Microbial Diseases of the Skin: Staphylococcus and Streptococcus

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Microbial Diseases of the SkinStaphylococcus
and Streptococcus
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Skin

• Portals of entry
• Hair follicles
• Sweat ducts
• Sebum ducts
• Parenteral route

Figure 21.1
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Staphylococcal Skin Infections

• For clinical purposes coagulase-positive v.
  negative
• Correlation between coagulase expression and
  toxin production
• S. epidermidis
• Gram-positive cocci, coagulase-negative
• Up to 90 of normal skin microbiota
• Only pathogenic when skin barrier is broken
• Staphylococcus aureus
• Gram-positive cocci, coagulase-positive
• Most pathogenic of the staphylococci
• Various toxins, depending upon infecting strain

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Staphylococcal Skin Infections

• Common route of entry skin (hair follicles)
• Folliculitis Infection of the hair follicle
  (often occurs as pimples)
• Eyelash folliculitis Sty
• Folliculitis can progress to an abscess (boil)
• Abscess pus surrounded by inflamed tissue
• Boil can progress to a carbuncle
• Inflammation of tissue under the skin
• Always some risk of bacteria entering the
  bloodstream and producing toxins?sepsis

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Staphylococcal Skin Infections
Sites of infection and diseases caused by
Staphylococcus aureus
http//textbookofbacteriology.net
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Streptococcal Skin Infections

• Cause wide range of diseases
• Skin infections are usually localized, but can
  reach deeper tissue
• Group A streptococci (GAS) Streptococcus
  pyogenes
• Beta-hemolytic streptococci
• One of the most common human pathogens
• Carriers harbor GAS on skin and
  throat tissues

http//phil.cdc.gov
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Streptococcal Skin Infections

• Streptococcus pyogenes M protein
• Escape phagocytosis
• Helps cells adhere to mucous membranes

Figure 21.5
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http//www.gsbs.utmb.edu/microbook/ch013.htm
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Streptococcal Skin InfectionsS. pyogenes

• Impetigo
• Infection of epidermis
• Pustules rupture and crust over
• Erysipelas
• Infection of dermis
• Red, inflamed patches from local tissue
  destruction
• Sepsis if infection spreads to bloodstream

Figure 21.6, 7
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Streptococcal Skin InfectionsInvasive Group A
Streptococcal Infections

• Invasive GAS (Flesh-eating bacteria)
• Necrotizing fasciitis
• Rare
• Destruction of muscle, fat, skin tissue
• Exotoxin A, superantigen
• Streptococcal toxic shock syndrome
• Immune system contributes to damage
• Mortality 40

Figure 21.8
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Microbial Diseases of the Nervous System
Prions
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Infections of the Nervous SystemPrions

• Prions Infectious proteins
• Transmissible spongiform encephalopathies
• PrPC, normal cellular prion protein, on cell
  surface
• PrPSc, scrapie protein, accumulate in brain cells
  forming plaques or aggregates

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Prions

• Creutzfeldt-Jakob disease (humans)
• Spongiform encephalopathy

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Prions
PrPSc
PrPc
PrPSc acquired or produced.
PrPSc interacts with PrPC at the cell surface.
PrPC is converted to PrPSc.
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3
4
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PrPC expressed at cell surface.
Lysosome
Endosome
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6
7
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New PrPSc converts more PrPC to PrPSc. (chain
reaction)
PrPSc is endocytosed.
PrPSc accumulates inside cell
Figure 13.21
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Diseases of the Nervous SystemTransmissible
Spongiform Encephalopathies

• TSEs caused by prions
• Sheep scrapie
• Bovine spongiform encephalopathy (Mad cow
  disease)
• Chronic wasting disease
• Creutzfeldt-Jakob disease, Kuru, Fatal familial
  insomnia
• Prion infection from ingestion, transplant or
  inheritance
• Spongiform degeneration of brain
• Rapidly progressive dementia at end-stages
• Chronic, fatal

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Diseases of the Nervous SystemTransmissible
Spongiform Encephalopathies

• Incubation times measured in years/decades
• Slowly progressive
• No inflammation
• Extremely rare

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Microbial Diseases of the Cardiovascular
SystemAnthrax
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The Cardiovascular System

• BloodTransports nutrients to and wastes from
  cells throughout our bodies
• Problem it can also transport pathogens!

Figure 23.1
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Microbial diseases of the bloodAnthrax

• Bacillus anthracis, gram-positive,
  endospore-forming aerobic rod
• Found in specific soil types
• Endospores can last up to 60 years
• Primarily strikes grazing animals
• Ingested with grass?fatal sepsis
• Cattle are routinely vaccinated
• Three forms cutaneous, gastrointestinal,
  inhalational

http//textbookofbacteriology.net
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Microbial diseases of the bloodAnthrax

• Severity of infection depends on portal of entry
• Cutaneous anthrax
• Endospores enter through minor cut, dont usually
  enter bloodstream
• Low-grade fever and malaise
• 20 mortality (without Abx)
• lt1 mortality with Abx
• Gastrointestinal anthrax
• Ingestion of undercooked food contaminated with
  endospores
• Ulcerative lesions along GI tract
• 50 mortality

Figure 23.7
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Microbial diseases of the bloodAnthrax

• Inhalational anthrax
• Inhalation of endospores
• Up to 60 days before germination
• Initially cough, mild fever, mild chest pain, so
  typically no Abx given
• 100 mortality
• High probability of
  entering bloodstream ?
  septic shock

http//www.arches.uga.edu/f150ga/
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Microbial diseases of the bloodAnthrax

• Infection begins when macrophages engulf
  endospores
• Endospores germinate inside of macrophages
• Bacteria multiply, eventually kill macrophages
• Release of bacteria into bloodstream?
  replication and toxin production
• Toxins cause edema and target/kill macrophages,
  effectively disabling defenses
• Capsule doesnt initiate a protective immune
  response
• Septic shock is often the cause of death

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Microbial Diseases of the Respiratory
SystemTuberculosis
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Lower Respiratory System

• Ciliary escalator keeps the lower respiratory
  system sterile

Figure 24.2
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Microbial Diseases of the Lower Respiratory
SystemTuberculosis

• Mycobacterium tuberculosis
• Acid-fast rod
• Obligate aerobe
• Generation time gt 20 hr
• Transmitted from human to human
• Airborne droplets reach alveoli
• Bacilli are usually phagocytized and killed by
  macrophages

Figure 24.9
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Microbial Diseases of the Lower Respiratory
SystemTuberculosis
Some bacilli may survive inside macrophages
More macrophages are recruited -ineffective at
killing -walled-off lesion (tubercle)
Figure 24.10.1
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Microbial Diseases of the Lower Respiratory
SystemTuberculosis
Weeks later, many macrophages die -release
bacilli into center of tubercle -bacilli do not
grow well here -may heal (calcified
lesions) -may become dormant infection
Figure 24.10.2
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Microbial Diseases of the Lower Respiratory
SystemTuberculosis
Air-filled cavity may form in mature
tubercle -active growth of bacilli
Cavity grows and may rupture, releasing bacilli
into bronchiole -disseminated throughout
lungs, blood and lymphatics ?TB infection in
other tissues
Figure 24.10.3
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Microbial Diseases of the Lower Respiratory
SystemTuberculosis

• Diagnosis Tuberculin skin test screening
• current or previous infection (or
  vaccination)
• Followed by X-ray or CT, acid-fast staining of
  sputum, culturing bacteria

Acid-fast bacillus (AFB) smear (sputum)
Figure 24.11
www.cdc.gov
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Microbial Diseases of the Lower Respiratory
SystemTuberculosis

• Vaccination recommended only for children at high
  risk
• Treatment of TB Prolonged multiple antibiotic
  therapy
• Prolonged nature?patients less likely to complete
  prescribed regimen?emergence of multi-drug
  resistant TB (MDR-TB)
• Also XDR-TB (Extensively drug resistant TB)

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Microbial Diseases of the Digestive
SystemDental Caries, Food poisoning and
Helicobacter
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Normal Microbiota of the Digestive System

• gt300 species in mouth
• Large intestine 100 billion bacteria/gram feces
• 40 fecal mass is microbial cell material
• Assist in polysaccharide breakdown, some
  synthesize vitamins
• Mostly anaerobes and facultative anaerobes
• Bacteriodes, E. coli, Enterobacter, Klebsiella,
  Proteus

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Bacterial Diseases of the Upper Digestive System
Dental Caries
Figure 25.3b
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Dental Plaques CariesPolymicrobial Infections
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Dental plaque diversity
Prescotts Principles of Microbiology
www.gaba.com
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Bacterial Diseases of the Upper Digestive System
Dental Caries
Figure 25.4
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Bacterial Diseases of the Lower Digestive System

• Symptoms usually include diarrhea,
  gastroenteritis, dysentery
• Often with abdominal cramps, nausea and vomiting
• Dysentery severe diarrhea with blood or mucus
• Treated with fluid and electrolyte replacement
• Infection pathogen enters GI tract and
  multiplies
• Incubation from 12 hr to 2 wk
• Time for colonization, growth and toxin
  production
• Typically fever evolves
• Intoxication ingestion of preformed toxin
• Symptoms appear 1-48 hr after ingestion
• No colonization is necessary

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Staphylococcal Food Poisoning

• Staphylococcus aureus one of the most common
  causes
• Onset of food poisoning symptoms 1-6 hours after
  ingestion of contaminated food
• Intoxication
• S. aureus is tolerant of high osmotic pressure
  and low moisture
• Somewhat resistant to heat
• Most competitors are eliminated (cooking, osmotic
  pressure)
• Multiplies on food, releasing enterotoxin as it
  grows
• Enterotoxin type A Superantigen exotoxin
• Survives up to 30 minutes of boiling!
• Triggers vomiting reflex cramps and diarrhea
  follow
• Recovery within 24 hours

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Staphylococcal Food Poisoning

• S. aureus is present on skin, in nasal secretions
• Contaminated hands
• Best prevention strategy adequate refrigeration

Figure 25.6
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Escherichia coli Gastroenteritis

• Sources contaminated, undercooked meat raw
  vegetables
• Pathogenic E. coli strains fimbriae for
  attachment and toxins that cause GI disturbance
  (gastroenteritis)
• Low infective dose lt100 bacteria
• Attach to intestinal mucosa and release toxin
  into lumen
• Infection

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Escherichia coli Gastroenteritis

• Enterohemorrhagic E. coli (EHEC) produce Shiga
  toxin
• 50 of feedlot cattle may have enterohemorrhagic
  strains in their intestines (asymptomatic)
• E. coli O157H7 serotype most common
  cause of outbreaks in US
• O cell wall antigen
• H flagellar antigen
• Severe cases (6) severe colon inflammation
  with bleeding (hemorrhagic colitis)
• Can progress to affect kidneys (hemolytic uremic
  syndrome)

www.sciencenews.org
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Helicobacter Peptic ulcer disease

• Helicobacter pylori
• Cause of majority (70-95) of peptic ulcer
  disease cases
• Not identified until 1983
• B. Marshall and Kochs Postulates
• 40 of adults harbor H. pylori
• Only 1-15 develop ulcers
• Neutralizes stomach acids so it can thrive
  (urease)
• Causes a drop in protective gastric mucus
  production

Figure 11.11
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Helicobacter Peptic ulcer disease
Figure 25.13
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Helicobacter Peptic ulcer disease
www.helico.com

• H. pylori increases risk of stomach cancers
• 70-90 of stomach cancers are associated with
  chronic H. pylori infections

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Microbial Diseases of the Urinary SystemCystitis
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Normal Microbiota of the Urinary System

• Urinary bladder and upper urinary tract sterile
• gt1,000 bacteria/ml or 100 coliforms/ml of urine
  indicates urinary tract infection

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Urinary Organs
Valves to prevent backflow from bladder (shields
kidneys from infections)
Figure 26.1
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Diseases of the Urinary SystemCystitis
Pyelonephritis

• Cystitis infection of the urinary bladder
• Difficult, painful urination (dysuria)
• Presence of white blood cells in urine (pyuria)
• Eight times more common in females vs. males
• Shorter urethra thats closer to anal opening
• Often caused by E. coli
• Antibiotic-sensitivity tests may be required
  before treatment
• 25 untreated cases lead to pyelonephritis
• Inflammation of one/both kidneys
• If chronic, scar tissue develops, impairs kidney
  function
• 75 due to E. coli