Exam VI - Respiratory & Genital Infections Flashcards Preview

Microbiology > Exam VI - Respiratory & Genital Infections > Flashcards

Flashcards in Exam VI - Respiratory & Genital Infections Deck (94)
Loading flashcards...


Streptococcus pyogenes
Group A beta-hemolytic strep, GAbS
Transmission: Respiratory droplets
Incubation 2-4 days
Symptoms: Abrupt onset fever, sore throat with exudate (suppurative = pus generating), may have abdominal pain, nausea, vomiting
Diagnosis: rapid strep test
At risk population: children


Streptococcus pyogenes

Gram-positive cocci in pairs or chains
Catalase negative
Beta-hemolytic on blood agar plate
M Protein: antiphagocytic and antigenic variation
SPE: Streptococcal pyrogenic exotoxins; encoded by phage with many enzymes; pyro = fever causing


Scarlet Fever

caused by streptococcus pyogenes
Potential complication of strep throat due to pyrogenic exotoxin with symptoms 1-2 days after pharyngitis
Sandpaper rash
Starts on face spreads to body, not on palms or soles
1 week duration then desquamation
Strawberry tongue


Rheumatic Fever

caused by streptococcus pyogenes
Potential complication of strep throat
Antibodies made against the S. pyogenes M protein (during original pharyngitis infection) cross react with
protein on heart valves and joints
Damage heart valves over time causing endocarditis leading to scarring of heart valves, stenosis, regurgitation, and rheumatic heart disease (RHD)
Polyarthritis - multiple joints affected


Corynebacterium diphtheria

Gram positive, club shaped (rod), non-motile
Catalase positive
Humans are the only reservoir
Respiratory: transmission respiratory aerosols
Cutaneous: transmission skin contact

Virulence Factor
Diphtheria toxin: phage mediated produced at site of infection that disseminates through the blood and binds to receptors on heart, throat, and nerve cells


Mechanism of Action: diphtheria

Same as P. aeruginosa Exotoxin A (AB toxin)
ADP-ribosyl transferase
Inactivates elongation factor 2
Inhibits host protein synthesis


Respiratory diphtheria

Incubation 2-4 days
Attach and multiply in the pharynx- location of infection
Exotoxin causes tissue damage
Formation of thick gray pseudomembrane exudate - will bleed if tested with swab
Malaise, sore throat, fever, exudative pharyngitis, bill neck
Potential complications: myocarditis and neurotoxicity


Cutaneous diphtheria

Gains entry to subcutaneous tissue through break in the skin - immunocompromised
Chronic, non-healing ulcer - necrosis due to toxin


Diagnosis of diphtheria

Selective agar: cysteine tellurite blood agar
Tinsdale agar
Tellurite: grayish black colonies
Cysteine: brown halos surrounding colonies


Bordetella pertussis

Gram negative (has LPS) coccobacillus (rod), aerobic
Disease: pertussis
highly contagious disease with uncontrolled violent coughing
High Risk Population: unvaccinated children and vaccinated teens (middle school, high school age)

Virulence factors:
Attachment: bind to ciliated epithelial cells = pertactin and filamentous hemagglutinin
Tissue damage caused by pertussis toxin
ADP ribosylating activity of G proteins, increased cAMP, increased resp. mucus
tracheal cytotoxin has a high affinity for cilia causing ciliostasis or death of cells leading to characteristic cough; also stimulates IL-1 resulting in fever via T cells


Pathogenesis of Bordetella pertussis (4)

1. Exposure: aerosol droplet inhalation
needs human reservoir
2. Attachment to ciliated epithelial cells via pertactin and filamentous hemagglutinin
3. Proliferation
4. Tissue damage via pertussis toxin and tracheal cytotoxin


Pertussis: 3 stages

7 to 14 day incubation

1. Catarrhal: coldlike symptoms, runny nose, sneezing, malaise, low fever, loss of appetite; highly transmissible, large # of bacteria
2. Paroxysmal: damage ciliated cells, impaired mucus clearance; prolonged coughing fits with inspiratory whoop, 40-50/day, vomiting exhaustion, ruptured blood vessels in the eyes
3. Convalescence: recovery


Diagnosis of Pertussis

Nasopharyngeal aspirate best
Classic: Bordet-Gengou medium
Current: Regan-Lowe agar
Inoculate at bedside
7-12 days incubation
PCR – best if available


Treatment of Pertussis, Tetanus, and Diphtheria

Acellular Vaccine - currently recommended
Inactivated pertussis toxin + Filamentous hemagglutinin + pertactin
Part of DTaP for children



Inflammation of the lungs accompanied by fluid filled alveoli and bronchioles
May involve: hemoptysis (coughing blood)
Caused by inhalation of aerosols, aspiration of normal flora (URT and GI), or hematogenous spread from another site of infection
nosocomial or community acquired
Types: typical vs. atypical


Typical Pneumonia

streptococcus pneumonia
Abrupt onset, fever, chills, congestion, shortness of breath (dyspnea), chest pain
****Productive cough
Streptococcus pneumoniae, Klebsiella pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus

Characteristics of bacteria: also known as pneumococcus, lobar pneumonia, gram positive, pairs or chains, alpha hemolytic, blood agar, CAPSULE, adhesin, IgA protease, pneumolysin: lyses ciliated epithelial cells


Typical Pneumonia: Causes, Dx, and Tx

Fall & winter, CAP (community acquired pneumonia)
Predisposing factors: viral infection, influenza, HIV, alcoholism, children, elderly, splenectomy

Diagnosis: sputum sample - rust colored
Microscopy - gram positive cocci and numerous PMNs, antigen agglutination (secreted in urine as well as sputum)
Alpha hemolysis
Optochin sensitive

Pneumovax: 23 most common capsule serotypes, PPSV23; adult
Pneumococcal conjugate vaccine: PCV13, children


Atypical Pneumonia

Organisms not seen with Gram stain (except Lp)
fever, headache, malaise, myalgia, nausea, diarrhea, many neutrophils, dry hacking cough
***Nonproductive cough (no sputum)

Mycoplasma pneumoniae
Chlamydophila spp.
Legionella pneumophila
Coxiella burnetii


Mycoplasma pneumoniae

Primary atypical pneumonia, community acquired
Symptoms: atypical pneumonia; persistent nonproductive cough, excessive sweating
May last several weeks to months; lack of seasonality
"walking pneumonia"
Characteristics: smallest free living microbe, no cell wall, capsule, adhesin (attachment to the base of the cilia)
Transmission: inhalation of aerosols

Dx: usually can not see the bacteria with microscopy, large number of PMNs, grows very slowly in culture, 2-6 weeks, *cold agglutinins*


Chlamydophila pneumonias

Characteristics: gram negative, CAP, obligate intracellular bacteria; mild infection
TWAR: Taiwan Acute Respiratory Agent
Transmission: respiratory droplets
Symptoms: mild fever, sore throat, malaise, persistent cough; atypical pneumonia

Diagnostics: Microscopy/Gram stain: no organisms seen
large number of PMNs
Elementary body: body that gains entry to the cell and survive; most active
Reticulate body: when ready to multiply it starts the second stage



Chlamydophila psittaci
Parrot fever
Disease of birds can be transmitted to humans


Legionnaires’ Disease

Legionella pneumophila; atypical pneumonia
Characteristics: gram negative, does not Gram stain well, intracellular
Water cooling towers and air conditioning units
Environment: amoeba
Human: alveolar macrophages
Transmission: inhalation of aerosolized droplets
Symptoms: abrupt onset of fever, headache, pleurisy, chills, myalgia, dry cough; complications involving GI tract, CNS, liver and kidneys are common
Pontiac Fever: strong immune system means that this infection will probably go away on its own


Legionnaires' Disease: Risk and Dx

Risk factors: smokers, COPD, high alcohol consumption, elderly, immunosuppressed, renal transplant patients, or patients on dialysis

Culture: fastidious (picky) - buffered charcoal yeast extract agar (BYCE) with iron salts and cysteine
Fluorescent antibody staining
Antigen can be detected in urine


Common Causes of Nosocomial Pneumonia

Pseudomonas aeruginosa, S. aureus, H. influenza
Enterics: Enterobacter , Klebsiella, E. coli, Serratia marcescens - if they go anywhere else other than GI via vomiting = problems


Pseudomonas aeruginosa

Gram-negative rod, ubiquitous, capable of growing on many substrates and temperatures ranging 4-42 C, aerobic, and forms a biofilm - Alginate capsule
Motile: flagella and pili
Opportunistic and nosocomial infections; highly antibiotic resistant
Characteristic color and sweet grape like odor
Oxidase positive


P. aeruginosa: CF

Risk factors: cystic fibrosis - colonized by S. aureus first then with P.aeruginosa by 5 yrs old - lifelong
Burkholderia cepacia is also another lung bacteria that affects those with CF
These bacteria cause the immune system to cause the damage (indirectly)
Most CF patients die from P. aeruginosa lung associated infections (90%)
Research very hard because alginate in P. aeruginosa contributes to the biofilm formation
Fresh isolates of P. aeruginosa from CF patients are mucoidy, but in vivo and in vitro switching in the mucoidy phenotype via quorum sensing in culture
Hospitalized on ventilation- high risk



Aspiration of respiratory or gastric material
Risk factors: dental work and loss of consciousness
mixture of Bacteroides and Fusobacterium - necrotizing, lung abscesses, empyema (formation of pus in pleural cavity)
***copious amounts of foul smelling sputum


Potential Bioterrorism Agents

Q fever


Bacillus anthracis

Gram positive rods occurring in chains
Aerobic, non-motile, forms resistant endospores
Spores remain viable for years in soil, dried or processed hides; present in air, water, soil and vegetation
Three types: cutaneous, inhalation, and GI

Inhalation: capsule (polyglutamic acid capsule (AA)) + anthrax toxin
Transmission: inhalation of endospores (spores have no taste or smell)
Initial - sore throat, mild fever, myalgia, cough
After several days - severe coughing, nausea/vomiting, lethargy, confusion, shock, death


Anthrax Toxin

Major virulence factor secreted by B. anthracis
Encoded by plasmid pXO1 carrying three toxin genes
A/B toxin
Three component proteins:
Protective antigen (PA)
Edema factor (EF)
Lethal factor (LF)
*these cause tissue damage, edema, and cell death
High mortality rate