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Gram Positive Pathogens Flashcards

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1
Q

Gram Positive Cell Walls

A
  • Composed primarily of peptidoglycan
  • may also contain teichoic acids (negatively charged)
    Help maintain cell envelope
    Protect from environmental substances
    May bind to host cells
  • some gram + bacteria have layers of proteins on surface of peptidoglycan
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2
Q

Gram + pathogens

A
  • stain purple when gram stained
  • Two major groups based on DNA - G and C within genome - actually many taxonomic phyla
    1. Low G + C bacteria (cocci and bacilli)
    2. High G + C bacteria (Bacilli/Pleomorphic
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3
Q

Cocci - Low G + C - Gram +

A

Staphylococcus aureus, Streptococcus pyogenes (GAS), Streptococcus pneumoniae, Enterococcus faecalis

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4
Q

Bacilli - Low G/C content - Gram +

A

Bacillus, Clostridium difficile, listeria monocytogenes

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5
Q

Bacilli/Pleomorphic - High G/C Content

A

Mycobacterium tuberculosis

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6
Q

Staphylococcus

A

Normal members of every humans, microbiota, can be opportunistic pathogens, common inhabitant of the skin and mucous membranes, spherical cells arranged in irregular clusters, lack spores and flagella, may have capsules, come in different species ie: aureus
- facultative anaerobe’s, salt tolerant, tolerant of desiccation, radiation, and heat, they survive on environmental surfaces

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7
Q

Staphylococcus Aureus - Gram + - low G/C

A
  • most virulent strain associated with disease in humans
  • facultative anaerobe
  • salt tolerant - tolerate on human skin
  • gram-positive - spherical cells irregular clusters
  • present in most environments frequented by humans, readily isolated from fomite, carriage is mostly in anterior nares, skin, nasal pharynx , intestine
  • Predisposition to infection: poor hygiene and nutrition, tissue injury, pre-existing, primary infection, diabetes, immuno deficiency
  • carriage rate for healthy adults: 2O - 60%
  • MRSA carriage varies 1-5%
  • causes MRSA (methicillin resistance staph aureus)
  • infection occurs upon breaching physical barriers (only takes a few hundred)
  • structures allow it to hide from phagocytes, produce enzymes, produce toxins
  • Virulence Factors: coagulate +, penicillinase (resistant to penicillin by inactivating it), leukocidin (lyses neutrophils/macrophages), enterotoxin (induce nausea, vomit, diarrhea), exfoliative (desquamation of skin), toxic shock syndrome toxin (induce fever, vomit, rash, organ damage)
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8
Q

Effects of Staph diseases

A
  • causes cutaneous diseases (skin)
  • toxigenic/noninvasive diseases
  • spider bites can cause staph infection from staph aureus bacteria
  • systemic
  • Skin: boils, carbuncles, impetigo, scalded skin syndrome, osteomyelitis
  • Cardio/lymph: endocarditis, toxic shock
  • Gastrointestinal: food intoxication
  • Respiratory: pneumonia
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9
Q

Folliculitis - cutaneous

A

Superficial inflammation of hair follicle, usually resolved with no complications, but can progress

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10
Q

Furuncle - cutaneous

A

Boil; inflammation of hair, follicle, or sebaceous gland, progresses into abscess or pustule

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11
Q

Carbuncle - cutaneous

A

Larger and deeper lesion, created by aggregation and interconnection of a cluster of furuncles

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12
Q

Impetigo (pyoderma) - cutaneous

A

Bubble like swellings that can break and peel away most common in newborns
- superficial lesions that break inform highly contagious crust
- Often in school children
- Associated with insect bites, poor hygiene, and crowded living

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13
Q

Food intoxication - toxigenic

A

Ingestion of heat stable enterotoxin’s;  gastrointestinal distress - typically only vomiting occurs

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14
Q

Scalded skin syndrome - toxigenic

A

Toxin includes bright, red flush, blisters, then desquamation of the epidermis

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15
Q

Toxic shock syndrome - toxigenic

A

Toxemia leading to shock and organ failure

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16
Q

Osteomyelitis - systemic

A

Infection is established in the metaphysis; abscess forms
- forms biofilms on bones

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17
Q

Bacteremia

A

Primary origin is bacteria from another infected site or medical devices; endocarditis possible

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18
Q

Endocarditis

A

Very aggressive “ acute endocarditis” - often fatal 

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19
Q

Pneumonia

A
  • common cause of post influenza, bacterial pneumonia
  • staph aureus likes to live in nose
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20
Q

Clinical concerns for Staph infections

A
  • 95% have penicillinase and are resistant to penicillin and ampicillin
  • MRSA carries multiple resistance
  • some strains have resistance to all major drug groups, except VANCOMYCIN
  • Abscesses have to be surgically perforated
  • Systemic infections require intensive lengthy therapy
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21
Q

Treating Staph

A
  • S. aureus: resistant forms can still be treated with cephalexin, sulfa drugs, tetracyclines, or clindamycin,
  • MRSA: treated with vancomycin, ceftaroline, linezolid, daptomycin - typically two of these are used in combination to reduce further drug resistance
  • VISA and VRSA: quinupristin/dalfopristin is the last drug of choice
22
Q

Prevention of staph infections

A
  • hospital workers who carries S aureus nasally may be barred from nurseries, operating rooms, and delivery rooms
  • Carriers can be treated for several months with a combination of Antimicrobic drugs like Bactroban, and the dicloxacillin
  • Hygiene and cleansing
  • A vaccine is currently in trials
23
Q

Characteristics of Streptococcus and Enterococcus

A
  • Gram-positive spherical cocci - arranged in long chains; commonly in pairs
  • non-spore forming, nonmotile
  • Facultative anaerobe
  • Can form capsules and slime layers
  • Catalase -
  • have peroxidase system
  • Those parasitic forms are fastidious and require and enriched media
  • Small, non-pigmented colonies
  • Sensitive to drying, heat, and disinfectants
24
Q

Streptococcus sub groups

A
  • Lancefield groups: based on cell wall Ag-17 groups (A, B, C)
  • based on hemolysis
    1. Beta hemolytic: complete hemolysis (Clear)
  • Most serious strep pathogen
  • Strict parasite
  • Inhabits throat, nasopharnyx, sometimes skin
    2. Alpha hemolytic: partial hemolysis (opague - greenish)
  • 
25
Q

Streptococcus pyogenes (GAS) - Gramn+ Low G/C - Group A

A
  • catalase negative
  • facultative anaerobe
  • non motile
  • small, non pigmented colonies
  • long changed of spherical cocci
  • sensitive to drying, heat, disinfectants
  • Occurs in humans only
  • No carriers
  • Transmission occurs through contact, droplets, food, and fomite
  • Portal of entry: skin or pharynx
  • Children become affected for cutaneous and throat infections
  • Systemic infections, and progressive immune sequelae are possible if untreated
  • virulence factors:
  • Skin: Impetigo, Erysipelas, necrotizing, fasciitis
  • Card/Lymph: scarlet fever, rheumatic fever
  • Respiratory: pharyngitis (step throat) , sinusitis
  • Urogenital: glomerulonephritis
    1. surface antigen (carbohydrates (protest against lysozyme), fimbriae (adherence), M-protein (contributes to resistance to phagocytosis), hyaluronic acid capsule (provokes no immune response), C5a protease: hinders, complement, and neutrophil response
    2. Extra cellular toxins: streptolysins, erythrogenic toxin (pyrogenic), super antigens
    3. Extra cellular enzymes: streptokinase (digest, fibrin, clot) , hyaluronidase (breaks down, connective tissue), DNase (hydrolyzes DNA)
26
Q

Streptolysins

A

Hemolysins
- Type O (SLO)
- Type S (SLS)
both cause cell and tissue injury

27
Q

Erythogenic Toxin (pyrogenic)

A

Induces fever and typical red rash

28
Q

Superantigens

A

Strong monocyte and lymphocyte stimulant; cause the release of tissue necrotic factor

29
Q

Eryspipelas

A

Pathogen enters through broken skin and spreads to the dermis and subcutaneous tissue; can be superficial, or become systematic

30
Q

S. Pyogenus - Systemic Infections

A
  • Scarlet fever, septicemia, pneumonia, streptococcal toxic shock syndrome, necrotizing, fasciitis
31
Q

Sequalae of Group A Streptococcus Infections ( long term complications)

A
  • rheumatic fever: fall is over or subclinical, pharyngitis in children; carditis with extensive valve damage possible, arthritis, cholera, fever
  • Acute glomerulonephritis: nephritis, increased blood pressure, occasionally heart failure, can become chronic leading to kidney failure
32
Q

Treatment for group A streptococcal infections

A

Both group A and B are treated with penicillin
- Long-term penicillin prophylaxis for people with a history of rheumatic fever or recurrent strep throat 

33
Q

Streptococcus Pneumoniae - Low G/C - Gran +

A
  • causes 60-70% of all bacterial pneumonias
  • small, lancet shaped cells arranged in pairs and short chains
  • culture requires blood or chocolate agar and growth improved by 5-10% CO2
  • Lack catalase and peroxidases - cultures dies in O2
  • *main virulence factor is large capsules
  • 90 different capsular types have been identified
  • causes pneumonia and Ottis media
  • virulence factor: polysaccharide capsule (protein adhesion, mediates binding of cells to epithelial cells of pharynx), secretory IgA protease (destroys IgA), pneumolysin (lyses epithelial cells)
  • 5-50% of all people carry it as normal biota in the nasopharynx; infections are usually endogenous - very delicate, does not survive long outside of its habitat
  • pneumonia occurs when cells are aspirated into the lungs of susceptible individuals - young children, elderly, immune compromised, persons living in close quarters are predisposed to it
  • pneumococci multiply and induce an overwhelming inflammatory response
  • gains access to middle ear by way of Eustachian tube, causing Ottis media
34
Q

Treatment of pnemococcal infections

A
  • traditionally with penicillin G or V
  • increased drug resistance
  • two vaccines available
    1. Capsular antigen vaccine for older adults and other high risk people - effective for 5 years
    2. Conjugate vaccine for children 2-23 months
35
Q

Enterococcus faecalis - low G/C - Gram +

A
  • previously classified with group D streptococci
  • reclassified as separate genus
  • all enterococci live in intestinal tracts of animals
  • normal colonists of human large intestine
  • form short chains and pairs
  • found in human colon (rarely pathogenic here)
  • cause opportunistic urinary, wound, and skin infections, typically in debilitated persons
  • can cause disease if introduced to other parts: Trauma and surgury - surgeons need to use their nose
  • important cause of nosocomial infections
  • enterococcus grows with bile
36
Q

Treatment of enterococcus faecalis

A
  • difficult to treat
  • often resistant to antimicrobials like Vancomycin (VRE - vancomycin resistant enterococcus)
  • usually requires combined therapy
  • prevention is difficult in health care settings, patients often have weak immune systems, good hygiene and aseptic techniques minimize transmission
37
Q

Endosperm forming bascilli

A
  • bacillus and clostridium
  • endospore: dense survival unit that develops in a vegetative cell in response to nutrient deprivation
  • most endospoee forming bacteria are gram +, motile, rod-shaped
  • resistant to heat, drying, radiation, chemicals, factor for survival, longevity, ecological niche, pathogenicity or spore formers
38
Q

Bacillus - low G/C - Gram +

A
  • aerobic
  • catalase +
  • endospore forming, motile rods, mostly saprobic
  • versatile in degrading complex macromolecules
  • source of antibiotics
  • primary habitat is soil
  • two species
    1. Bacillus anthracis: causes anthrax
    2. Bacillus cereus: cause of one type of food poisonimhb
39
Q

Clostridium - low G/C - gram +

A
  • anaerobic
  • catalase -
  • 120 species with oval or spherical spores produced only under anaerobic conditions
  • synthesize organic acids, alcohols, and exotoxins
  • cause wound infections, tissue infections, and food intoxications
40
Q

Treatment for clostridium

A
  • vaccinate if available, degerm (immediate cleaning of dirty wounds, deep wounds, compound fractures, infected incisions
  • remove it by debridement of disease tissue, or flushing of alimentary canal and amputation of affected limb
  • kill it though large antibiotic doses and hyperbaric oxygen therapy in tissues
  • neutralize toxin by administering antitoxins (passive immunotherapy if available)
41
Q

Clostridium difficile

A
  • C-diff or CDI
  • Second most common intestinal disease after salmonellosis in industrialized countries
  • caused by clostridium difficile (a normal resident of intestine) in low numbers (diversity and balance)
  • produces enterotoxins that damage intestines
  • major cause of diarrhea in hospitals
  • increasingly common in community-acquired diarrhea
42
Q

Treatment and Prevention of C-diff

A
  • antibiotic associated colitis (relatively non-invasive; treatment with broad spectrum antibiotics kills the other bacteria, allowing C. Difficile to overgrow
  • mild cases respond to fluid and electrolyte replacement and withdrawal of antimicrobials
  • severe infections treated with oral vancomycin or metronidazole and replacement cultures
  • compromised barriers lead to secondary infections, like severe ulcerative colitis
43
Q

Listeria monocytogenes - low G/C - gram +

A
  • non-spore forming
  • ranging fro, coccobacili to long filaments
  • 1-4 flagella and lack capsules (intracellular motility from actin polymerization not flagella)
  • resistant to cold, heat, salt, pH extremes, and biel
  • virulence attributed to ability to replicate in the cytoplasm of the cells after inducing phagocytosis; avoids humoral immune system
  • primary reservoir in soil and and water; animal intestines
  • can contaminate foods and grow during refrigeration
  • Listeriosis: most cases associated with dairy products, poultry, and meal - 20% death rate
  • often mild or sub clinical in normal adults
  • immunocompromised patients (pregnancy), fetuses, and neonates; affects brain and meninges
44
Q

Mycobacterium - high G/C content - gram +

A
  • irregular bacilli - Pleomorphic
  • acid fast stain
  • strict aerobes
  • catalase +
  • do not form capsules, flagella, or spores
  • grows slowly
  • numerous pathogenic strains: M. Tuberculosis
45
Q

Mycobacterium Tuberculoses - high G/C - gram +

A
  • tubercle bacillus (long, thin rod that grows in Sinuous masses or strands called cords
  • produces no exotoxins or enzymes that contribute to infectious Ed’s
  • virulence factors: contain complex waxes and cord factor that prevent destruction in lysosomes or by macrophages
  • predisposing factors: inadequate nutrition, debilitation of the immune system, poor access to medical care, lung damage, and genetics
  • estimate 1/3rd of world population and 15 million in US carry tubercle bacillus; highest rate in US occurring in recent immigrants
  • bacillus very resistant; transmitted by airborne respiratory droplets
  • 5-10% of infected people develop clinical disease
  • untreated, the disease progresses slowly; majority of TB cases contained in lungs
  • clinical tuberculosis divided into: primary tuberculosis, secondary tuberculosis ( deactivation or reinfection)m disseminated (extra pulmonary) tuberculosis
46
Q

Primary TB

A
  • infectious dose is 10 cells
  • phagocytoses by alveolar macrophages and multiply intracellularly
  • after 3-4 weeks immune system attacks, forming tubercles, granulomas consisting of a central core containing bacilli surrounded by WBC - tubercles
  • if center of tubercle breaks down into necrotic, caseous lesions, they gradually heal by calcification
47
Q

Secondary TB - Latent & recurrent

A
  • if patient doesn’t recover from primary TB, reactivation of bacilli can occur
  • tubercles expand and drain into the bronchial tubes and upper respiratory tract
  • gradually, patient experiences more severe symptoms - violent coughing, greenish or bloody septum, fever, anorexia, weight loss, fatigue
  • untreated, 60% mortality rate
48
Q

Extra pulmonary TB

A
  • during the course of reactivated YB, bacilli disseminate to regional lymph nodes, kidneys, long bones, genitalia tract, brain, and meninges
  • these complications are grave
  • people that are immunosuppressed are particularly susceptible
49
Q

Detecting TB

A
  1. Tuberculin Sensitivity (immunologic testing, in vivo)
    - Mantoux test: local intrader,al injection of purified protein derivative (PPD); look for red wheal to form in 48-72 hours - induration; established guidelines to indicate interpretation of result based on size of wheal and specific population factors
  2. In vitro TB test: CDC gas accepted two new indirect methods based on blood tests - advantages of these - QuantiFERON TB Gold Test and T spot TB test
  3. Chest X-rays: non-diagnostic, used to rule out pulmonary TB - post + PPD
  4. Acid-fast staining: of Delhi, or other specimens - Ziehl/Neelsen stain and Fluorescence staining
  5. Cultural isolation and biochemical testing: provide the most accurate diagnosis - long time
50
Q

Managemnet and Prevention of TB

A
  • 6-24 months of at least 2 drugs from a list of 11
  • many strains of M. Tuberculosis are resistant to at least one of the drugs commonly used for treatment
  • the most common treatment begins with an initial phase of forum drugs: isoniazid (INH), rifampin (RIF), ethambutol (EMB), and pyrazinamide (PZA) - taken daily for 8 weeks
  • after this, a continuation phase involves daily doses of INH and RIF for 18 weeks
  • a one pill regimen called Rifater contains INH, RIF, and PZA - EMB can be supplemented if needed
  • MDR and XTR-TB becoming a major problem - vaccine based on attenuated “bacilli calmatteguerin” strain of M. Bonus is used in other countries no US

Microbiology (8 decks)

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