Download RT Bugs Chart

Upper Respiratory Tract Infections
BACTERIAL AND FUNGAL:
Location of Infection
Causative Agent
ORAL INFECTION
Oral Anaerobes
Virulence Factors
Lymphocyte Activators: induce
inflammatory response
Etiology
Caused by normal flora
Polymicrobic
Complement activation/PMN
content release: tissue damage
Form localized abscesses
Pathogenesis
Chronic Marginal Gingivitis: between
teeth and gums
-PMNs/lymphocytes enter CT attached
to tooth (inflammation)
-No bacterial invasion
-Can occur in 2 weeks w/o tooth care
Periodontitis: teeth and supp. tissue
-Progressive gingivitis (bone
resorption, loss of ligament, loss of
entire tooth)
-Bacterial invasion may occur
Actinomyces israelii
--
Normal flora: colonizes
mucosal surfaces
(oropharynx to lower
intestine)
Endogenous infection: only
occurs upon penetration of
epithelial barrier (low O2
tension)
Viridans Streptococci
Candida albicans
Glucans: polysaccharides that
permit attachment to teeth
Adhesion: mannoprotein binds
fibronectin receptors
Invasion:
-Invasive hyphae bind fibronectin,
collagen, and laminin
-Proteases and elastases
Normal flora: of oral and
nasopharyngeal cavity
Predisposing Factors:
-Abx (diminish normal flora)
-Compromised immune
system
-Disruption of mucosa (ie.
catheter or cancer
chemotherapy)
-Diabetes (increased
glucose and surface R)
Acute Necrotizing Ulcerative Gingivitis
(Trench Mouth):
-Ulceration of gingiva (bone resportion
and tooth loss)
-Bacterial invasion occurs
Follows mouth trauma:
-Inflammatory sinuses fill with pus and
bacteria from initial site of infection
-Slow progressing
Thoracic Actinomycosis: may occur if
sinus extension or aspiration occurs
Polymicrobic infection: also GNRs in
sinuses
Dental Cavities: S.mutans
Subacute Bacterial Endocarditis: tooth
extraction leads to transient
bacteremia and colonization of
damaged heart valves
Stomatitis: inflammation of the oral
cavity
-Oral Thrush: multiple white plaques
loosely adherent to tongue or palate
-Inflammatory patches on esophagus
Clinical ID
Diagnosis: via Sx
Mixed anaerobes not
differentiated
Abscesses may be
sampled: must be
cultured in anaerobic
conditions
-Mostly G(-) rods and
PMNs
Shape: G(+) filamentous
rod- looks like fungi
Culture:
-Sulfur granules (yellow
granules- diagnostic)
-Anaerobic or
microaerophilic
-Slow growth
Shape: G(+) cocci
Biochemical:
-Catalase (-)
-No Lancefield group
Specimen: scrapings of
infected mucosa
-KOH or Gram stain
shows budding round
yeast with hyphae
-Germ tube formation
EAR/SINUS INFECTION
Streptococcus
pneumoniae
Polysaccharide Capsule: primary VF
-Anti-phagocytic
-Prevents complement deposition
-Abs to it confer immunity
Cell Wall TA and PG: inflammation
Predisposition for URTIs:
-High carriage rate
Predisposition for Acute
Otitis Media:
-Viral infection
-Allergies
-Infant (short/pliant
Eustachian tubes)
Acute Otitis Media: middle ear inf.
-Eustachian tube inflammation
-Bacteria enters middle ear from
nasopharynx
Sinus Infection: acute and chronic
sinusitis in all ages
Needle Aspiration:
difficult cases
-OM: pus behind
tympanic membrane
-S: sinus wall puncture or
catheterization
Predisposition for Sinusitis:
-Viral Infection
-Allergies
-Anatomical blockage
Haemophilus
influenzae
Polysaccharide Capsule: primary VF
-Antiphagocytic
-Antigenic variation
-Polyribitol phosphate capsule with
6 serotypes (a-f)
IgA Protease: colonization
Non-Pilus Adhesins: tissue tropism
(direct to mucosal surfaces)
PHARYNX INFECTION
Streptococcus
pyogenes
(GAS)
Facilitating Immune Evasion:
M protein:
-Anti-phagocytic
-80 different serotypes
-Antigenic variation
Protein G:
-Binds Fc portion IgG Abs
Hyaluronic Acid Capsule:
-Antiphagocytic
Facilitating Colonization:
Protein F:
-Bind nasopharyngeal epithelium
-Regulated by O2 levels
M Protein:
-Binds epidermis (impetigo)
Normal Flora: high carriage
rate in URT
-Most have no capsule (nontypeable)
Predisposing Factors for
Otitis Media/Sinusitis:
-Viral infection
-Displacement of flora to
sterile sites
Transmission: person to
person spread via droplets
Diagnosis: clinical exam
-OM: swollen tympanic
membrane (pus
formation)
-S: symptoms and
radiography
Otitis Media and Sinusitis:
-Most causes of OM are non-typeable
(therefore, not affected by Hib vaccine)
-Common in kids under 5
-If caused by Hib, can lead to
meningitis
Shape: G(+) lancet
shaped diplococcic
Biochemical:
-No Lancefield group
-Optochin sensitive
Diagnosis: clinical exam
Needle aspirate: in
difficult cases (as above)
Shape: G(-) coccobacillus
Growth: fastidious (needs
factor X and V)
Most common bacterial cause of
pharyngitis: but usually due to viruses
Scarlet Fever: may occur with
pharyngitis (due to Spe)
-Rash (Face  trunk and extremities)
-Strawberry tongue
Post-Streptococcal Sequelae:
-Rheumatic Heart Disease (~3 weeks
after pharyngitis)
-Acute Glomerulonephritis (more
commonly following skin infection)
Capsular serotyping
Throat swab of tonsils
and pharynx:
-Culture on BAP for Bhemolysis
-Aggulitination test for
Lancefield group A (rapid)
Biochemical Tests:
-Catalase (-)
-Bacitracin sensitive
High titers anti-SLO Abs:
in patients with
rheumatic fever
Corynebacterium
diphtheria
Exotoxins:
SLO: oxygen labile
SLS: oxygen stable
-B-hemolysis
-Form pores in cell membranes
Spe A-C (Erythrogenic/Scarlet Fever
Toxins):
-SpeA only produced by some
lysogenized GAS
-Superantigens (similar to Staph
exotoxins)
-Cytokine release
-Toxic Shock Like Syndrome
Diphtheria Toxin: only VF
-AB toxin (polypeptide with nicked
chain between A and B)
-B binds EGF precursor on cell
membrane
-A is enzymatic subunit (ADPribosylates elongation factor 2 to
halt translation)
Tox Genes:
-Carried by bacteriophages
-Synthesis negatively regulated by
iron (production is on when iron is
low, such as in human host)
Bordetella pertussis
(Whooping Cough)
Filamentous Hemagglutinin (FHA)
and Pili:
-Adhesin for binding mucosal
epithelial cells
-Directs organism to MØ
-Agglutinates RBCs
Pertussis Toxin (Ptx):
-AB toxin
-B subunit made of 5 non-identical
subunits (binding)
-A subunit (enzymatic) ADPribosylates Gi, preventing Gs from
being turned off (increase cAMP)
Invasive Adenylate Cyclase:
-Enters cell directly to ↑ cAMP
-Requires calmodulin
Rare in US: due to
immunization
Bacterial Toxinosis with NO invasion:
-DT responsible for ALL pathogenesis
Diagnosis: based on
clinical symptoms
Only lysogenized strains
produce DT: required for
pathogenesis (can
lysogenize in vivo and
convert to toxin producing
strain)
Manifestations of DT Cytotoxicity:
-Pseudomembrane formation (can
cause suffocation)
-Systemic manifestations (organ
damage to heart and CNS)
Throat swab: difficult
because it is a normal
resident flora in many
people
Transmission: droplet
spread or contact with
cutaneous infection/fomite
-Can have asymptomatic
carriers of toxinogenic
strains
Only infects humans: often
seen in infants and
preschoolers
Transmission: HIGHLY
contagious; droplet spread
-Adults can be carriers and a
source of infection for
unvaccinated newborns
Shape: G(+) club shaped
rods (remain attached
after division-“Chinese
Letters”)
Whooping Cough: acute bronchitis
with violent/paroxysmal cough
-Can also cause edema and
hemorrhages in the brain
Deep Nasopharyngeal
Cultures: needs to be
cultured immediately
(does not survive well)
Pathogenesis:
-FHA directs organism to adhere to
bronchial epithelium
-Toxins kill ciliated cells and interfere
with phagocytosis
-Systemic effects due to TOXIN
-Local inflammatory response to
BACTERIA in bronchi leads to cough
Growth:
-CAP with cephalosporins
(to inhibit G positive)
Shape: G(-) coccobacillus
(resembles H.flu)
Direct fluorescent Ab
detection: should still
confirm with culture
Lower Respiratory Tract Infections
BACTERIAL AND FUNGAL:
Causative Agent
Virulence Factors
Streptococcus pneumoniae
Polysaccharide capsule: primary VF
-Over 90 serotypes
-Anti-phagocytic
-Prevents complement deposition
-Evasion of lung surfactant
-Abs to it confer immunity
Pneumolysin: sulfhydryl activated cytolysin
-Damages membranes (like SLO)
-Binds cholesterol on cell membrane
-Acts on several cell types (PMN, monocytes,
pulmonary epithelium)
-Several functions (immune evasion, spread
to bloodstream, inflammation via
complement activation)
Etiology
Human pathogen only: many
asymptomatic carriers
Transmission: person to person
(droplet)
Most common cause of acute
bacterial pneumonia: in all age
groups
Polysaccharide Capsule:
-Anti-phagocytic
-Antigenic variation
-Serotype B most virulent
Normal Flora: common in URT
-Both encapsulated and nonencapsulated (more common)
Transmission: person to person
(droplet)
Common Age: 2-5 years old
Legionella pneumophilia
Existence inside amoeba:
-More resistant to disinfectants
-Can survive winter inside cyst of amoeba
Clinical ID
Sputum Gram Stain: issue because
of contamination with polymicrobic
saliva
Acute Pneumonia: infection of lung
parenchyma
-Cough with productive sputum (purulent
and rusty red color)
-Inflammation  ↑ vascular permeability
 fluid accumulation  suffocation
Radiology: bronchopneumonia or
lobar consolidation
Secondary Complications:
-Bacteremia (due to inflammation and
damage to endothelial cells)
-Acute Purulent Meningitis
Cell Wall TA/PG: inflammation
-Causes fever and lung damage
-Activate alternative complement pathway
-Production of IL1 and TNF
Haemophilus influenzae
Pathogenesis
Organism establishes in LRT:
-Aspiration from middle RT
-Compromised cough reflex permits entry
(stroke, alcoholism, viral infection,
anesthesia)
-Alveolar Abs NORMAY clear it
Parasite of freshwater and soil
protozoa: found in cooling
towers, AC systems, plumbing,
respiratory equipment etc.
Transmission: inhalation (no
person-to-person spread)
Generally low virulence in
humans: most people have Abs
because of ubiquity
Pneumonia:
Encapsulated: similar to pneumococcal
pneumonia
-Higher virulence/blood culture more likely
(+) with Hib infection
-Less common as normal flora
Non-encapsulated: less virulent
-Predisposing factors include chronic
bronchitis, emphysema, COPD
Acute Epiglottitis: also possible
Legionnaire’s Disease: severe pneumonia
with high mortality rate
-2 to 10 day IP
Pontiac Fever: nonpneumonic febrile
illness (mild flu-like symptoms); may be
due to inhalation of dead or low virulence
strains
-1 to 2 day IP
Disseminated Disease: rare
Blood Culture: detects bacteremia
-Latex agglutination for Abs
Shape: G(+) lancet shaped
diplococcic
Biochemical:
-Alpha hemolytic
-No Lancefield grouping
-Capsular serotyping
-Quelling reaction
-Optochin sensitive
-Bile soluble (distinguish from
viridians strep)
Samples:
-Sputum
-Blood cultures (positive in 10-15%
of patients; higher with Hib)
Shape: G(+) coccbacilli
Growth: fastidious (requires X and
V)
Urine EIA test for soluble Ag
Does not Gram stain well:
-Silver stain (thin, pleiomorphic G(-)
rod with filamentous forms)
Growth (slow): requires L-cysteine,
amino acids, and ferric ions; also
needs buffered medium (pH rest.)
Organism rarely found in sputum
Disease Process:
-Tropism for lung alveoli and bronchioles
-Surface protein binds C3 to enhance its
own phagocytosis (“coiling”); can also have
bacteria-induced phagocytosis (no C3
bound)
-Intracellular parasite in monocytes and
macrophages (multiplication normally
inhibited in activated MØ)
Acinetobacter spp.
Mycoplasma pneumoniae
Antibiotic Resistance: innately resistant to
many classes of antibiotics
Adhesin: binds sialic acid containing
glycolipids or glycoprotens on bronchial
epithelial cells
Hydrogen peroxide: damages tissue
Superoxide: damages tissue
AutoAb generation: may occur; reactive to
lymphocytes, smooth muscle, brain and lung
tissue
Environmental organism: lives
in soil, water and on the skin of
healthy people (esp. health care
workers)
Frequent cause of nosocomial
infections
Common in teenagers
Transmission: droplet spread
(low ID)
Protein Expression in MØ:
-Prevent phagolysosome fusion
-Prevent acidification of endocytotic vesicle
-Induce accumulation of ribosomes and
mitochondria around phagosome
-Facilitate iron scavenging from transferrin
Pathogenesis (in immunocompromise):
-Pneumonia
-Serious blood or wound infections
Walking Pneumonia: less severe than
other bacterial pneumonia
Disease Process:
-Colonization of bronchial epithelium
interferes with ciliary action
-Inflammation and exudates contribute to
pathogenesis
Secondary infection site: otitis media (nonpurlent)
Chlamydia pneumoniae
Life Cycle:
-Elementary body (infectious stage)
-Reticulate body (metabolically active and
replicates in the cell)
Humans are only host: over ½
of adults are seropositive but
reinfection can occur
Sequelae: immunopathology results due to
cross reactive Abs
-Hemolytic anemia
-Aseptic meningitis
-Pancreatitis
Pharyngitis
Bronchitis
Atypical/Walking Pneumonia: school aged
children and young adults
Similar clinical picture to M.pneumoniae
Shape: G(-) coccobacillus
No Cell Wall:
-No Gram stain
-No B-Lactam treatment
Bound by triple membrane
containing sterols
No organism in sputum
Diagnosis:
-Circulating Ag
-Complement fixing Ag
(ELISA)
Shape: G(-) outer membrane with
no cell wall; coccobacillus
Glycogen (-) inclusions
Detection: immunofluorescence of
outer membrane proteins or PCR
Staphylococcus aureus
Causes infection secondary to
some other lung insult: for
example, a viral infection
Acute Pneumonia
Empyema: purulent infection of the pleural
space (spread from infected lung)
Lung Abscess: complication of acute or
chronic pneumonia
Samples:
-Sputum
-Lung abscess aspirate (may also
use radiology to diagnose)
-Blood culture (if disseminated)
Shape: G(+) cocci in clusters
Biochemical:
-Catalase and coagulase (+)
Mycobacterium
tuberculosis
Mycolic Acid (Cord Factor):
-Resistance to drying/disinfectants
-Promotes hypersensitivity granuloma
-Promotes inflamm. response/tissue damage
Lipoarabinomamman: cell wall glycolipid
-Suppresses T cell proliferation
-Prevents MØ activation
Incidence highest amongst AIDS
patients and immigrants
XDR TB: ~1% are extensively
drug resistant
Transmission: aerosol inhalation
Primary Infection: Gohn complex
formation (granuloma) and enlarged LNs
-unapparent most of the time
Progressive Primary TB: ~5% of primary
infections; infection does not resolve and
disseminates (bloodborne or miliary)
Reactivation TB: commonly reactivates at
the apex of the lung (highest O2)
-Increased risk with age, alcoholism,
diabetes or decrease immune function)
Sulfolipids: inhibit MØ phagosome-lysosome
fusion
Antibiotic susceptibilities required
Tuberculin Skin Test:
-Inject PPD (autolyzed bacteria,
lipid, polysaccharides and NSs)
-Causes DTH reaction (local
induration and erythema) if (+)
PPD+:
-Current infection (granuloman
formation)
-Previous exposure (but not
necessarily disease)
-BCG vaccine
Catalase: degrades hydrogen peroxide
Disseminated TB: either due to progressive
primary or reactivated
-Via lymph or erosion of necrotic tubercle
in lung
-Infects liver, spleen, kidney, bone, or
meninges
Ammonia Production: prevents acidification
in phagolysosome
PPD-:
-No exposure
-Prehypersensitivity stage (within 6
weeks of exposure)
-Loss of sensitivity (disappearance
of Ag from primary complex)
-Anergy (immunocompromise)
Specimen Collection: sputum,
biopsy or blood (if disseminated)
Pseudomonas aeruginosa
Adhesins:
-Protein pilus adhesin (bind asialoGM1)
-Non-pilus adhesin (binds mucus)
CYSTIC FIBROSIS!
Nosocomial infections: water
borne
Acute pneumonia
Empyema
Abscesses
Staining: Acid Fast Stain
Growth: very slow; Lownstein
Jensen or Middlebrook agar
Rapid ID:
-rRNA/DNA probes
-PCR to detect common insertion
sequence
Sample: sputum
Shape: G(-) rods
Biochemical: oxidase (+), aerobic
Alginate: polysaccharide capsule for biofilm
formation; regulated in response to
environmental signals
Infections in CF:
-CF patients have defect in CFTR leading to
decreased sialylation of surface glycolipid
(asialoGM1)
-Alginate gel + excess mucus leads to
barrier to phagocytosis AND antimicrobials
-Anti-pseudomonal Abs may be defective
-Lung tissue damage due to persistent
colonization and elastase release
-Rarely spreads beyond lungs!
Elastase: protease that degrades lung elastin
Exotoxin A: ADP ribosylation EF2
Aspergillus spp. (Fungus)
Multiple Drug Resistance:
-Mutations leading to loss or porins
-Alteration of LPS
No dimorphic growth phase
Infectious conidia: germinate to mold form
Hyphae: bind fibrinogen and complement
components
Histoplama capsulatum
(Fungus)
Dimorphic growth phase:
-Mold in the environment (produces
infectious conidia)
-Pathogenic yeast in tissue
Common environmental mold:
emerging cause of nosocomial
infections
Conditions caused:
-Acute pneumonia
-Lung abscesses
Predisposing Factors
-Asthma
-Chronic bronchitis
-TB
-Immunosuppression
Structure:
-Septate hyphae with conidia
-Mold form grows rapidly, easily
identified
Transmission: inhalation of
infectious conidia
Radiology: fungus ball in
pulmonary cavity
Farmer’s Lung or Allergic
Aspergillosis
Environmental source: bird and
bat droppings (Central and
Southeastern US)
Transmission: inhalation of
conidia (no person to person)
Exposure is common but disease is rare:
-Primary infection site is lungs
-Grows inside MØ and produces granuloma
similar to TB (can disseminate to organs of
reticuloendothelial system)
Normal Immune Response:
-T cell activation of MØ prevents
intracellular growth
-Long-term immunity to re-infection
Blastomyces dermatitidis
(Fungus)
Dimorphic growth phase: similar to
Histoplasma
Difference: yeast cells exist extracellularly,
NOT in MØ
Samples:
-Lung aspiration
-Bronchial lavage
-Biopsy
Distribution: middle and SE US
Transmission: inhalation of
conidia
More common in males
Chronic Pneumonia: PMN infiltration and
granuloma formation (mimics pulmonary
tumor or TB)
Radiology: granuloma similar to TB
Sputum: NOT USEFUL
Blood or biopsy required
Growth (Slow): BAP or Sabouraud
agar
Structure: dimorphic; mold forms
tuberculate maccroconidia (finger
like projects with spores)
Detection: widespread exposure
and cross reactivity to other
pathogens
-DTH skin reaction to mycelial Ag
-Complement fixing Ab test
-Immunodiffusion
-DNA probes
Large yeast cells with broad buds
Slow growth: ~4 weeks
Serodiagnosis: hard because of
cross-reactivity with other fungi
Dissemination possible:
-Chronic infection of skin and bone most
common
-Possible even in subclinical infections
Coccidiodes immitis
(Fungus)
Dimorphic Growth Phase:
-Mold (produces arthroconidia)
-Spherule (invasive tissue form that
produces reproductive endospores)
Valley Fever: common in SW US
Transmission: inhalation of
arthroconidia
Immune Response:
-T cell mediated
-Cytokine-activated macrophages
-Large yeast cells can resist oxidative and
non-oxidative killing mechanisms
Usually mild disease: acute pulmonary
infection with cough, chest pain and
myalgia
Chronic Pneumonia: if decreased T cell
response
-Dissemination possible (skin, bones, joints,
meninges), although rare
Disease Process:
-Arthroconidia inhaled and are
phagocytosed (PMNs, MØs)
-Spherule grows too large for phagocytosis
and bursts, releasing endospores, which
are endocytosed and prevent
phagolysosome fusion (inflammatory rxn)
-Inflammation results in granuloma
formation
Pneumocytsis
carinii/jirovecii (Fungus)
Protozoan: based on morphology and drug
susceptibility
Fungus: based on rRNA and sequence
homology with other fungi
Very common infection of
generally low virulence: causes
PCP in immunocompromise
-Premature infants
-Chemo patients
-Organ transplants patients
-AIDS (presenting
manifestation)
-Use of corticosteroids
-Leukemia
Immune Response:
-Cell-mediated immunity to arthroconidia
and endospores
-T cell anergy can result in chronic infection
(due to heavy pathogen load after spherule
burst)
-Progressive diffuse pneumonia
-Other concurrent infections are common
-Alveoli filled with desquamated cells,
organisms, monocytes and fluid (foamy
appearance)
Symptoms: typical pneumonia signs absent
-Mild/low grade fever
-Non-productive cough
-Progressive dyspnea, cyanosis, hypoxia
-Death by asphyxiation
Detection of spherules in
histological sections
Complement Fixing Ab titers
predict outcome:
-Low: good CMI response
-High: disseminated and T cell
anergy
Skin test of limited value: due to
common exposure
Other ID Methods:
-Immunodiffusion
-DNA probe
Sample: sputum (induced with
hypertonic saline)
-Only useful in AIDs b/c of ↑
number of organisms
-Extracellular cysts and trophs
-Scattered cysts in contact with
alveolar cells (characteristic of
latent infection)
DNA VIRUSES CAUSING RESPIRATORY INFECTIONS:
Virus
Characteristics
Epstein Barr Virus
Genome: linear dsDNA
(Gammaherpesvirus)
Enveloped
Replication: nucleus
Pathogenesis
Transmission: saliva
Site of Primary Infection: URT
Spread to B Lymphocytes:: up to 10% may
become infected (heterophile Ab secretion
and lymphocytosis)
Diseases
Young Children: infection usually asymptomatic
-Fever and sore throat most common
-May also cause diarrhea, otitis media, infectious mono (less common)
Adolescents/Adults: asymptomatic disease less common
-Infectious Mono: fever, sore throate, anorexia, lymphadenopathy,
hepatosplenomegaly, lymphocytosis, heterophile Abs
Cancer:
-Burkitt’s Lymphoma (malaria may be a cofactor)
-Nasopharyngeal carcinoma (Southern China; genetic, dietary and
environmental cofoactors)
-Hodgkin’s Lymphoma (EBV detected ~50% of cases)
Cancer in Immnocompromise:
-Post-transplant lymphoproliferative disorders and lymphomas
-X-linked lymphoproliferative
-AIDS associated lymphomas (tend to occur in CNS)
Cytolomegalovirus
(Betaherpesvirus)
Genome: linear dsDNA
Enveloped
Replication: nucleus
Transmission: virus shed in urine, saliva and
other body fluids
Hairy Oral Leukoplakia: in mouth of AIDs patients
-White, wart like lesions on the side of the tongue (NOT TUMORS)
Usually asymptomatic: may cause infectious mono-like disease
(heterophile Ab negative)
Immunocompromise: CMV pneumonia and retinitis possible
Adenovirus
Genome: linea dsDNA
Non-enveloped: icosahedral
-Fibers at vertices (characteristic)
Replication: nucleus
Transmission:
-Respiratory spread (most common); will still
spread to GI tract
-Fecal/oral spread
-Iatrogenic spread (ie. to conjunctiva)
Bind: CAR receptor and integrin co-receptor
on host cell
Infect: mucosal epithelial cells of the
respiratory tract, GI tract and eye
Viral Entry: endocytosis
Viral Release: cell lysis (inefficient, but a lot of
viral particles made)
Neonatal/Fetal CMV: major problem
-Risk of death, mental retardation and deafness
Acute Respiratory Infections: highly infectious
-Fever, sore throat, cough, nasal congestion, tonsillitis
Acute Respiratory Disease: military recruits (mild URI  pneumonia)
-Vaccine available for military use only
Pneumonia: possible complication of any Adenovirus RTI
-Common cause of childhood pneumonia or pneumonia in
immunocompromise
Pharygoconjunctival Fever: conjunctivitis + URTI (often from pools)
Epidemic Keratoconjunctivitis: minor corneal abrasions required
GI Disease: only Type 40 /41 (infant gastroenteritis)
Urethritis/Cystitis: uncommon (Type 27)
Parvovirus B19
(Parvoviridae)
Genome: linear ssDNA
Non-enveloped: icosahedral
Replication: nucleus
(AUTONOMOUS)
Many infections are asymptomatic:
-Infection in school age children more
common
-Abs increase with age
Transmission: respiratory route,
transplacental (if primary B19 infection in
pregnant woman)
Erythema Infectiosum (Fifth Disease):
First Phase: non-specific flu-like symptoms
-Viremia
-Formation of IgM-parvovirus immune complexes
Second Phase: deposition of immune complexes
-Erythematous rash
-Arthritis
Transient Aplastic Crisis: in people with hemolytic anemia
-Replicates in bone marrow (erythroid precursors)
-Transient reduction in RBC production that is not a major problem in
normal indiciduals
Immunocompromise: chronic infection of BM  persistent anemia
Congenital B19: can cause hydrops fetalis (fatal anemia of fetus)
-No abnormalities in survivors