Microbiology Flashcards
Common URIs
nasopharynx =
viruses! rhinovirus
coronavirus, coxsackie A/B, influenza C
Common URIs
oropharynx =
streptococcus pyogenes (“GpA Strep”)
corynebacterium diptheria
EBV, adenovirus, enterovirus
Common URIs
middle ear/parasinuses =
streptococcus pneumonia
haemophilus influenzae (non-encapsulated)
(think how pneumonia can cause otitis media)
also - moraxella catarrhalis, GpA strep
Common URIs
epiglottis =
haemophilus influenzae type b
(think how pneumonia can cause epiglottitis
Streptococcus Pyogenes/GpA Strep
ID/Diagnosis
Gm+ cocci in chains
catalase negative (=streptococci, not staphylococcus)
beta-hemolytic (clear hemolysis)
bacitracin sensitive (= streptococcus pyogenes)
ASO+ (anti-streptolysin O Ab is present)
confirm via commercial test w/ latex beads
*even if rapid test (RADT) is –ve, perform a GAS culture
Streptococcus Pyogenes/GpA Strep
Clinical Presentation
pharyngitis = inflammation of oropharynx, petechiae on soft palate; possibly nausea, vomiting, abdominal pain
*Suppurative
pharyngitis (rarely w/ scarlet fever)
pyoderma - impetigo, erysipelas, cellulitis
necrotizing fasciitis (toxin mediated)
streptococcal toxic shock syndrome (toxin mediated)
*Nonsuppurative
rheumatic fever (M proteins, molecular mimicry)
glomerulonephritis (immune mediated)
Streptococcus Pyogenes/GpA Strep
Virulence
M Protein - anti-phagocytic, molecular mimicry
Streptokinase (ASO+) - converts plasminogen to plasmin
Hyaluronidase - breaks down connective tissue
DNase - digests DNA
Streptococcus Pyogenes/GpA Strep
Treatment
Penicillin G
Haemophilus Influenzae
ID/Diagnosis
Gm– coccobacilli (= haemophilus)
oxidase +
chocolate agar + hemin (X factor) + NAD+ (V factor)
5-10% CO2
*slide agglutination test - determine type a-f
Haemophilus Influenzae
Clinical Presentation
Encapsulated (type b) bacterial meningitis (most common cause) epiglottitis pneumonia - kids, adults w/ COPD etc Unencapsulated (normal flora) otitis media + sinusitis, conjunctivitis
Haemophilus Influenzae
Virulence
6 capsular types, type a-f
type b capsule = polyribose-ribitol-phosphate (PRP, Hib)
PRP is anti-phagocytic
also - adhesive pili, factor that dysregulated ciliary beating, protease that degrade IgA
Haemophilus Influenzae
Treatment
vaccination = Hib polysaccharide protein coupled to diptheria toxoid
tx - 3rd generation cephalosporin or ampicillin
Corynebacterium Diphtheriae
ID/Diagnosis
Gm+ bacilli - “Chinese letters”
catalase +, non-motile, non-spore forming
black colonies on potassium tellurite
*diphtheroids are normal flora; differentiate pathogenic corynebacterium via PCR
Corynebacterium Diphtheriae
Clinical Presentation
any mucus membrane
pseudomembrane + airway obstruction
myocarditis, polyneuritis (nerve palsy)
Corynebacterium Diphtheriae
Virulence
diphtheria toxin, toxin AB
prevents protein synthesis in all cells
ADP-ribosylates and inactivates EF-2
Corynebacterium Diphtheriae
Treatment
antibiotics, antitoxin (horse, potential for serum sickness)
vaccination - DTaP, contains inactivated toxoid AB
Rhinovirus - Transmission
respiratory droplets
direct contact
starts with R, transmitted via Respiratory droplets
RSV - Transmission
respiratory droplets
direct contact
“respiratory” SV, transmitted via “respiratory” droplets
Adenovirus - Transmission
respiratory droplets direct contact \+ fecal-oral \+ contaminated water (ADenovirus has ADditional methods of transmission)
EBV - Transmission
saliva, the “kissing disease”
Rhinovirus - Target Cells
respiratory epithelial cells of nose (lower temp, 88-90F)
RSV - Target Cells
epithelial cells of URT
Adenovirus - Target Cells
mucoepithelial cells, “adeno”id cells
EBV - Target Cells
epithelial and “B” cells
Rhinovirus - Clinical Presentation
Common Cold - incubation (2-4 days), self-limiting
rarely, bronchopneumonia (kids) or chronic lung injury (COPD, asthmatics, immunocompromised)
RSV - Clinical Presentation
URT, Croup, Bronchiolitis
Croup = cold + tachypnea, wheezing, cyanosis
self-limiting (7-10 days)
*immunity is not long-lived, can have repeated infections
Adenovirus - Clinical Presentation
Pharyngitis, Acute Respiratory Disease (*military recruits)
self-limiting (7-10 days)
Conjuntivitis, Pneumonia
EBV - Clinical Presentation
Pharyngitis, Mononucleosis- self-limiting (2-3 weeks)
swelling, redness and white patches on tonsils; swelling of lymph nodes (Cervical Lymphadenopathy)
Rhinovirus, RSV, Adenovirus, EBV
Diagnosis and Treatment
Ddx - symptoms, viral culture, PCR, ELISA, DFA (direct fluorescent antibody), serology. EBV can be detected via atypical lymphocytes (CD8 CTL) and agglutination tests for heterophile antibody.
*Vaccines
rhinovirus - none due to >100 serotypes
RSV - none, limited success treatment with ribavirin or RespiGam (passive immunity)
adenovirus - none, live tablet now available in military
EBV - none
Rhinovirus, RSV, Adenovirus, EBV
Structure
Rhinovirus: +ssRNA, icosahedral, nonenveloped
RSV: –ssRNA, helical, enveloped
Adenovirus: dsDNA, icosahedral, nonenveloped
EBV: dsDNA, icosahedral, enveloped
RSV has F (fusion) and G (attachment) proteins.
*RNA viruses start w/ R; RSV is only helical virus; viruses with 3 letter abbreviation are enveloped
Rhinovirus, RSV, Adenovirus, EBV
Replication and Cell Cycle
RNA viruses (rhinovirus and RSV) replicate in cytoplasm; DNA viruses (adenovirus, EBV) replicate in nucleus.
Rhinovirus - released via cytolysis.
RSV - released via exocytosis, forms syncytium.
Adenovirus - lytic (mucoepithelial cells) or latent (adenoids).
EBV - released via exocytosis or lysis.
Influenza Viruses
Orthomyxoviruses - Characteristics
–RNA, 8 segments, enveloped
HA (haemagglutinin) and NA (neuraminidase) spikes
type A - antigenic shift and drift, most disease
type B - antigenic drift
type C - stable, cause of cold-like symptoms
Influenza Viruses - Replication
- HA binds sialic acid moiety, enters cell.
- Acidic pH (via M2 ion channel) facilitates particle disassembly and envelop fusion.
- Replication and protein synthesis.
- NA cleaves HA-sialic acid bond, facilitation virus release.
Influenza Viruses - Pathogenesis
- Short incubation (1-4 days).
- Replicates in respiratory epithelium; no viremia.
- Damage to respiratory epithelium renders susceptible to secondary infections (pneumonias).
- Interferons and cytokines produce symptoms of disease.
- Immunity via IgA in respiratory tract (can still infect others).
Influenza Viruses - Clinical Presentation
Primary Infection - HIGH fever (IL-1), etc.
Complications - secondary bacterial pneumonia, viral pneumonia (severe disease -> ARDS), myositis, cardiac involvement, neurologic symtoms.
Influenza Viruses - Vaccines
QIV - Quadrivalent Inactivated Vaccine
2 type A, 2 type B
intramuscular injection
healthy persons > 6 mo.
LAIV - Live Attenuated Influenza Vaccine
2 type A, 2 type B
nasal spray (Flumist)
healthy persons btw 2 and 49 years
H1N1 Monovalent Vaccine (Swine Flu)
pregnant women, caregivers of children < 6mo., kids 6 mo.-24 years, persons 24-64 with health conditions that put them at risk
Influenza Viruses - Treatments
NA Inhibitors = OseltaMIVIR (Tamiflu) and ZanaMIVIR (Relenza) - inhibits viral shedding, type A and B
M2 Inhibitors = AMANTIDINE, RiMANTIDINE - give early, blocks M2 channel, increases pH in endosome, prevents viral disassembly; type A ONLY
Mycobacterium TB - Epidemiology
Exposed? 30% are infected.
Infected? 5% develop disease w/in 2 years.
Latent infection? 5% develop disease w/in lifetime.
Active infection? 10-20% develop non-infectious extra-pulmonary disseminated disease.
Mycobacterium TB - Clinical Presentation
fever/night sweats, cough/hemoptysis, weight loss, fatigue, chest pain
Mycobacterium TB - Risk Groups
Exposure - close contacts, foreigners, healthcare workers, low socio-economic class
Development of Dz - HIV/AID, IV drug users, immunocompromised, other medical conditions (type 1 diabetes, renal impairment, cancer, etc)
Mycobacterium TB - Pathogenesis
Primary TB - caseating granulomas, Ghon Complex = primary lesion (TB w/in macrophage) + infected adjoining lymph node -> calcify.
Reactivation TB - rupture of granuloma, cavitation on CXR, usually in apices of lung.
Miliary TB - small lesions in multiple organs.
also…lymphadenitis (associated with M. bovis and milk), meningitis, Pott’s disease (vertebrae, posts m.)
Mycobacterium TB - Diagnosis
PPD Test (purified protein derivative)
Interferon Gamma Release Assays - more sensitive, can be used in persons vaccinated with M. bovis-derived vaccine
CXR - latent (Ghon) v. active (cavitary lesion)
Culture for acid-fast bacilli! Gold-Standard
Mycobacterium TB - Treatment
Latent - 9 mo. isoniazid
Active - 9 mo. RIPE = rifampin, isoniazid, pyrazinamide, ethambutol; consider DOT (direct observed therapy)
Mycobacterium TB - Vaccine
BCG Vaccine - live attenuated M bovis
not used in US due to adverse reactions, waning of immunity @ 10 years, false + PPD
