Microbiology Flashcards
Gram positive structure
Cell wall present; major surface antigen
Composition:
- Peptidoglycan
- Lipoteichoic acid–> TNF, IL-1 induction
Gram negative structure
No cell wall, only outer membrane
- Site of Endotoxin= LPS (lipopolysaccharide)= major surface antigen
Composition:
- Lipid A–> activate macrophages–> increased TNF and IL-1
- Antigen= O polysaccharide
- Periplasm= space between cytoplasmic membrane and outer membrane; contains hydrolytic enzymes (beta-lactamases)
Spore structure
Resistant to dehydration, heat, chemicals
- Must autoclave (121 C for 15 min)
Composition:
- Keratin-like coat
- Dipicolinic acid core
- Peptidoglycan
Seen in:
- Soil: B. anthracis, Clostridium perfringens, c. tetani
- Other: B. cereus, C. botulinum, Coxiella burnetti
Gram-positive cocci
Staphylococcus
Streptococcus
Gram-negative cocci
Neisseria
Gram-positive rod
Clostridium Corynebacterium Bacillus Listeria Mycobacterium (high lipid= acid fast) Gardenerella (gram variable)
Gram-negative rods
Almost everything else:
- Enterics:
- E. Coli
- Shigella
- Yersinia
- Klebsiella
- Proteus
- Enterobacter
- Serratia
- Vibrio
- Campylobacter
- Helicobacter (silver stain+)
- Pseudomonas
- Bacteroides - Respiratory:
- Haemophilus (pleomorphic)
- Legionella (intracellular; silver stain +)
- Bordetella - Zoonotic
- Francisella
- Brucella
- Pasteurella
- Bartonella
- resistant to Penicillin G (gram-negative outer membrane inhibits Pen G/Vanco from entering)
- Susceptible to Ampicillin, amoxicillin
Spirochetes
Gram-negative (too thin)
- Leptospira
- Borrelia
- Treponema
Pleomorphic bacteria
Giemsa-stain
- Rickettsiae (intracellular)
- Chlamydiae (intracellular, no muramic acid)
Bacteria with no cell wall
Mycoplasma= no staining
- Sterols with no wall
Giemsa-positive
Certain Bugs Really Try my Patience:
- Chlamydia
- Borrelia
- Rickettsiae
- Trypanosomes
- Plasmodium
Carbol Fuschin stain (Ziehl-Neelsen)
Acid-fast organisms
- Nocardia
- Mycobacterium
India ink positive
Cryptococcus neoformans
- can also stain with mucicarmine
Exotoxin
Derived from gram + and gram -
- Secreted from cell
- Polypeptide
- Located on plasmid/bacteriophage
- Highly toxic
- Antigenic= Induces antitoxins (titer antibodies)
- Vaccine= toxoids
- Destroyed at 60C (besides staph enterotoxin)
Seen in: Tetanus, botulism, diphtheria
Endotoxin
LPS= structural component of outer cell membrane in gram negative; released when lysed (NOT secreted)
Activates:
- Macrophages:
- IL-1–> fever
- TNF–> fever, hypotension
- NO–> hypotension - Complement
- C3a–> hypotension, edema
- C5a–> neutrophil chemotaxis - Tissue factor
- Coagulation cascade–> DIC
- Located on Bacterial chromosome
- Low toxicity
- Causes: Fever, shock
- Mode of action:Induces TNF and IL-l
- Antigenic: Poorly antigenic
- Vaccines= none
- Stable at 100C for 1 hour
Seen in: meningococcemia, gram-negative sepsis
Obligate aerobes
Nagging Pests Must Breathe
- Nocardia
- Pseudomonas aeruginosa
- Mycobacterium tuberculosis (apices of lung)
- Bacillus
Obligate anaerobes
Can’t Breathe Air
- Clostridium
- Bacteroides
- Actinomyces
Seen in GI tract, pathogenic anywhere else
** Can’t treat with aminoglycosides= need O2 to enter cell
Obligate intracellulars
Rickettsia
Chlamydia
Facultative intracellular
Now Listen Sally, Yer Friend Bruce Must Leave
- Neisseria
- Listeria
- Salmonella
- Yersinia Pestis
- Francisella
- Brucella
- Mycobacterium
- Legionella
Encapsulated bacteria
Positive Quellung reaction–> swelling
SHiNE SKiS
- Streptococcus pneumoniae
- Haemophilus infiuenzae type B
- Neisseria meningitidis
- Escherichia coli
- Salmonella
- Klebsiella pneumoniae
- group B Strep.
Catalase-positive
Degrades H2O2 before converted to microbicidal products by Myeloperoxidase (MPO) PLACESS for your cats: - Pseudomonas - Listeria - Aspergillus - Candida - E. Coli - S. Aureus - Serratia
Urease-positive
CHuck norris hates PUNKSS:
- Cryptococcus
- H. pylori
- Proteus
- Ureaplasma
- Nocardia
- Klebsiella
- S. epidermidis
- S. saprophyticus
IgA protease
Enzyme cleaving IgA–> colonize respiratory mucosa: SHiN
- S. pneumoniae
- H. influenza (B)
- Neisseria
** These can all take up naked DNA from environment as well= Transformation
Protein A
S. Aureus
- Binds Fc region of Ig–> no opsonization/phagocytosis
M Protein
Group A strep
- Prevents phagocytosis
Pigment-producing bacteria
Actinomyces Israelii= yellow (Israel= yellow sand)
S. Aureus= yellow (pus/gold)
Pseudomonas aeruginosa= blue/green (pyocyanin)
Serratia marcescens= red (maraschino cherry)
Novobicin
Used to ID catalase-positive, coagulase-negative staphylococci
- Staph Saprophyticus= resistant
- Staph Epidermis= sensitive
Optochin
used to ID catalase-negative alpha-hemolytic streptococci:
- Viridans= resistant
- Penumoniae= sensitive
Bacitracin
Used to ID Catalse-negative, beta-hemolytic streptococci:
- Agalactiae= resistant
- Pyogenes= sensitive
Alpha-hemolytic bacteria
Partial hemolysis; green ring around colonies
- Strep pneumo
- Strep viridans
Beta-hemolytic bacteria
Complete hemolysis; clear ring around colonies:
- Staph aureus
- Strep pyogenes (group A)
- Strep agalctiae (group B)
- Listeria monocytogenes
Staphylococcus aureus
Gram positive cocci, Clustered
Catalase positive
Coagulase positive
Virulence factor= Protein A (binds Fc-IgG–> prevents phagocytosis)
Causes:
- Inflammatory disease: skin infections, organ abscesses, pneumonia
- Acute bacterial endocarditis
- Osteomyelitis - Toxin-mediated disease:
- Toxic shock syndrome (TSST-1)= superantigen, binds MHC II receptor–> T-cell activation–> IFN-gamma, IL-2 release
- scalded skin (exfoliative toxin)
- rapid-onset food poisoning (preformed enterotoxins)
* * Activates T-cells (IL-2) and macrophages (IL-1, TNF) - MRSA: resistant to beta-lactams (altered penicillin-binding protein)
Treatment:
- Nafcillin (Naf for Staph- EXCEPT MRSA)
- Vancomycin for MRSA
THINK:
- Pus, empyema, abscess
- Surgical wound
- chronic granulomatous disease (Catalase-positive microbes)
Staphylococcus epidermidis
Gram positive cocci
Catalase positive
Coagulase negative
Novobicin sensitive (vs staph saprophyticus)
Infects prostehetic devices, IV catheters (biofilm)
- Seen in normal skin flora
- Contaminates blood cultures
Resistant to penicillins, tx with Vancomycin
Staphylococcus saprophyticus
Gram positive cocci
Catalase positive
Coagulase negative
Novobicin resistant (vs staph epidermidis)
Causes UTIs
Streptococcus pneumoniae
Gram positive cocci; lancet shaped Catalase negative alpha-hemolytic Capsule (+ quelling) Optochin sensitive (vs strep Viridans) IgA protease
Causes:
- Meningitis
- Otitis media
- Pneumonia (rusty sputum)
- Sinusitis
- Sepsis, splenectomy in Sickle cell
Streptococcus viridans
Gram positive cocci Catalase negative alpha-hemolytic No capsule Optochin resistant (vs strep pneumo)
Causes:
- Dental caries (normal flora in mouth= strep mutans)
- Subacute bacterial endocarditis (strep sanguis)
Strep pyogenes
Group A strep Gram positive cocci Catalase negative beta-hemolytic Bacitracin sensitive (vs strep agalactiae)
M-protein (prevents opsonization–> blocking phagocytosis)
Exotoxin=
- streptolysin O
- Protein degrades cell membrane (lyse RBCs)- test for ASO antibodies - Exotoxin A: brings MHC II and T-cell receptors together–> release IFN-gamma, IL-2 release–> Toxic shock-like syndrome
- Streptokinase= plasminogen activator (blocks clotting)
Causes:
- Pyogenic:
- Pharyngitis
- Cellulitis
- Impetigo (precedes glomerulonephritis, pharyngitis) - Toxigenic:
- Scarlet fever (spares face, strawberry tongue, throat)
- Toxic shock-like syndrome
- Necrotizing fasciitis - Immunologic:
- Rheumatic fever (polyarthritis, carditis, subcutaneous nodules, erythema marginatum, Sydenham’s chorea)
- Acute glomerulonephritis
- Post strep glomerulonephritis= deficiency of complement due to fixation in renal tubules
- ASO titer to detect infection (antibodies to streptolysin O)
- Host antibodies to M-protein–> rheumatic fever
Strep agalactiae
Group B strep Gram positive coci Catalase negative Beta hemolytic (Produces CAMP factor--> increased hemolysis) Bacitracin resistant (vs strep pyogenes) Hippurate test positive
Causes:
- Illnesses mainly seen in babies (due to colonization of vaginal flora): Pneumonia, meningitis, sepsis
- Screen women at 35-37 weeks
- Prophylaxis with penicillin
Enterococci
Group D strep Gram positive cocci Catalase negative Non-hemolytic/variable hemolysis Grows in Bile and 6.5% NaCl
Enterococci faecalis, faecium:
- Penicillin G resistant
- Cause UTI, biliary tract infections, subacute endocarditis
- Vancomycin-resistant strains= nosocomial infection
Streptococcus bovis
Group D strep Gram positive cocci Catalase negative Non-hemolytic Grows in Bile (no NaCl)
Colonizes gut
- Colon cancer patients: subacute endocarditis, bacteremia
Corynebacterium diphtheriae
Gram positive rod (club-shaped)
Black colonies in cystine-tellurite agar
Metachromatic (blue and red) granules
AB Exotoxin= (B=binds, A= active–> EF-2)
- B-prophage encoded–> inhibits protein synthesis (ADP-ribosylates elongation factor= EF-2)
- Test= Elek’s test
Causes:
- Pseudomembranous pharyngitis (gray-white)
- Lymphadenopathy
- Myocarditis
- Arrhythmias
** Toxoid vaccine= induces production of IgG against exotoxin B (toxin causes disease, not bacteria)
Clostridium tetani
Gram-positive rod
Spore-forming
Obligate anaerobe
Exotoxin= Tetanospasmin
- Tetanus toxin–> cleaves neurotransmitter-releasing proteins (SNARE)
- Blocks glycine, GABA release (inhibitory neurotransmitters) from Renshaw cells in spinal cord
- Causes spastic paralysis, trismus (lockjaw), risus sardonicus)
Tx: passive vaccine
Clostridium botulinum
Gram-positive rod
Spore-forming
Obligate anaerobe
Exotoxin= botulinum toxin
- Cleaves SNARE proteins (blocking neurotransmitter release)
- Inhibits ACh release at NM junction–> flaccid paralysis
- Adults= ingest preformed toxin
- Babies= spores in honey–> floppy baby)
Tx: passive vaccine
Clostridium perfringens
Gram-positive rod
Spore-forming
Obligate anaerobe
Exotoxin= alpha toxin (lecithinase= phospholipase)
- Phospholipase degrades tissue, cell membranes–>
- Causes myonecrosis (gas gangrene)
- Hemolysis
Clostridium difficile
Gram-positive rod
Spore-forming
Obligate anaerobe
Exotoxins:
- Toxin A = enterotoxin binding brushborder of gut)
- Toxin B = cytotoxin binding enterocytes–> pseudomembranous colitis
- Secondary to antibiotics (clindamycin, ampicillin)
Treatment:
- Metronidazole
- Oral vancomycin
Bacillus anthracis
Gram-positive rod
* Polypeptide capsule (D-glutamate containing)
Spore-forming
Exotoxin= anthrax (Edema factor)
- Mimics adenylate cyclase (increased cAMP)
- Calmodulin-dependent adenylate cyclase–> increases cAMP in smooth muscle–> vasodilation (edema), suppressed neutrophil funciton)
Forms:
- Cutaneous–> black eschar (painless ulcer)–> bacteremia, death)
- Pulmonary–> flu-like symptoms–> fever, pulmonary hemorrhage, mediastinitis, shock (Woolsorter’s disease)
Bacillus cereus
Gram-positive rod
Spore-forming
Obligate aerobe
Enterotoxin= Cereulide
- Food poisoning (enterotoxin in rice= “reheated rice syndrome)
- Emesis: rice, pasta–> N/V in 1-5 hours
- Diarrhea: GI pain, watery, non-bloody in 8-18 hours
Listeria Monocytogenes
Gram positive rod
Facultative intracellular
Catalase positive
Beta hemolytic
Forms “actin rockets”–> move cell to cell
- Tumbling motility
Ingested from unpasteurized milk/cheese, deli meats
Causes:
- Amnionitis
- Septicemia
- Spontaneous abortion
- Meningitis in immunocompromised
- Gastroenteritis in healthy (self-limited)
Vaginal transmission
Causes:
- Granulomatosis infantiseptica
- Neonatal meningitis
- Tx= ampicillin
Actinomyces
Long, branching filament (resembles fungi) Gram-positive Anaerobe NOT acid-fast Found in normal oral flora
Causes:
- Oral/facial abscesses that drain–> sinus tracts
- Yellow “sulfur granules”
Tx: Penicillin
Nocardia
Long, branching filament (resembles fungi) Gram-positive Aerobe Acid fast Found in soil
Causes:
- Pulmonary infections in immunocompromised
- Cutaneous infections (post-trauma) in healthy
Tx: Sulfonamides
Mycobacterium tuberculosis
Gram-positive rod
Carbol-Fuschin (Ziehl-Neelsen) stain
Acid fast (lipid membrane)
Obligate aerobe (lung apices)
Facultative intracellular
* Cord factor in virulent strain–> TNF-alpha release, inhibited macrophage maturation
* Sulfatides (surface glycolipids) inhibit phagolysosomal fusion
Primary TB:
- Nonimmune host infected–> Ghon complex:
1. Heals (fibrosis)–> immunity/hypersensitivity
2. Progressive lung disease (immune compromised)
3. Severe bacteremia–> Miliary TB
4. Preallergic lymphatic/hematogenous dissemination–> dormant–> reactivate later in life
Secondary TB:
- Partially immune hypersensitized host (adult) reinfected)
1. Fibrocaseous cavitary lesion (upper lobes)
2. Reactivates
Reactivated TB= Extrapulmonary TB
- CNS (parenchymal TB/meningitis in base of brain)
- Vertebral body (Pott’s disease)
- Lymphadenitis
- Renal
- GI
Symptoms:
- Fever, night sweats, weight loss, hemoptysis
Tx:
- Prophylaxis= Isoniazid (INH)
- Therapy= Rifampin, Isoniazid, Pyrazinamide, Ethambutol (RIPE for tx)
Mycobacteria Kansasii
Gram-positive rod
Carbol-Fuschin (Ziehl-Neelsen) stain
Acid fast (lipid membrane)
Obligate aerobe (lung apices)
Facultative intracellular
* Cord factor in virulent strain–> TNF-alpha release, inhibited macrophage maturation
* Sulfatides (surface glycolipids) inhibit phagolysosomal fusion
Pulmonary TB-like symptoms
Mycobacterium avium-intracellulare
Gram-positive rod
Carbol-Fuschin (Ziehl-Neelsen) stain
Acid fast (lipid membrane)
Obligate aerobe (lung apices)
Facultative intracellular
* Cord factor in virulent strain–> TNF-alpha release, inhibited macrophage maturation
* Sulfatides (surface glycolipids) inhibit phagolysosomal fusion
Disseminated non-TB disease in AIDS, resistant to multiple drugs
** Prophylaxis with azithromycin (CD4+ < 50)
Tx: Azithromycin, Rifampin, Ethambutol, Streptomycin
Mycobacterium leprae
Gram-positive rod
Carbol-Fuschin (Ziehl-Neelsen) stain
Acid fast (lipid membrane)
Obligate aerobe (lung apices), likes cool temps
Facultative intracellular
* Cord factor in virulent strain–> TNF-alpha release, inhibited macrophage maturation
* Sulfatides (surface glycolipids) inhibit phagolysosomal fusion
Reservoir in USA= armadillos
Causes Leprosy. 2 forms:
1. Lepromatous= lethal
- Communicable
- Low cell-mediated immunity, humoral Th2 response only
Tx: Dapsone, rifampin, clofazimine (2-5 years)
- Tuberculoid= hypoesthetic hairless skin plaques (“glove and stocking” loss of sensation)
Tx: Dapsone, Rifampin (6 months)
Lactose-fermenting enteric bacteria
Gram-negative rods
Grow pink colonies on MacConkey’s agar:
Fast fermenter= Lactose in KEE
- Klebsiella
- E. coli
- Enterobacter
Slow fermenter=
- Citrobacter
- Serratia
Neisseria Gonococci
Gram-negative diplococci
Ferments Glucose (Gonococci)
Produces IgA proteases
Facultative intracellular
Grown on special agar: Thayer-Martin agar (or VPN agar)—an agar plate containing antibiotics (vancomycin, colistin, nystatin, and TMP-SMX)
- NO vaccine available (rapid antigenic variation in pilus)
- STD
Causes:
- Septic arthritis
- Neonatal conjunctivitis
- PID
- Fitz-Hugh-Curtis syndrome (adhesions due to PID; infection of liver capsule)
Tx: Ceftriaxone (+ azithromycin/doxycyclin for chlamydia coinfection)
Neisseria Meningococci
Gram-negative diplococci Ferments Maltose and glucose (MeninGococci) Produces IgA proteases Facultative intracellular Encapsulated (polysaccharide capsule)
Grown on special agar: Thayer-Martin agar (or VPN agar)—an agar plate containing antibiotics (vancomycin, colistin, nystatin, and TMP-SMX)
- Vaccine (none for Type B)
- Found in respiratory, oral secretions
Causes:
- Meningococcemia
- Meningitis
- Waterhouse-Friderichsen syndrom
Tx: Ceftriaxone, Pen G
** Rifampin, ciprofloxacin, ceftriaxone in close contacts
Haemophilus Influenza
Gram negative Coccoid rods Requires factor V and X to grow in culture (chocolate agar) IgA protease Encapsulated
- Vaccine= type B capsular polysaccharide conjugated to diphtheria toxoid (2-18 months)
- Nontypable strains cause mucosal infections (no vaccine available)
Causes:
- Epiglottitis (cherry red)
- Meningitis
- Otitis media
- Pneumonia
Tx: Ceftriaxone (meningitis)
* Rifampin prophylaxis in close contacts
THINK:
- Pediatric infection (epiglottitis)
Legionella pneumophilia
Gram-negative rod
Facultative intracellular
Silver stain
Grown on charcoal yeast extract with iron, cysteine
- Aerosol transmission from water source
- Detected in urine
- Labs show hyponatremia
Causes:
- Legionnaire’s disease= severe pneumonia, fever, GI, CNS symptoms
- Pontiac fever= mild flu-like syndrome
Tx: Macrolide (protein synthesis), quinolone (topoisomerase II)
Pseudomonas aeruginosa
Gram negative rod (enteric) Obligate aerobe Catalase positive Lactase NON-fermenting Oxidase positive Blue-green pigment, grape-like odor
Motile, oxidase positive
Produces:
- Endotoxin (fever, shock)
- Exotoxin A (inactivates EF-2)
- Elastase (breaks down vessel walls)
Causes: PSEUDOmonas - Pneumonia (chronic in CF pts due to biofilm) - Sepsis - External otitis - UTI - Drug use - Osteomyelitis (diabetic/drug user) \+ Hot tub foliculitis, wound/burn infections \+ MEO in diabetics
Tx:
- Aminoglycoside + extended-spectrum penicillin (piperacillin, ticarcillin)
Enteroinvasive E. Coli (EIEC)
Gram-negative rod
Lactose fermenting
Virulence factors:
- P fimbriae (cystitis/pyelonephritis)
- K capsule (pneumonia, neonatal meningitis)
- LPS endotoxin (septic shock)
Mechanism:
- Invades intestinal mucosa–> necrosis, inflammation
Manifestation: similar to Shigella
- Invasive
- Dysentery (blood, pus in stool)
Enterotoxigenic E. Coli (ETEC)
Gram-negative rod
Lactose fermenting
Virulence factors:
- P fimbriae (cystitis/pyelonephritis)
- K capsule (pneumonia, neonatal meningitis)
- LPS endotoxin (septic shock)
Mechanism:
- Labile toxin: overactivates adenylate cyclase–> increased cAMP–> Cl- secretion in gut–> H20 moves out of cells
- Stable toxin: overactivates guanylate cyclase–> increased cGMP–> decreased resorption of NaCl /H20 in gut
- NO inflammation/invasion
Manifestation: traveler’s diarrhea
Enteropathogenic E. Coli (EPEC)
Gram-negative rod
Lactose fermenting
Virulence factors:
- P fimbriae (cystitis/pyelonephritis)
- K capsule (pneumonia, neonatal meningitis)
- LPS endotoxin (septic shock)
Mechanism:
- Adheres to apical surface, flattens villi
- Prevents absorption
Manifestation:
- Pediatric diarrhea
Enterohemorrhagic E. Coli (EHEC)
Gram-negative rod
Lactose fermenting
Virulence factors:
- P fimbriae (cystitis/pyelonephritis)
- K-1 capsule (pneumonia, neonatal meningitis)
- LPS endotoxin (septic shock)
Mechanism:
- O157:H7= most common–> Shiga-like toxin
- Shiga-like toxin (SLT)= inactivates 60S ribosomal subunit by removing adenine from rRNA
- Endothelial swelling, narrowed lumen–> hemolysis, reduced renal blood flow
- Damaged endothelium–> thrombocytopenia
Cuases:
- Dysentery (Shiga-like)
- Hemolytic-uremic syndrome (HUS) due to cytokine release in response to SLT–> vascular damage–> capillary thrombus formation–> anemia, thrombocytopenia, acute renal failure, increased bleeding time
Klebsiella
Gram negative rod
Lactose fermenter
Polysaccharide capsule (mucoid colonies)
4As:
- Aspiration pneumonia
- Abscess (lungs/liver)
- Alcoholics
- diAbetics
- can also cause nosocomial UTI: positive urease test
Salmonella
Gram negative rod Lactose non-fermenter Oxidase negative Facultative intracellular Encapsulated
- Flagellated
- Hematogenous dissemination
- Animal reservoir
- Produce hydrogen sulfide
- Invades intestinal mucosa–> monocytic response
Causes:
- Bloody diarrhea
- Non-typhoidal= appendicitis mimicker
- Typhi= Typhoid fever (humans only): rose spots on abdomen, fever, headache, diarrhea
- Osteomyelitis in sickle cell pts
Tx: Antibiotics prolong symptoms
Shigella
Gram negative rod
Lactose non-fermenter
Oxidase negative
Shiga toxin= inactivates 60S ribosomal subunit by removing adenine from rRNA
- No flagella
- Cell to cell transmission
- Reservoir= humans/primates
- Invades intestinal mucosa–> PMN infiltration
- Shiga toxin–> Cytokine release–> HUS: due to cytokine release in response to Shige toxin–> vascular damage–> capillary thrombus formation–> anemia, thrombocytopenia, acute renal failure, increased bleeding time
Tx: antibiotics shortens excretion of organism in feces
Campylobacter jejuni
Gram negative comma-shaped
Oxidase positive
Grows at 42C
Transmitted through poultry, meat, unpasteurized milk
Causes:
- Bloody diarrhea (esp. children)
- Guillain-Barre syndrome, reactive arthritis
- Mimics appendicitis
Vibrio cholerae
Gram negative comma-shaped
Oxidase positive
Grows in alkaline media
Mechanism:
- Cholera toxin Activates Gs of adenylate cyclase–> increased cAMP–> increased Cl- secretion, H20 efflux
Causes:
- Profuse rice-water diarrhea (common in developing countries)
Tx: rehydration
Yersinia enterocolitica
Gram negative rod
Facultative intracellular
Mechanism:
- Transmitted from pet feces, contaminated milk, pork
Causes:
- Mesenteric adentitis (Crohn’s, appendicitis mimicker)
H. Pylori
Curved Gram-negative rod
Silver stain
Urease positive (urease breath test)- alkaline environment created in stomach
Causes:
- Gastritis
- 90% duodenal ulcers
- Increased peptic ulcer, gastric adenocarcinoma, B-cell lymphoma risk
Tx: triple therapy:
- PPI
- Clarithromycin
- Amoxicillin/ Metronidazole
Spirochetes
Borrelia (BIG)= Wright/Giemsa stain
Leptospira
Treponema= dark field microscopy
Leptospira interrogans
Spirochete
Water contaminated with animal urine (triathletes in tropics)
Causes:
- Flu-like symptoms
- Jaundice
- Photophobia with conjunctivitis
- Weil’s disease= icterohemorrhagic leptospirosis: severe; jaundice, azotemia (liver, kidney dysfunction), fever, hemorrhage, anemia
Borrelia Burgdorferi
Spirochete (visualized with Wright/Giemsa stain)
Lyme disease:
- Transmitted by Ixodes tick
- Reservoir= wood mouse
- Stages:
1. Erythemia migrans (bull’s eye), flu-like
2. Neurologic (Bell’s palsy), cardiac (AV node block)
3. Musculoskeletal (chronic monoarthritis, migratory polyarthritis), neurological (encephalopathy, polyneuropathy), cutaneous