Microbiology Exam 4 Study Guide

anatomy of respiratory tract

composed of upper tract and lower tract

lower tract is blocked by the mucociliary escalator

infections can move from upper tract to lower tract; disease in the lower tract is more severe

URT (upper respiratory tract) normal flora

1) corynebacterium diphtheriae

2) streptococcus pneumoniae

3) haemophilus sp.

4) neisseria meningitidis

5 general upper respiratory tract diseases

1) sinusitis

2) pharyngitis

3) tonsillitis

4) epiglottis

5) laryngitis

sinusitis

inflammation in the lining of the sinuses; sinuses fill with fluid, causing pressure to build

if it lasts more than 10 days, it is likely bacterial and you need antibiotics

common causes of sinusitis

viral infections - common cold

haemophilus influenzae

streptococcus pneumoniae

staphylococcus aureus

pharyngitis (sore throat)

lining of the throat becomes inflamed

pain, itchiness, redness, white patches

common causes of pharyngitis

viral infections - common cold or flu

streptococcus pyogenes (strep throat)

tonsilitis

infection and swelling of the tonsils

spots or a film on tonsils

common causes of tonsilitis

viral - flu or common cold

streptococcus pyogenes

streptococcus pneumoniae

epiglottitis

inflammation of the epiglottis, which blocks the airway

a medical emergency; death within hours

common cause: haemophilus influenzae

laryngitis

inflammation of the voice box; vocal cords become irritated and voice is lost

common causes of laryngitis

viral - flu or common cold

streptococcus pyogenes

streptococcus pneumoniae

candida sp.

bacterial diseases of the upper respiratory tract (URT)

1) strep throat

• rheumatic fever

• scarlet fever

2) diphtheria

strep throat

streptococcus pyogenes

• group A (GAS)

characterized by white streaks on tonsils

rheumatic fever

develops 2-4 weeks after an untreated group A streptococcal infection (strep throat)

M protein: virulence factor that plays a central role in developing this disease

always treat strep throat with antibiotics

scarlet fever

caused by GAS (group A streptococcus pyogenes) that triggers a distinctive red, sandpaper-like rash

toxin: erythrogenic toxin that participates in toxemia

toxemia (scarlet fever)

clinical state where toxins produced by GAS enter the bloodstream, triggering systemic symptoms like high fever, “sandpaper” rash, and strawberry tongue

toxin vs. toxemia

toxin: poisonous substance produced by a living organism (bacteria, plants, animals)

toxemia: medical condition characterized by the presence + spread of toxins directly within the bloodstream

diphtheria

bacterial infection caused by corynebacterium diphtheriae

non-virulent strains are normal flora

tough, grayish membrane of fibrin, dead tissue, and bacteria

diphtheria toxin

diagnosis of diphtheria

must verify presence of diphtheria toxin

toxin vaccines: DTaP vaccine (children) and Tdap vaccine (teens/adults)

viral diseases

1) common cold

2) influenza

common cold

usually viral (caused by a virus)

• rhinovirus: adults have immunity to most of the strains

• coronaviruses: primary cause in adults

additional causes of common cold

adenoviruses

coxsackieviruses

signs of common cold

sneezing

runny nose

headache

sore throat

cough

nasal congestion

cough may linger due to damage to airways

influenza

enveloped, RNA virus

influenza strains A, B, and C; most infections are A

the flu

difficult to distinguish from other respiratory infections

can test through lateral flow for antigens or PCR for viral nucleic acids

how do flu viruses get their names?

influenza subtypes

when antigenically different, new subtype

why is the flu vaccine new every year?

antigenically different: when an antigen is not recognized by the same antibody anymore

genomes mutate over time (antigenic drift)

influenza can swap RNA segments w/ other influenza viruses (antigenic shift)

antigenic drift

minor mutations where subtype remains the same

vaccines become less effective over time

antigenic shift

causes large changes over a short period of time

often the source of epidemics

flu vaccine

every year, flu scientists meet and predict the next season’s flu strains and subtypes

takes 1 year to make the flu vaccine

each seasonal vaccine is trivalent (protect against 3 different flu viruses)

defense mechanisms of the lower respiratory tract

blocked by the mucociliary escalator

little to no normal flora

alveolar macrophages

diseases of the lower respiratory tract (LRT)

1) bronchitis

2) pleuritis

3) pneumonia

bronchitis

inflammation of the bronchi marked by cough and wheezing

pleuritis

smooth pleural lining gets inflamed and rubs together

pneumonia

infection and swelling of lung tissue → difficulty breathing

bacterial is usually more serious due to pus

sputum

thick mucus coughed up from lungs

sputum culture

less than 10 squamous epithelial cells

greater than 25 WBC per low power field on gram stain

bacterial diseases of the lower respiratory tract (LRT)

1) whooping cough

2) primary pneumonia

3) atypical/walking pneumonia

• mycoplasma pneumoniae

• chlamydophila pneumoniae

• legionnaires disease

4) tuberculosis

5) secondary pneumonia

whooping cough

bordetella pertussis

reportable disease

pertussis virulence factors

1) pertussis toxin

2) tracheal toxin

3) filamentous hemagglutinin

stop mucocilliary escalator and allows entry to lower respiratory tract

pertussis toxin

causes systemic symptoms

halts phagocytosis

increases mucus production

tracheal toxin

damages ciliary cells

filamentous hemagglutinin

attaches to ciliated epithelial cells and impedes ciliary action

diagnosis of pertussis

characteristic whoop

prevention of pertussis

vaccine: DTaP

primary pneumonia

streptococcus pneumoniae

also called pneumococcal pneumonia

pyogenic coccus (capable of forming pus)

prevention for primary pneumonia

vaccines: PNEUMOVAX (elderly) or PCV 13 (for kids)

atypical or “walking” pneumonia

describes a milder form of pneumonia

bacterial causes of atypical/”walking” pneumonia

1) mycoplasma pneumoniae

2) chlamydophila pneumoniae

3) legionella pneumophila

mycoplasma pneumonia

bacteria have no cell wall

chlamydophila pneumoniae

intracellular life cycle

legionnaires pneumophila

also called “legionnaires disease”

inhalation of bacteria → form contaminated water

associated with outbreaks

legionnaires considerations

test water temps to ensure bacteria can’t grow

tuberculosis (TB)

mycobacterium tuberculosis

intracellular bacteria

TB (tuberculosis) disease

immune cells form a wall around infection, called a tubercle

this allows TB to go “latent”

disruption of the wall will cause bacteria to spread, and disease is “reactivated”

tubercle

specific term for a granuloma (cluster of immune cells) in the lungs

extrapulmonary or miliary TB

active tuberculosis disease

greenish or bloody sputum

epidemiology of TB

increasing drug resistance

serious problem with AIDS

diagnosis of TB

use tuberculin skin test (TST) or purified protein derivative (PPD)

if symptomatic, use an AFB smear

also use X-ray and PCR

treatment of TB

prolonged antibiotics (6 months)

viral causes of pneumonia and other diseases

1) respiratory synctial virus

2) SARS/MERS

3) COVID-19

respiratory syncytial virus

common and dangerous infection of infants; premature infants at highest risk

life-threatening in elderly

new vaccine for pregnant mothers and elderly

SARS and MERS

2 separate diseases caused by 2 separate coronaviruses

disease starts like influenza, but becomes severe (pneumonia, hypoxia, respiratory failure)

COVID-19

also known as SARS-Cov-2

SARS-CoV-2 was more contagious and less deadly than SARS/MERS

fungal diseases

1) histoplasmosis

2) coccidiomycosis

3) aspergillosis

4) pneumocystis pneumonia

histoplasmosis

histoplasma capsulatum

infects macrophages

can be confused w/ TB, granulomas form in lung

spread from the droppings of birds and bats

AIDS and immune compromised at high risk

coccidioidomycosis (valley fever)

coccidioides immitis

TB-like

spores spread by soil and wind

AIDS

aspergillosis

produces aflatoxins which are carcinogens

pneumocystis pneumonia

must be treated

occurs in infected infants and immunosuppressed individuals (AIDS)

paragonimiasis

parasitic infection characterized by lung flukes (paragonimus sp.)

caused from undercooked crabs/crayfish

look for eggs in sputum

what can give you a positive PPD or TST?

active, latent, extrapulmonary, and cured TB

BCG vaccine

past exposure

points of entry in the skin

1) wounds

2) pores

3) circulation

skin defenses

keratin and cell sloughing (desquamation)

high salt and oils (sebum) make environment unfavorable for microbes

also contain antimicrobial peptides

normal flora of the skin

staphylococcus epidermidis

corynebacterium diphtheriae

candida sp. (fungus)

staphylococcus aureus

lesions

changes to skin caused by infection; includes rashes, pustules, warts, and abscesses

we describe lesions by skin color or texture changes

diagnostic indicators

specific signs that indicate a disease

macule vs. papule

macule: flat and discolored lesion (vitiligo)

papule: raised and solid lesion (wart)

maculopapular rash

type of lesion that combines flat, discolored spots (macules) with small, raised bumps (papules)

vesicle vs. pustule

vesicle: fluid filled lesion filled with a clear fluid (blister)

pustule: fluid filled lesion filled with pus (acne)

pus

comprised of dead white blood cells and dead bacterial/fungal cells that is usually a sign of infection

purulent

describes a fluid that contains pus

abscess

deep tissue pustule

decreased blood flow

antibiotics don’t penetrate well; must drain to improve blood flow

considerations for lesion treatment

the deeper in the skin the infection goes, the more serious it is

-itis

infection of inflammation of (ex: folliculitis)

-emia

in the blood (ex: septicemia)

bacterial infections and skin

1) dermatitis (pseudomonas)

2) staphylococcus aureus

3) group A strep (GAS): streptococcus pyogenes

dermatitis

pseudomonas aeruginosa

gram-negative rod

pustules or papular lesions

naturally very antibiotic resistant

staphylococcus aureus

gram + cocci bacteria

diseases associated: impetigo, folliculitis, cellulitis, necrotizing fasciitis, MRSA skin infections, toxic shock syndrome (TSS)

virulence factors of S. aureus

capsule

coagulase (allows bacteria to clot plasma, shielding themselves from the host immune response)

protein A (prevents antibodies from binding to bacteria)

how does S. aureus protein A work?

1) protein A binds to the Fc region of host antibodies + Fab regions of B cell receptors

2) binds antibodies backwards → prevents immune cells from recognizing + engulfing the bacterium

toxemia

toxin enters bloodstream to cause disease

bacteria are not present at the site of symptoms + not in the blood

TSST-1

toxin released by S. aureus that causes toxic shock syndrome

severe symptoms - fever, rash, skin shedding

methicillin resistant staphylococcus aureus (MRSA)

MRSA is a methicillin resistant strain of S. aureus that is a serious and prevalent threat

hospital vs. community associated MRSA

hospital associated (HA-MRSA): mecA gene is present and it’s resistant to all antibiotics except vancomycin

community associated (CA-MRSA): contains mecA gene and PVL gene as an extra virulence factor; sensitive to many other antibiotics

streptococcus pyogenes

group A Streptococcus (GAS) causes various skin infections

gram positive cocci

GAS virulence factors

capsule

M protein

SPE A and SLO cause toxemias

GAS Necrotizing Fasciitis

toxemia associating with SPE A and SLO

“flesh eating” disease

rapid disease course

treatment for GAS

antibiotic treatment is a must due to the dangerous potential sequelae associated w/ GAS (ex: rheumatic fever)