pneumonia detection

gram-positive

H. influenzae pneumonia detection

gram-negative

M. pneumoniae pneumonia detection

no cell wall

Bacterial pneumonia vaccine

conjugate - S. pneumonia and H. influenzae

Mycobacterium tuberculosis respiratory disease

tuberculosis

Tuberculosis

leads to chronic cough, chest pain, hemoptysis

Tuberculosis progression

inflammatory response initiated after phagocytosis and recruitment of macrophages
> tubercles form due to chronic inflammation
> tubercles rupture, bacteria spreads
> lesions heal to form calcified Ghon complexes

Tuberculosis virulence factors

waxy mycolic acid

Mycolic acid

protects against digestion after phagocytosis

Tuberculosis detection

tuberculin skin test, chest X-ray, vaccine available

Bordatella pertussis respiratory disease

pertussis (whooping cough)

Pertussis

leads to "whoop" sound during cough
- vaccine

Whooping cough progression

starts off mild
> uncontrollable coughing spasm
> convalescence; long recovery period, chronic cough

Pertussis virulence factors

- adhesin
- A-B exotoxin; pertussis toxin
- cytotoxin that damages ciliated epithelial cells

Viral respiratory diseases

- rhinoviruses, coronaviruses, adenoviruses
- influenza virus, viral pneumonia
- tend to be more mild than bacterial

Rhinoviruses, coronaviruses, adenoviruses

common cold; irritation of mucosa leading to inflammatory response
> runny nose, pharyngitis, no fever

Viral influenza

> fever, chills, body aches
different types based on different combinations of the two spike proteins

Viral influenza spike proteins

- hemagglutin (H) for viral entry
- neuraminidase (N) for viral exit

Evolutionary change of influenza virus

- antigenic drift
- antigenic shift
requires new vaccines to be developed every year

Antigenic drift

result of small mutations causing slight changes in the spike proteins

Antigenic shift

result of large changes due to gene reassortment; can occur when host is infected with multiple influenza viruses

Viral pneumonia

caused by influenza virus, adenoviruses, etc
- signs + symptoms vary

Viral respiratory diseases leading to skin rashes

- measles
- varicella-zoster virus

Measles

virus enters respiratory system > viremia + macular rash
> rash on face to extremities
- high fever + Koplik's spots
- vaccine

Koplik's spots

white spots that form inside the cheek

Varicella-zoster virus diseases

- chickenpox
- shingles

Chickenpox

viremia > pustular rash on face to extremities
> lesions burst, form crusts
> virus moves along sensory nerves to dorsal ganglia where it becomes dormant
- vaccine

Shingles

reactivated chickenpox virus later in life
> moves along sensory nerves > painful lesions
- not contagious itself
- vaccine

Bacteremia

bacteria in the blood

Septicemia

bacteria reproducing in the blood

Viremia

viruses in the blood

Toxemia

toxins in the blood

Systemic inflammatory response syndrome (SIRS)

inflammation so severe that it damages host tissues + organs more than actual infection
> sepsis

Sepsis

excessive production of excess cytokines leading to damaging inflammation

Infections of the heart

- pericarditis
- myocarditis
- endocarditis

Percarditis

inflammation of the membrane surrounding the heart (pericardium)

Myocarditis

inflammation of the heart muscle (myocardium)

Endocarditis

inflammation of the inner lining of the heart (endocardium)

Vasculitis

inflammation of the blood vessels

Lyphangitis

inflammation of lymph vessels

Ischemia

reduced blood flow to tissues

Necrosis

tissue death

Bacterial pathogens of the circulatory system

- S. aureus
- C. perfringens

S. aureus circulatory disease

toxic shock syndrome