Microbiology II Flashcards
What pathogens can be found at the nasopharynx?
Mainly viruses
- rhinovirus
- coronavirus
What pathogens can be found at the oropharynx?
Strep pyogenes (Group A Strep)
Corynebacterium
Diphtheriae
Epstein-Barr virus
adenovirus
enterovirus
What pathogens can be found in the middle ear and parasinuses?
Strep pneumoniae
Haemophilus influenzae (non-typeable)
Moraxella catarrhalis
Group A Strep
What pathogens can be found on the epiglottis?
Haemophilus influenzae Type b
What are characteristics of Group A Strep?
Streptococcus pyogenes
- Gram + cocci in chains
- Catalase negative
- Beta-hemolytic
- Bacitracin sensitive
What are symptoms of pharyngitis and what is the most notable cause of pharyngitis?
Symptoms:
nausea
vomiting
abdominal pain
Complications:
peritonsillar abscesses
scarlet fever
cervical adenitis
otitis media
strep. TSS
Group A Strep
How does Group A Strep cause rheumatic heart disease?
M protein is a virulence factor of S. pyogenes that allows it to go undetected by the immune system due to its molecular mimicry of cardiac proteins
S. pyogenes infections can lead to anti-cardiac antibodies produced by the immune system
These antibodyes are responsible for deposits and thickenign of leaflets leading to RHD
What are characteristics of Haemophilus Influenzae bacteria?
Gram -
Coccobacilli
(curved ends on short rods)
Oxidase positive
Growth Requirements:
Fastidious
X Factor (hemin, heat stable)
V Factor (NAD or NADP, heat labile)
Grown on Chocolate agar
What is the most agressive capsular type of H. Influenzae? Why?
H. influenzae Type b
(HIb)
Type b capsule is polyribose-ribitol phosphate
Capsule is:
Antiphagocytic
Non-encapsulated forms are normal flora in the URT
What are types of diseases are caused by H. influenzae?
Meningitis - 90% die w/o treatment
Epiglottitis - obstructive, cherry red epiglottis, life threatening
Pneumonia - often complicated by empyema
Bacteremia
Cellulitis
Septic arthritis
What infections are caused by non-typeable H. influenzae?
Acute otitis media
sinusitis
- may follow viral infection
Exacerbations of COPD
Conjuctivitis (daycare settings)
What is treatment for H. influenzae?
3rd generation Cephalosporin
If susceptible to ampicillin, use that
Why must polysaccharide vaccines be protein conjugated for children?
Infants cannot make antibody responses to polylysaccharides because they are T-independent antigens.
The conjugate vaccine allows the infant to make an antibody response (and evoke memory cells) because the protein part of the conjugate engages T cells and allows the polysaccharides to be presented as T-dependent antigens.
What is the causative agent of diptheria?
Corynebacterium diphtheriae
What are characteristics of Corynebacterium diptheriae?
Gram + rods
(“chinese letters”)
catalase +
non-motile
non-spore forming
Produce diptheria toxin in mucus membranes
Produce Pseudomembranes that may occlude airway
What is the pathogenesis of diphtheria?
Organisms enter URT –> Colonize mucose –> Produce diptheria toxin
Diptheria toxin causes:
Myocarditis
Neuritis
Necrosis
(causes pseudomembrane)
What is Diptheria toxin?
Toxin produced by Corynebacterium Diptheriae that is encoded on a lysogenic phage (can be transduced to other corynebacterium species)
Three domains:
A = active domain
B = binding domain
T = transmembrane domain
Mode of Action:
Inhibits protein synthesis and kills cells
What is treatment for Corynebacterium Diptheriae infections?
**Antitoxin** to treat diptheria toxin Horse origin (test for sensitivity)
Antibiotic to eradicate organisms
What are the characteristics of rhinovirus?
Non-enveloped
+ssRNA genome
Icosahedral capsid
Small in size
>100 serotypes
ICAM-1 is primary cellular receptor used to infect respiratory epithelial cells
Temperature Sensitive
88-90deg F
How is rhinovirus transmitted?
aerosol droplets
(sneezing)
direct contact with infected surface
What is the rhinovirus replication cycle?
Cytoplasmic:
Rhinovirus binds to ICAM-1 –> enters epithelial cell
+ssRNA is translated by cell’s ribosomes
+ssRNA is transcribed by virus’s RNA polymerase
Proteins and RNA are assembled
Virus exits by Lysis of cell
What are symptoms of rhinovirus? How long do they last?
Infection of about 2-4 days (self-limiting)
Symptoms:
Nasal discharge
Nasal congestion
Sneezing
Sore throat
Edema and erythema of nasal mucosa
Muscle aches
fatigue
headache
loss of appetite
In rare cases of children: bronchopneumonia
How does someone become immune to rhinovirus?
No Vaccines
Mucosal IgA in nasal secretions are protective
Type I interferons control viral spread but causes pathogenesis
Immunity is serotype specific
>100 serotypes
At what point does a Respiratory Syncytial Virus infection become life threatening?
Primary infection occurs in epithelial cells of URT producing a mild, self-limiting illness
In children <8 months old, virus can spread to LRT, causing:
Bronchitis
Pneumonia
Croup
What are characteristics of Respiratory Syncytial Virus (RSV)?
Enveloped
-ssRNA genome
Helical Capsid
Two major envelope proteins:
Attachment (G) protein
Fusion (F) protein
Aggregated F proteins cause syncitia
Encodes its own RNA-dependent-RNA Polymerase
What is the RSV replication cycle?
Cytoplasmic
It’s a -ssRNA virus that causes cytoplasmic inclusion bodies:
RNA is transcribed by the virus’s RNA-dependent-RNA polymerase
Then RNA is translated into proteins
How is RSV diagnosed?
NAsal washings, nasal aspirates or swab samples are useful for antigen detection
Rapid diagnosis by:
DFA
IFA
ELISA
Viral culture is carried out in cell lines
Molecular assays such as RT-PCR
How is RSV treated?
No liscenced vaccine
Ribavirin has been used but has limited efficacy
Oxygen treatment and hospitalization for infants with severe brochiolitis
What passive immunotherapy is used against RSV?
RespiGam: polyclonal antibody used to prevent serious LRT infection for infants and bone marrow recipients
Synagis: monoclonal antibody (anti-F reactive Ab) for pediatric patients at high-risk of RSV (i.e. babies on ventilators)
What virus is known to cause outbreaks on epidemic levels for military training centers?
Adenovirus
What are characteristics of adenovirus?
Non-enveloped virus
ds linear DNA
Icosahedral capsid
51 known serotypes
Replicates in nucleus
What are the phases of adenovirus replication?
In nucleus:
Immediate early:
E1A genes transcribed
Early:
E1B, E2A, E2B, E3, E4, some virion proteins transcribed
Late:
Late genes, mostly virion proteins
What proteins allow for adenovirus to be infectious?
Hexon and Penton bases extend fibres out of the capsid
–> attach to cells and activate viral infection
What respiratory diseases are caused by adenovirus?
- Febrile, undifferentiated URI
- Pharyngoconjunctival fever
- Acute respiratory disease
(military recruits) - Pertussis-like syndrome
- Pneumonia
How is immunity of adenovirus mediated?
- *Humoral:**
- neutralizing Ab’s are protective against some serotypes
Cell-mediated:
CD8 CTL responses are critical in controlling infection
- severe infections are common in people with cellular immune defects
Adenovirus encodes proteins that play role in immune invasion:
- down regulates MHC class I
- inhibits TNF mediated lysis
How is adenovirus diagnosed?
Detection of Antigen:
Rapid diagnosis from nasopharyngeal aspirates or throat washings
Virus Isolation
Serology
PCR Assays
How is adenovirus treated?
- Symptomatic treatment
- Self-limiting: 7-10 days
- new live tablet vaccine approved in 2011 used by military during basic training
What classification of virus is Epstein Barr?
gamma Herpesvirus:
- restricted host-range
- infects epithelial cells and lymphocytes
- latent in lymphocytes and/or endothelial cells
- can cause cancer
What are characteristics of EBV?
All Herpesviruses have identical morphology:
Enveloped
linear dsDNA
Icosahedral capsid
encodes its own DNA-dependent DNA pol
encodes numerous host protein homologues to evade immune responses
replicates in nucleus
What does EBV infection cause? What are the symptoms?
Infectious mononucleosis
Symptoms:
Fatigue
Malaise
Throat soreness and reddening
Tonsil reddening, swelling, white patches
Cervical adenopathy
What about EBV is thought to be the cause of cancer?
EBV latency
How is infectious mononucleosis diagnosed?
- Atypical lymphocyte
(Downey cells = CD8 CTL) - Agglutination test for heterophile Abs
(using fresh horse or sheep RBCs) - EBV Ab ELISA
- PCR for EBV genes
How is EBV treated?
No vaccine:
Symptomatic treatment
Infectious Mononucleosis is self limiting
- rapidly controlled by immune response
- symptoms can linger for weeks
What are the major components of mycobacterial cell envelopes?
Waxes
Mycolic acids
polysaccharides
peptidoglycan (murein)
Phenolic Glycolipid I (PGL-1)
Lipoarabinomannan (LAM)
–> Acid Fast staining
What is the pathogenesis of TB?
Infectioin that requires cell-mediated immunity for control
- Ab response is not effective
No toxins involved
There is an active and latent
infection does not mean disease
What is the life cycle of M. tuberculosis?
- Mycobacterium enters alveoli and infects alveolar macrophage
- Infected macrophages release cytokines attracting monocytes, further spreading infection
- Immune cells wall of the site of infection with a fibrouls cuff, encapsulating bacilli, foamy macrophages, and the center becomes a necrotic, caseatign granuloma
- The granuloma can burst, further spreading infection
How can M. tuberculosis infection lead to disease?
Infection of the alveoli in people with little to no hypersensitivity/cell-mediated immunity (immune-compromised) become infected with a progressively systemic disease and eventually death
Infection in people with DTH and CMI –> disease is contained; bacteria live but fail to replicate –> Ghon complex appears in 15% of cases
Ghon complex appears >5 years later in 25% of cases
- leading to:
progressive systemic disease and death,
clinical TB (pulmonary or extrathoracic)
or
no disease
How does reactivation of TB occur?
- viable bacteria w/in lesions are the source of reactivation
- Usually found in upper lung
- Triggers:
Diminished immune response
Malnutrition
Aging
What is a Ghon complex?
Some individuals develop the Ghon complex in primary infection of TB in which:
an area of lung inflammation is associated with enlarged hilar lymph nodes
What people are at higher risk of being exposed to TB?
- Persons in close contact w/someone w/known or suspected TB infection
- Foreign-born persons from areas known to have TB
- Residents & employees of high risk congregate settings (i.e. nursing homes)
- Health care workers who serve high risk clients
- Medically underserved, low-income populations
- high risk racial or ethnic minority
- persons who inject illicit drugs
What people are at higher risk of developing TB disease once infected?
- HIV infected
- recently infected
- persons with certain medical conditions
- persons who inject illicit drugs
- History of inadequately treated TB
How is TB diagnosed in the laboratory?
- Sputum smear - need minimum of 10^4 bacilli/ml for + smear
- culture (“gold standard”) - slow, takes 2-3 weeks to form colony
- Tuberculin skin test (PPD or Mantoux)
What is a PPD test?
Purified Protein Derivitive (Of Tuberculosis)
- intradermal injection of purified protein
+ test produceswheal 6-10mm in diameter
(diameter of + test depends on risk of patient)
reaction must be read in 48-72hrs
What can cause a false-positive PPD?
Nontuberculous mycobacteria
BCG vaccination
What can cause a false-negative PPD?
Anergy
(lack of rxn by the body)
Recent TB infection
Very young age (<6 mo. old)
live virus vaccination
overwhelming TB disease
Why is it important to culture TB?
it is required to isolate bacteria for:
drug susceptibility testing
(deterine best route of treatment)
genotyping
How is TB treated?
Generally in drug combinations: Isoniazide, Pyrazinamide, Rifampin
First line drugs:
Isoniazid
Pyrazinamide
Rifampin
Rifapentine
Ethambutol
Second line drugs:
Cycloserine
Ethionamide
Streptomycin
(many more)
What is BCG?
Bacile de Calmette et Guerin
- Live, attenuated vaccine for TB derived from Mycobacterium bovis
Not used in US b/c:
- adverse rxns
- Immunity wanes in ~10yrs
- Interferes w/use of PPD
What is the pathogenesis of Influenza?
Primary Infection
Secondary infection
(re-infection)
What is the development of primary infection of influenza?
- Short incubation period
- local virus replication in respiratory epithelium
- damages to epithelium and ciliated columnal epithelial cells (renders airway susceptible to bacterial infection)
- No viremia
- macrophage and lymphocyte infiltrate
- interferon and cytokines cause fever, aches, edema
- direct virus damage and immmune response kill infected cells
- Stimulation of Abs and virus-specific T cells
- Clearance of virus from tissues
- immunity mediated by IgA in respiratory tract
What are clinical features of influenza?
- Abrupt onset of symptoms:
headache
fever
chills
myalgia
malaise
sore throat
non-productive cough
runny or stuffy nose
What are characteristics of the Influenza Virus?
neg. RNA virus (segmented RNA)
Enveloped
Haemagglutinin (HA) and Neuraminidase (NA) spikes
3 types: A, B, C
What are complications of influenza?
Secondary bacterial pneumonia:
following improvement, fever reappears, cough, purulent sputum
Viral pneumonia:
Relentless progression of illness, dyspnea, hypoxia, cyanosis, severe inflammatory reaction in alveoli, edema –> ARDS
Myositis and cardiac involvement
Neurologic symptoms
(Guillain-Barre syndrome, encephalopathy, encephalitis, Reye’s syndrome)
What are the three types of Influenza virus?
Type A: Undergoes antigenic shift and drift
Type B: undergoes antigenic drift only
Type C: relatively stable, doesn’t cause serious human disease
What is the purpose of Haemagglutinin and neuraminidase on influenza viruses?
HA: viral attachment and membrane fusion
HA1/HA2 binding site (a disulfide bond) must be cleaved for infection to expose fusion peptide
NA: virus release from infected cells and disaggregation
How does replication occur for influenza virus?
- Virus binds sialic acid moiety on glycoproteins and glycolipids
- transcription and replication occur in nucleus
(virus includes its own RNA-dependent RNA pol) - Steal 5’ capped termini of cellular mRNAs as primers for virla mRNA transcription
- Budding from plasma membrane
- frequent genetic reassortment occurs
How is influenza diagnosed?
- samples obtained from respiratory secretion
(throat swab, nasal wash, throat wash, nasopharyngeal aspirate) - Virus grown in fertilized eggs or in cell cultures
- Detect virus replication by cytopathic effects, immunofluorescence, hemagglutination, or hemadsorption
- determine serotype by hemagglutination-inhibition test
- or rapid diagnoisis by RT-PCR based tests
What is antigenic shift?
Occurs as a result of the segmented genome of flu virus and reassortment of viral genomes in the large animal reservoirs of the virus
What is antigenic drift?
Occurs as a consequence of the mutations introduced by viral RNA dependent RNA polymerase during replication of flu virus
What are the two vaccine types used against influenza?
Trivalent Inactived Vaccine:
2 Type A, 1 Type B
Chemically inactived vaccine
Induces serum antibodies
Live Attenuated Influenza Vaccine:
2 Type A, 1 Type B, nasal spray
Induced mucosal immunity
What do antiviral therapies for influenza target?
Neuraminidase: (responsible for virus release from cell)
Oseltamivir
Zanamivir
Ion Channel (M2): (facilitates virus dissembly and HA maturation)
Amantadine
Rimantadine
What is Amantadine and Rimantadine?
Antiviral therapies for influenza
- blocks Ion channel activity of M2 protein
- prevents H+ entry into viral interior thereby inhibiting viral dissembly
- also inhibits maturation of HA during virus assembly
- **reduces disease severity only if given early
- only for Type A Influenza**
What is the function of M2 in influenza life cycle?
- lowers the pH in virla particle to facilitate dissociation of the ribonucleoprotein complexes form the M1 protein
- facilitates HA maturation and egress by equillibrating pH of Golgi and cytoplasm during assembly
How is pneumonia classified?
It is an infection of the lung parenchyma
- Acute*: Fairly sudden onset with progession of symptoms over a few days
- Community Acquired
- Hospital Acquired (think Gram- rods)
Subacute or Chronic
What is a “typical” pneumonia?
high fever
shaking chills
chest pain
lobar consolidation on CXR
What are common causes of Typical pneumonia?
- Strep. pneumoniae (community acquired)
- Staph. aureus (CAP)
- Haemophilus influenzae (CAP)
- Gram - enterics (hospital acquired)
What is an “atypical” pneumonia?
less severe illness (“walking pneumonia”)
Insidious Onset
Dry cough
headache
other systemic complaints
CXR diffuse pattern: looks worse than symptoms suggest
What are common causes of “atypical” pneumonia?
Mycoplasma pneumonia
Chlamydia pneumonia, psittaci
Legionella pneumophila
Influenza, or other virus
Coxiella burnetti
What are characteristics of Strep. pneumoniae?
Gram +, lancet shaped cocci
Catalase negative
Alpha-hemolytic
Diplococcus bacteria
Sensitive to optichin
Bile soluble (Enzymes cause lysis of colony in bile salts)
Colonies are mucoid b/c of capsule
What is a major virulence factor of Strep. pneumoniae?
Capsular polysaccharides:
Capsule interferes with deposition of C3b on bacterial surface
Therefore, no recognition of C3b-coated organisms by complement receptors on phagocytes
**Anti-capsular Abs provide type-specific immunity
What are risk factors for Strep. pneumoniae?
Viral infection of URT
(particularly influenza)
Compromised pulmonary function
(alcoholism, general anesthesia)
Age
(elderly or <2)
Ethnicity
(blacks, American indians, alaska natives)
Basic immunity impaired
Serotype of S. pneumoniae present in URT
What is the pathogenesis of pneumococcal pneumonia?
Organism colonizes pharynx and gains access to lung/alveoli
Phagocytized by macrophages (stops infection)
OR
Multiplys in edematous fluid (continues infection)
Exudate spills into bronchiles and adjoining alveoli
Inflammatory response, air displaced
Centrifugally spreading lesion leads to resolution or death
What are signs and symptoms of pneumococcal pneumonia?
- It’s usually lobar –> oldest part of lesion in center
- sudden onset of fever, chills, pleuritic pain, rusty sputum
- positive blood cultures
What are possible complications of pneumococcal pneumonia?
Direct:
lung abcess
Via blood:
empyema
pericarditis
meningitis
intrapleural abscess
septic arthritis
What is the therapy for pneumococcla infections?
Many isolates of Strep. pneumoniae are now penicillin resistant
- no distinct drug regimen
- Conjugate vaccine is available for prevention
What bacterial agents commonly cause atypical pneumonia?
Mycoplasma pneumoniae
Chlamydia pneumoniae
Chlamydia psittaci
Coxiella burnetti
What are common viral agents of atypical pneumonia?
Adenovirus
parainfluenza virus
EBV
RSV
What are characteristics of Mycoplasma bacteria?
Lack cell wall (no peptidoglycan)
–> no target for antibiotics
Unit membrane containing sterols
Pleomorphic
too small to filter out
Facultative aerobes (except M. pneumoniae)
Grow slowly
Reproduce via binary fission
What is the pathogenesis of M. pneumoniae?
Entry via respiratory route
- *Bacteria attach to epithelial cells of LRT**
- tight association, but no invasion
- Bacterial attachment factor: P1 adhesin
- Cell membrane receptor: neuraminic acid-containing glycoprotein
Induction of ciliostasis
Deterioration of cilia in respiratory epithelium, both structurally and functionally
Caused by production of Community Acquired Respiratory Distress Syndrome toxin (CARDS toxin)
Bacteria are phagocytized by activated macrophages; cytokine production –> local inflammation
Vigorous CMI –> severe clinical case
How is M. pneumoniae diagnosed?
- Diagnosis of elimination
- Culture: very difficult; restricted to specialized labs
- Serology: >4-fold rise in specific M. pneumoniae Ab
- Test for Cold hemagglutinins (not specific)
What are cold hemagglutinins?
IgM antibodies that bind I antigen of human RBCs produced in 1-2 weeks after initial infection (i.e. M. pneumoniae)
–> able to agglutinate RBCs at 4deg C
What is the treatment for Mycoplasma pneumoniae?
- Antimicrobial therapy shortens period of symptoms
- Antibiotics of choice:
Tetracycline
Erythromycin or azithromycin
beta-lactams NOT effective (no cell wall)
- No vaccine available
What are the characteristics of Chlamydiaceae?
- Enveloped
- Obligate intracellular bacteria
- Contain DNA, RNA, and 70s Ribosomes
- divide by binary fission
- carry plasmids; infected by bacteriophage
- Similar to Gram (-) bacteria, but no detectable peptidoglycan
(sensitive to cell wall antibiotics)
What are the developmental forms of Chlamydia?
Elementary Bodies:
Extracellular
Infectious form
metabolically Inactive
Disulfide cross-linked outer membrane proteins
Reticulate Bodies:
Intracellular
Replicative form
Metabolically Active
Osmotically fragile
How does Chlamydia enter the cell?
Elementary bodies (infectious form) enter through "Parasite-specified endocytosis"
- Rapid internalization through receptor-mediated Clathrin-coated endocytosis
How is C. pneumoniae Pneumonia diagnosed?
Culture: difficult; restricted to specialized labs
Serology: IgM titer of >= 1:64
or 4-fold rise in IgG in acute and convalescent serum, measured 4 weeks apart
–> have to wait for recovery for diagnosis
What is an increased risk factor for Chlamydia psittaci?
Working with Birds: poultry industry workers, vets, exotic bird owners
–> Zoonotic infection:
“Parrot fever” - wasting disease of birds
Spontaneous abortion in sheep (and humans)
What are clinical features Psittacosis and how is it transmitted?
Clinical Features:
Abrupt onset
Fever, headache, myalgia, mild cough
abnormal Chest exam
Confusion/altered concious state
Transmission:
Inhalation of aerosolized organism in dried feces or respiratory tract secretions
direct contact with infected bird
How is psittacosis diagnosed and treated?
Diagnosed through culture of C. psittaci from respiratory tract or serology
Treatment:
Doxycycline
macrolides (azithromycin, erythromycin)
What are risk factors for Legionnaire’s disease?
Immunosuppression
Cigarette smoking
renal failure
Age > 50yrs
AIDS
hematologic malignancies
lung cancer
Males > women
What are characteristics of Legionella?
Gram (-) slender bacilli
–> don’t take Gram stain well
Specific growth requirements:
Amino acids
Iron and other trace metals
–> Buffered Charcoal Yeast Extract Agar
Slow growing
L. pneumophila predominant species in human disease
How is legionella spread?
- most commonly spread through aerosols
- A/C cooling towers
- Whirlpool spas
- sink taps and shower heads
- replicates anywhere btwn 5deg and 63deg C
- loves biofilms
How does legionella infect it’s host?
Ameobas or Macrophages:
“coiling phagocytosis” - special mechanism of uptake of legionella
- Phagosome does not acidify, does not fuse w/lysosome
- Phagosome surrounded by ER studded with ribosomes
- Legionella multiplies in phagosome
- phagosome ruptures
- host cell lyses, bacteria escape
What is Pontiac Fever?
Form of Legionellosis in Pontiac, MI:
Influenza-like
- fever, chills, myalgia, headache
- no evidence of pneumonia
- self-limiting
- no agent cultured
- retrospectively determined to be legionella
What are the approaches to diagnosing Legionellosis?
-
Urine sample
- LPS antigen detectable by ELISA -
Bronchoalveolar lavage (broncheolar machrophages)
Fluorescence staining on specimens
or
Dieterle’s Silver Stain instead of gram stain
or
DNA probes on specimens
or
Culture on Buffered Charcoal yeast extract agar -
Acute and convalescent sera
- 4-fold Ab rise
What is the treatment for Legionella?
Macrolides:
Azithromycin, Erythromycin
Fluoroquinilones:
Ciprofloxacin, Levofloxacin
What are characteristics of pseudomonas aeruginosa?
Gram (-) rods
Flagellated
Strict aerobes
Use oxidative metabolism
NONFERMENTERS
Mucoid capsule makes for a slimy and sticky culture
Oxidase (+)
Growth on MacConkey (Lac -) agar
Pigment production: pyocyanin (green)
Glucose oxidation
Artificial grape-like odor
What type of patients are most vulnerable to pseudomonas?
Why?
Cystic Fibrosis
–> chronic, recurrent pneumonia
Why:
- P. aeruginosa infections often become permanent
- >80% adults with CF are chronically infected
- P. aeruginosa and other agents for biofilms and become surrounded with breakdown products of bacteria and immune cells
- Matrix makes bacteria more resistant to both antibiotics and immune system
–> mucous of CF lungs is a perfect place for Ps. to stick to and grow
What are the most recognized Ps. aeruginosa diseases?
- pneumonia in CF patients
- burn infections
- hospital acquired infections
- cellulitis
- folliculitis (hot tub folliculitis)
- urinary tract infection
- swimmer’s ear
What antibiotics are useful in treating pseudomonas?
Aminoglycosides
Carbapenems
Carboxypenicillins
Ureidopenicillins
Extended-spectrum cephalosporins
fluoroquinolones
monobactam
What is a dimorphic fungi?
Organims that exists as mold in nature and as yeast in vivo
What is the morphology of Histoplasmosis?
Mold form:
White or brown hyphal colonies
Conidia:
Large spherical ones with spikelike projections
small, oval microconidia
grows slowly, can grown on cycloheximide
Yeast form:
Intracellular
uninucleate
oval
Thin walled
How is histoplasmosis spread?
Mold lives in soil w/high nitrogen content
- areas contaminated by bird or bat droppings
Outbreaks are associated with soil disturbances:
- exposure to caves and bird roosts
- excavation and demolition of old buildings
What is the pathology of histoplasmosis?
Spores –> Lungs –> yeast form –> into macrophages –> Reticuloendothelial system (RES)
- multiply within macrophages
- travel to hilar and mediastinal lymph nodes
- spread throughout the entire RES (lungs, LN, liver, spleen, bone marrow)
- Macrophages become fungicidal –> develop necrosis with fibrous encapsulation (granuloma) –> Ca++ deposition occurs over several years
**Pathophysiologically same as TB
What is the most common clinical presentation of histoplasmosis?
Asymptomatic
(or just not sick enough to go to the Dr)
What are the three pulmonary syndromes common with Histoplasmosis?
- *Acute:**
- usually mild, self-limiting (10-14d)
- fever, sweats, cough, occ HA and GI complaints
- diffuse pulmonary infiltrates and hilar/mediastinal LN involvement
Subacute:
Presents over weeks
- fever, sweats, cough, weight loss
- hilar/mediastinal lymphadenopathy
- possibal focal or patchy pulmonary infiltrate
Chronic:
Inability to clear infection
Same symptoms as subacute
What are some ways histoplasmosis infection can present other than pulmonary involvement?
(note these are not completely void of pulm. involvment)
- *Mediastinitis:**
- freq. complication of pulmonary histo
- can lead to acute pericarditis and cardiac tampanode
Progressive Disseminated Histo:
- Patients with compromised cell-mediated immunity
and patients on TNFa inhibitors
- fever, wt loss, sweats
- hepatosplenomegaly and lymphadenopathy
- hematologic abnormailities due to bone marrow involvement
- respiratory distress
- possible GI, adrenal, CNS, mucosal involvement
How are histoplasmosis infections diagnosed?
Culture (“gold standard” but slow)
Fungal stain
Serology (doesn’t say if infected, only if they have been infected in their lives)
Antigen (good for disseminated disease)
What is the treatment for histoplasmosis?
Primary self-limited: none
Moderate disease: Itraconazole
Severe disease: Amphotericin B
What is the morphology of blastomycosis?
Mold:
White to tan filamentous mold
Round to oval conidia on terminal hyphal branches
Yeast:
Spherical
multinucleated
Thick “double-contoured” walls
Reproduce by formation of buds
What is the pathogenesis of blastomycosis?
Inhalation of conidia into alveoli –> organisms change to yeast form in lungs –> multiply by budding –> hematogenous dissemination may occur before immunity develops
What is the clinical presentation of blastomycosis?
Most cases are asymptomatic
Those symptomatic get:
- Pulmonary infection: acute pneumonia
- Cutaneous: verrucous or ulcerative
- Bone: osteomyelitis
- Genitourinary: prostatitis and epididymoorchitis
How is blastomycosis diagnosed?
Histopathology (biopsy)
Culture
Serology (poor specificity)
What is the treatment for blastomycosis?
Mild disease: itraconazole
Severe disease: amphotericin B
What is the morphology of coccidioidomycosis?
Mold:
Grows quickly in culture 25deg C
Arthroconidia = funcgal spores that form by segmentation of pre-existing fungal hyphae
Usually barrel-shapped and alternating as they are separated by disjunctor cells
Yeast: (usually in lung)
Arthroconidia become spherules
Spherules produce endospores
Rupture of spherule results in release of endospores, which become new spherules
What is the clinical presentation of coccidioidomycosis?
Most common: Self-limiting pneumonia
Symptoms: fever, cough, chest pain, fatigue, shortness of breath, chills, muscle and joint aches, night sweats, weight loss
–> can last for several months
- *Dissemination to skin, bone, and meninges** is possible
- -> generally afflicts those with immunosuppresion
How is coccidioidomycosis diagnosed and treated?
Diagnosis:
Direct microscopic eval of sputum
Culture @ 25deg C (must tell lab you think coccidio b/c of possible spreading)
Serology (rising titers is bad prognostic sign)
Treatment:
Mild to moderate: Fluconazole or itraconazole
Severe: amphotericin B
What is the morphology of paracoccidioidomycosis?
Limited to tropical and subtropical Central and S. America
Yeast form:
variable size
oval to round with multiple buds (“pilot wheel”)
What is the clinical presentation of paracoccidioidomycosis?
- Usually asymptomatic
- acute, subacute, chronic pneumonia
- disseminated: lymphadenopaty, organomegaly, and BM involvement
- chronic mucocutaneous ulcers
- meningitis
How is paracoccidioidomycosis diagnosed and treated?
Diagnosis:
Direct microscopy
tissue biopsy
culture
Treatment:
Itraconazoole
Severe: amphotericin B
HIV+ patients: TMP/SMX prophylaxis
