Microbacterias Flashcards
Streptococcus pyogenes
Gram postive cocci in chains
Beta Lysis (same as staph)
Flaking desquamation of skin
Temperature 102
Exudative tonsils
Anterior cervical lymphadenopathy
Facial flushing
Sandpaper erythematous rash
Strawberry tongue
Molecular mimicry
Virulence factors:
1. Hyaluric acid capsule- helps him to evade the immunogenic and antiphagocytic
- M protein- Resist antiphagocytic, Binds to serum factor H and inhibits activation of complement and C3b
- Hyaluronidase- Breaks down connective tissue for the bacteria to enter.
- SPE (Streptococcal Pyrogenic Exotoxin) Erythrogenic toxin- Causes of Scarlet fever. This Is a super antigen phage coded.
- Streptomycin O & S- can lyse neutrophils.
Laboratory:
1. Rapid antigen detection test
2. Bacitracin sensitive
3. Catalase negative
4. PYR postive
5. Check for ASO titer
Pancarditis
Corynebacterium diphtheriae
Gram positive Bacilli- club shaped
Transmitted by respiratory droplets
Fever 104 F
Extensive inflammation, swelling
Enlargement of cervical lymph nodes
Edema on neck (bull neck)
On throat- Thick dirty grey exudate
Leathery pseudomembrane
Bleeds when tried to remove
Leather like consistency
Laboratory
1. Albert stain- metachromatic granules ( club shape)
2. Potassium tellurite blood agar- Black colonies
3. Loeffler medium
4. Detection of toxin by Elek gel
Virulence factors:
1. Exotoxin A-B: inhibits synthesis by ADP ribosylation of EF-2 (elongation factor 2)
DTap- Diphtheria, tetanus, acellular, pertussis vaccine
Treatment:
Erythromycin
Penicillin G
Epstein Barr Virus
Bilateral, tender lymphadenopathy
Mild erythema of pharynx
Splenomegaly
Hepatomegaly
Transmited through saliva (kissing disease)
Latent infection of Target B cell binding to CD21
T cell are required to control the infection. Causing swelling of lymphoid organs and malaise.
Lab diagnosis:
1. Lymphocytosis with atypical lymphocytes (CD8 and NK cell) in the peripheral blood.
- Positive heterophiles antibody- monospot test
IgM for acute primary infection
IgG for past infection
ds DNA enveloped Icosahedral infection mononucleosis- ballerina skirt.
Complications
1. Nasopharyngeal carcinoma
2. Burkitt
3. Hodgkin and Non-Hodgkin
Herpes simplex Virus
Enveloped DNA virus
Remains latent in the trigeminal ganglion
Recurrent activation-travels along sensory nerves to the dorsal root ganglia (nerve cells near the spinal cord), where it remains latent.
Vesicular lesions- clears fluids
Ulcerative lesions with greyish exudate in the oral mucosa
Erythematous pharynx
Regional Lymphadenopathy
Laboratory:
1. Tzanck smear- multicellular giant cell
2. Fluorescent microscopy
Treatment
Acyclovir
Cytomegalovirus CMV
Monospots will be non-reactive (reactive in EBV)
Owls eye inclusion body- Intranuclear inclusions with perinuclear clearing.
Interstitial pneumonia in post transplant patients.
Adenovirus
Non-enveloped DNA virus Icosahedral
Replicates in the nucleus
Swimming pool conjunctivitis
Mild blanching rash on cheeks and torso
Direct contact with secretions
Contaminated ophthalmic solutions
Fecal Oral
Can caused:
1. Acute respiratory disease
2. Epidemic keratoconjutivitis
3. Pneumonia in the immunocompromised
4. Diarrhea
5. Cystitis
Coxsackie A virus
non-enveloped RNA virus
Transmission: Fecal oral route, direct contact
Mild fever, sore throat, difficulty in swallowing
Shallow yellow ulcers surrounded by red halos in the oral mucosa.
Thick walled gray vesicles on the palmar, feet and buttocks
Herpangina: Lesion ONLY on the mouth
Hemophilus influenzae
Encapsulated Gram negative pleomorphic coccobacilli
Chocolate agar Required X Hemin and V NAD for growth
it can grow in the chocolate agar because it has X and V
On blood agar can grow with presence of staph aureus. Induced hemolysis
Virulence factors:
1. Polysaccharide Capsule
2. IgA protease
3. Endotoxin lipopolysaccharides
EPIGLOTITIS
4 D. presentation: Distress, drooling, dysphonia, dysphagia
Tripod position- sitting leaning foward with neck hyperextended.
Inspirator stridor
Toxic looking child
Epiglottis swells up like a big thumb. Radiology shows edema of epiglottis like a thumb print sign.
Treatment:
Cephalosporins (betalactam) and Rifampin (DNA dependent RNA polymerase)
Conjugated vaccine works against polyribosylribitol phosphate type b. Does NOT neutralize the non-typable. Keeps causing otitis media, sinusitis and pneumonia.
Pseudomonas aeruginosa
Gram negative bacili
Green colonies
Oxidase positive- fruity odor
Motile
Non-lactose fermenter
slime capsule
Multidrug resistance
Centrimide agar- Only grow pseudomonas
Virulence factor:
1. Pili- adherence to host
2. Polysacharide slime layer- antiphagotic
3. Exotoxin A- ADP ribosylation of EF-2 (similar to diphtheria toxin)
4. Exoenzyme S- acts on regulatory G proteins. induces apoptosis
5. Elastase- damages collagen
6. Phospholipase C- damages membrane
7. Pyocyanin pigment- Stimulates IL-8 and C5a peptidase
Clinical:
1. Otitis externa:
chewing or yawning, itching in the ear, discharge from ear.
Can spread to the temporal bone, sigmoid sinus or base of skull.
- Sinusitis
- Hospital acquired pneumonia (ventilator associated and burns)
Moraxella catarrhalis
Gram negative diplococci
Non capsulated RNA
Catalase positive
Oxidase positive
Aerobic
Do not ferment anything
Potent producer of beta lactamase (antibody resistance) Slime
PMP-SMX
Fluroquinolones
Otitis media
sinusitis
COPD exarcerbations
Pneumonia
Rhinovirus
Picornavirus
Non enveloped RNA.
Sensitive to gastric acid
survive on fomites
Attaches to the nasal epithelium via ICAM-1
Replicates in the nasal epithelium causing ciliated columnar cells to slough off.
Parainfluenza virus
CROUP- Laryngotracheobronchitis
Respiratory droplets
Non-segmented ssRNA
enveloped. Replicates in the cytoplasm
F protein forms multinucleate syncytium giant cell.
Has 2 VAP
1. Hemagglutunin and neuraminidase
2. Fusion protein F- mediates the entry into the cell.
Steeple sign
Seal like bark
Narrowing and obstruction of the airway
Inspiratory stridor
Hoarness of voice because of edema of vocal cords
Bordetella pertussis
Gram negative cocco bacili
motile obligate aerobe
Highly contagious- respiratory doplets
Whooping cough
Coughing ends in them vomiting.
Complication:
Conjunctival hemorrhages- eye bruising
Rib fracture- from coughing so much
Culture: Bordet Gengou/ Regan Lowe
Cough plate method
Is a bacteria but in the blood count there are lymphocytes (that are suppost to be for virus)
The reason is because of the Adenylate cyclase toxin.
Virulence factors:
1. Fillamentous hemagglutinin (FHA) - mediates the attachment to the respiratory cilia.
- Pertussis toxin- increases adenylcyclase, increases cAMP, Increases insulin (hypoglycemia) and increases histamine sensitivity.
- Tracheal cytotoxi- causes the paroxysmal cough
- Hemolysin- Induces apoptosis of macrophages and bronchopulmonary cells.
- Adenylate cyclase toxin- Calmodulin dependent activation of cAMP that will impaired chemotaxis. The Lymphocytes stays in the blood that is why they are high in the blood count.
Vaccine:
DTaP
TDap
Respiratory syncytial virus (RSV)
RNA enveloped
Bronchiolitis
Highly contagious respiratory droplets
Common in children from 2-6mo
Inflammation of terminal bronchioles, necrosis and sloughing of epithelium of lining of bronchioles.
Fusion protein induces multinucleate giant cells.
Nasal flaring
Tachypnea
Child using the accessory muscles
Intercostal retraction and hyperinflation of chest
Expiration wheeze
Crepitations
Cyanosis
Measles
Koplik spots
Macular rash
Give rise to giant cell pneumonia
Influenza
ssRNA
Enveloped segmented the only one that replicates in nucleus
Orthomyxovirus
Two proteins:
1. Hemagglutinin- attachment to sialic acid on host cell
2. Neuraminidase- Detachment from host cell
Can thin the mucus and allows the virus to gain access
Matrix Protein (M)
Can cause secondary pneumonia
Severe desquamation of bronchial and alveolar epithelium.
Antigenic shift: Reassortment of genome segments from different human or animal strains. Random mixing and packaging of genome occurs after co infection producing new Hybrid virus. Pandemics
Antigenic drift: point mutations in the gen coding which alters viral antigenicity. The vaccine doesn’t work on the strain anymore. Reason for yearly outbreaks
Antivirals: Oseltamivir (Oral) and Zanamivir (inhalant) are Neuraminidase inhibitor. (influenza A and B)
Amantadine and Rimantadine: only for influenza A, neutralize the acid pH within the endosome.
Vaccine: Trivalent or quadrivalent.
Killed: Injectable for older than 50, Cardiopulmonary disease, people with high risk
Live: Nasal spray
Streptococcus pneumoniae
Encapsulated Gram postitive
Diplococci with plenty of neutrophils
Yellowish- brown sputum (rusty)
Left side pain
CXR: Left Lower lobe infiltrate
Upper airway colonization ( young children) and aspiration of bacteria into the lower airway (young, old and unconscious.
Alveoli infiltrated with RBC/neutrophils because the macrophages fails to phagocytose the bacteria. Causing consolation (liquid in alveoli) affecting the gas exchange.
Sickle cell, Asplenia, Multiple myeloma are at risk for fulminant sepsis.
Capsule: Polysaccharide antiphagocityc
IgA protease: Cleaves IgA
Teichoic acid: Stimulates inflammatory cytokines (C5a). Attachment along with the surface protein adhesins.
Phosphorylchloline: Bind to platelet activating factor receptor on endothelial cell to facilitate the entry into the cell. (AVOID OPSONIZING ANTIBODIES)
Pneumolysis: Cytotoxic to alveolar and pulmonary epithelium (stimulates TNF alpha, IL1, C3a and C5a)
Culture: Alpha hemolysis on blood agar
Optochin sensitive
Bile salts activate autolysis and is dissolved.
Quellung reaction: Capsule swelling with specific antibodies.
Antibiotic: Third generation cephalosporin.
Vaccine for people above 50. 23 talent pneumococcal. (marginal zone B cell produces IgM)
Vaccine for kids under 2yr is conjugated because they do not develop the marginal zone after age of 2.
Aspiration pneumonia
Suspect on history lost of consciousness due to stroke, heavy drinking, poor gag reflex, anesthesia.
Foul smelling greenish sputum
In Supine position- superior segment of the right lower lobe.
In the right sided position- the right middle lobe or upper lobe
In the standing/sitting position- is on the posteriorbasal segment of the right lower lobe.
CXR: Dense right lower lobe infiltrates
3 forms of aspiration:
1. Gastric content: leads to chemical burn of pulmonary parenchyma
2. Obstructing object
3. Oral flora: Mainly mixed anaerobes especially in people with poor oral hygiene.
WBC- neutrophils more than 80%
Klebsiella peumoniae
Cough productive foul smelling sputum- red currant jelly
Percussion in the right lower lobe is dull. (fluid or solid)
Capsulated Gram negative bacilli with plenty neutrophils
In Mac Conkey agar- Grows as mucoid lactose fermented because of the capsule.
Staphylococcus aureus as secondary pneumonia
Gram + cocci in clusters
Golden yellow in Mannitol salt agar
Beta lysis in blood agar
Catalase +
Coagulase +
MRSA/VRSA
CXR: patchy infiltrates with diffuse opacification. Bilateral nodular infiltrates. Lesions with abscess necrotic agents.
Complication: lung Empyema (pus accumulates in the pleural space)
Staphs abilities:
1. Adhesion- Fibrinogen binding protein
2. Protein A- Avoids opsonization by flipping the antibodies. Bind to the Fc portion of IgG
3. Has a cloaking of opsonins (invisible cap)
4. Resistance to oxidative burst killing (H2O2)
5. CHIPS- Chemotaxis inhibitory protein of stap- impair the phagocyte recruitment
6. SCIN- Staph complement inhibition
7. Antimicrobial resistance
Pathogenic
- Impetigo/folliculitis
- Enteritis ( vomiting/diarrhea)
- Toxic shock syndrome
- Post pneumonia
- Staph Scalded skin syndrome
- Food poisoning
Legionella pneumophilia
Atypical pneumonia
NO person to person transmission
is aerosolized/ environmental
Cruise ships, Water sports, Garden, Hotel showers, Hospitals
RISK group: Older than 50, Smokers, Alcoholics, COPD and Immunocompromised.
Acquired: Showers, Whirlpool<60 Celsius , Air-condition, respiratory therapy, Humidifiers.
Taken up by the alveolar macrophage and prevents phagosome lysosomal fusion, survives and keep replicating intracellular.
Macrophages release Type 1 Interferon to reduce replication and reduce the iron required by the bacterial for survival.
Can live between 20C -60 C degree.
DO NOT show up in gram stain
Hyponatremia- SIADH
Diarrhea
Non-productive cough
Alternate mental and headaches
Smoker
Urine antigen test is positive
CRX: patchy infiltrates
BAL: polymorphonuclear Leukocytes are seen.
Silver Stained bacilli Positive
BYCE- Buffered Charcoal yeast extract (love growing in iron)
Direct Fluorescent Antibody (DFA) positive
Obligate or facultative intracellular, enters respiratory tract upon inhalation.
T cell mediated activation Th1, IFN gamma, IL 2
Antibiotic treatment: Because is an intracellular we have to use and antimicrobial that can penetrate the WBC. Legionella has betalactamase so we cannot use beta lactase.
Ex: Azitromycin and Fluroquinolones (Levifloxacin and Ciprofloxacin)
Mycoplasma pneumoniae
Atypical pneumonia- Primary interstitial pneumonia. Community acquired
Transmitted human to human
Thickening of the alveolar septa rather than filling of alveoli.
CRX- fine granular infiltrates
Extracelullar, obligate aerobe. Adheres to the respiratory epithelium by complex of adhesion proteins, mainly P1 adhesion.
Mycoplasma produces hydrogen peroxide and damage the respiratory epithelium. The cilia is destroy (same as influenza). Inference with the normal clearance of the upper airway and allows the bacteria to spread to lower respiratory tract.
LACK OF CELL WALL- cannot use penicillin or cephalosporins
Do NOT show gram stain
Requires cholesterol media. Fried egg on culture
Hb is low (pallor) - Because Cross reacting Mycoplasma IgM antibodies destroy the RBC. (AUTOIMMUNE HEMOLYTIC ANEMIA)
TC raised
ESR raised.
Cold agglutinin antibody test. (IgM antibodies that bind to antigens on the surface of human erythrocytes at 4 Celsius) Hemolytic anemia
Direct Coombs test is positive.
Mycoplasma acts as super antigen- stimulating inflammatory cells to migrate to infective areas and release TNF alpha, IL 1 and later IL 6
Complication
1. Hemolytic anemia- Type 2 cytotoxic hypersensitivity
2. Raynaud phenomenon- vasospasm of digits. severe in sickle cell.
3. Erythema multiform- Type 4 hypersensitive- Steve Johnson syndrome.
Chlamydia pneumoniae
Atypical pneumoniae
Human pathogen that causes sinusitis, pharyngitis, bronchitis and atypical pneumoniae
Transmitted person-person by respiratory secretion.
They are 3 differences chlamydias
1. Chlamydia trachomatis- sexual contact transmission
2. Chlamydia psittaci- inhalation of dried bird feces. Atypical pneumonia
3. Chlamydia pneumoniae- Respiratory droplets. Atypical pneumonia
Obligated intracellular (like legionella), survive inside human host.
Elementary body/reticulate body
Cannot make ATP
Cell wall lacks peptidoglycan.
Weak endotoxin
Chlamydiae pneumonia has been associated with Atherosclerosis
Cytoplasmic inclusion bodies are helpful in identifying these organism. Seen in Giemsa stain or immunofluorescence
Replicative cycle:
1. The extracellular, elementary body enters an epithelial cell
2. Changes into a reticulate body that divides many times by binary fusion
3. The daughter reticulate bodies changes into elementary bodies and release from the epithelial cell
Antibiotic:
Doxycycline for adults
Macrolides for teenager/ children
Pneumocystis jirovecii
Obligated Extracellular fungal
CANNOT be cultured.
Staining: Grocott Gomori methanamine silver stain
Exclusively in immunosuppressed patients. most common in AIDS patients.
Oral thrush may be seen
Bilateral crackles on auscultation
CD4 count is less than 200
T cell deficiency
Major surface glycoprotein (MSG) of the organism attach to the host fibronectin, surfactant.
Grows over the surfactant layer of alveolar epithelium. Type 1 pneumocytes are DESTROYED and Type 1 pneumocytes have EXCESS replication.
Foamy exudate in alveolar spaces with plasma cell infiltrate. Alveoli is filled with monocytes (they become macrophages) resulting in the foamy.
Nocardia asteroides
Gram Positive bacilli
Catalase positive
Urease positive
Intracellular aerobic rod that form branched filaments.
Partially/ Weakly acid fast. (1%)
Mycobacteria- strong fast
Actinomycosis- non acid fast
Culture in 1-2 days
Sulfonamides are the antibiotics of choice
Aspergillosis
Exposure to Aspergillus in environment may cause allergic reactions in host.
Destructive, Invasive pulmonary and Disseminated disease in highly immunosuppressed individuals.
Are common thoughout the world
Within the hospital environment, it may be found in air, shower heads, hospital water storage tanks and potted plants
Inhalation of spores (conidia).
In normal person: Alveolar macrophage phagocytose spores and destroy by non oxidative mechanism.
In Neutropenic host: Spores germinate from hyphae, colonize and invade lung tissue and blood vessel.
The ones that survive the macrophage and turn into hyphae are countered by neutrophil which secrete reactive oxygen and kill the organism.
Catalase positive
Causes farmer lung- sinusitis
Lab: mold in agar (fluffy)
Rhinocerebral zygomycoses- Bacillus anthracis
Fruity odor- diabetic ketacidosis
Person working in a Wool factory
Spores are latent for 2 mo in the nasal.
NO person to person
Non-motile
Gram positive box car like bacilli
Blood agar: Medusa head colonies
Periorbital swelling
Ribbon like non-septate hyphae
Spores can be inhaled, conidia reach the distal alveolar and begin germinate. macrophage phagocyte conidia and neutrophils the hyphal.
Can invade the blood vessel and the brain
Paranasal swelling
Headaches
Mental lethargy
CRX: mediastinum Widening
Virulence factors:
Polypeptide capsule: Poly D glutamic acid
Protective antigen: binding portion
Edema factor: calmodulin dependent adenyl cyclase increase cAMP
Lethal factor: Protease increases secretion of TNF leading to necrosis.
Active immunization: Inactivating the anthrax toxin. Protective antigen.
Passive immunization: human monoclonal antibodies against Bacillus anthracis.
Hantavirus
Enveloped segmented ssRNA
Transmited by Rodent contact with excreta
Damage to capillaries, small vessels walls resulting vasodilation and congestion with hemorrhages
Leading to hypotension, oliguria and shock
Mycobacterium tuberculosis
Aerobic- grows in oxygenated tissues
Bacilli, non motile
60% is mycotic acid cell wall
Acid Fast due to high mycotic acid!!
Inhalation of aerosol droplets containing mycobacteria
Do not gram stain
High lipid content. Resist killing in macrophage, avoid phagocytosis
Has superoxide disputase and catalase fro intracellular survival
Suldatides: block the phagosome lysosome fusion
3 possible outcomes
1. clearance of bacteria
2. Primary active disease
3. Latent infection- years later, macrophage didn’t complete the work
- Mycobacteria TB bind to macrophage through complement receptor mannose receptor and lipoarabinomannan on cell wall. Blocks the formation of Phagolysosome.
- TH1 response after 3 weeks infection, TH1 is mounted, which it activated macrophages, enabling them to become bactericidal, which causes tissue damage.
- TH1 response orchestrates the formation of granuloma and caseous necrosis. TH1 secretes TNF which recruits monocytes from blood stream. Which IFN gamma activates the monocytes to transform into macrophages and aggregates to forms granuloma.
Caseating granuloma: has a necrotic region on the center. Necrosis is found in the TB lesion is dry, crumbling and cheesy.
Primary TB: Initial focus of infection. Ghon complex( Hilar lymph and lobe) and Ghan focus , enlarge lymph. Lower part of the upper lobe or upper part of lower lobe. Has fibrosis and calcification.
Secondary TB: Caseous necrosis after drainage of infectious material, creating a tuberculosis cavity. Site with high oxygen tension.
If necrotic focus breaks through the pleura: lymphatic invasion- Pneumothorax, tuberculous empyema.
Caseous material dispersed in the bronchial tree may lead to bronchopneumonia
Military Tuberculosis: Presence of multiple small tuberculous granuloma in many organs. ( invade the blood vessels)
Clinical:
Night sweats
Significant weight loss
Productive cough with purulent sputum production
Coin lesion (Ghon focus) in CRX
With the sputum:
Acid Fast 20%: ZIEHL NEELSEN and COLD KINYOUN
PPD skin test: Delayed hypersensitivity reaction. Positive indicates EXPOSURE. NOT ACTIVE
>5 patient with HIV or recent contact TB
>10 patient high risk , IV drug user
>15 no known risk factor
Quantiferon: more specific
immune cell from M tuberculosis and amount of IFN gamma release is measured. Not influenced by vaccine.
Culture takes 8 weeks ( Lowenstein Jensen agar)
BACTEC liquid medium takes 2 weeks detects radioactive carbon dioxide.
Multidrug resistance
Mycobacterium Avium
Acquired envioromental: NO human to human
water source, hot water, bird and animal excreta
Risk CD4 less than 50
Usually prenseted as pulmonary infection
MAC also infected via ingestion
Has fever, night sweats, anorexia, weight loss, hepatomegaly, splenomegaly, lymphadenopathy
Proxylaxis: azithromycin and clarithromycin
Treatment: Clarithromycin,ethambutol, Rifabutin, amikacin or fluoroquinolone.
Coccidiodes immitis
Dimorphic fungi, grows as mold in the alkaline soil.
Hyphae fragment to form rectangular arthrospores (infection form)
Eosinophilic response
Environment is Arthroconidia when it enters to the body it develops into spherules that produces endospores and are release into lungs
In the tissue they are spherules with endospores.
Night sweats, weight loss
erythematous, lumpy lesions
Type 4 sensitivity- 80% test positive for skin test
NO acid fast
NO gram stain
NO fungal stain
H&E stain reveals spherules with endospores
Multifocal consolidation
Calcification on healing lesions
Found in spoil- enhanced by bat and rodent drooping
Inhalation of spored may result in asymptomatic or self limited flue like illness.
Primary coccidioidomycosis- allergic reaction
Secondary - immune complex ( erythema multiform, nodosum)
Histoplasma capsulatum
Trabeculate microconidia the infecting form in the soil contaminated with bird/bat excreta
- Soil contaminated with bird droppings is whipped by the wind
- Microconidia are inhaled
- The patient develops mild pneumonitis
- In the tissue, the phase of infection, the yeast develop is phagocytose and multiplies by budding intracellular. Most patient recover
- In some case the phagocytes enter the blood and causes diseases.
CXR: Multiple nodular infiltrates in both lungs.
Enlarge hilar and mediastinal lymph nodes. Snowball/popcorn calcification.
NO acid fast
No Gram stain
NO fungal stain
Giemsa stain yeast is seen in macrophages
Dimorphism Yeast- body Mold- room
Blastomycosis
Verrucous skin lesion
Auscultation reveals crackles in the left lung
CXR: Multiple nodular lesions which some are cavitating in the left lower lobe.
Inhaled from the environment. In the lungs they change into yeast form recruit neutrophils. Transported into the lymph nodes and hematogenous spread.
Tissue response is granulomatous, skin shows verrucous lesions.
NO gram stain
NO acid Fast
Biopsy- H&E stain reveals Thick Walled Broad Based budding yeast.
