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Microbial Diseases of the
Skin:
Staphylococcus and
Streptococcus
Skin
• Portals of entry:
─ Hair follicles
─ Sweat ducts
─ Sebum ducts
• Parenteral route
Figure 21.1
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
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
Staphylococcal Skin Infections
Sites of infection and diseases caused by Staphylococcus aureus
http://textbookofbacteriology.net
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
Streptococcal Skin Infections
• Streptococcus pyogenes:
M protein
─ Escape phagocytosis
─ Helps cells adhere to
mucous membranes
Figure 21.5
http://www.gsbs.utmb.edu/microbook/ch013.htm
Streptococcal Skin Infections
S. 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
Streptococcal Skin Infections
Invasive 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
Microbial Diseases of the Nervous
System:
Prions
Infections of the Nervous System:
Prions
• 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
Prions
• Creutzfeldt-Jakob disease (humans)
─ Spongiform encephalopathy
Prions
PrPSc
PrPc
1 PrPC expressed at
cell surface.
2 PrPSc acquired or
produced.
3 PrPSc interacts
PrPC
with
at the
cell surface.
4 PrPC is converted
to PrPSc.
Lysosome
Endosome
5
New PrPSc
converts more
PrPC to PrPSc.
(chain reaction)
6 PrPSc is
endocytosed.
7 PrPSc
8
accumulates
inside cell
Figure 13.21
Diseases of the Nervous System:
Transmissible 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
Diseases of the Nervous System:
Transmissible Spongiform Encephalopathies
• Incubation times measured in years/decades
• Slowly progressive
─ No inflammation
• Extremely rare
Microbial Diseases of the
Cardiovascular System:
Anthrax
The Cardiovascular System
• Blood—Transports
nutrients to and wastes
from cells throughout our
bodies
─ Problem: it can also
transport pathogens!
Figure 23.1
Microbial diseases of the blood:
Anthrax
• 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
http://textbookofbacteriology.net
• Three forms: cutaneous, gastrointestinal, inhalational
Microbial diseases of the blood:
Anthrax
• Severity of infection depends on portal of entry
─ Cutaneous anthrax
◦ Endospores enter through minor cut, don’t
usually enter bloodstream
◦ Low-grade fever and malaise
◦ 20% mortality (without Abx)
−<1% mortality with Abx
─ Gastrointestinal anthrax
◦ Ingestion of undercooked food contaminated
with endospores
◦ Ulcerative lesions along GI tract
◦ 50% mortality
Figure 23.7
Microbial diseases of the blood:
• Inhalational anthrax
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/
Microbial diseases of the blood:
Anthrax
• 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 doesn’t initiate a protective immune response
─ Septic shock is often the cause of death
Microbial Diseases of the
Respiratory System:
Tuberculosis
Lower Respiratory System
• Ciliary escalator keeps the lower respiratory system
sterile
Figure 24.2
Microbial Diseases of the Lower Respiratory System:
Tuberculosis
• Mycobacterium tuberculosis
─ Acid-fast rod
─ Obligate aerobe
─ Generation time: > 20 hr
• Transmitted from human to
human
─ Airborne droplets reach
alveoli
◦ Bacilli are usually
phagocytized and killed
by macrophages
Figure 24.9
Microbial Diseases of the Lower Respiratory System:
Tuberculosis
Some bacilli may
survive inside
macrophages
More macrophages
are recruited…
-ineffective at killing
-walled-off lesion
(tubercle)
Figure 24.10.1
Microbial Diseases of the Lower Respiratory System:
Tuberculosis
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
Microbial Diseases of the Lower Respiratory System:
Tuberculosis
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
Microbial Diseases of the Lower Respiratory System:
Tuberculosis
• Diagnosis: Tuberculin skin test screening
─ + = current or previous infection (or vaccination)
─ Followed by X-ray or CT, acid-fast staining of sputum,
culturing bacteria
Figure 24.11
Acid-fast bacillus (AFB) smear
(sputum)
www.cdc.gov
Microbial Diseases of the Lower Respiratory System:
Tuberculosis
• 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)
Microbial Diseases of the
Digestive System:
Dental Caries, Food poisoning
and Helicobacter
Normal Microbiota
of the Digestive System
• >300 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
Bacterial Diseases of the Upper Digestive System:
Dental Caries
Figure 25.3b
Dental Plaques & Caries:
Polymicrobial Infections
Dental plaque diversity
Prescott’s Principles of Microbiology
www.gaba.com
Bacterial Diseases of the Upper Digestive System:
Dental Caries
Figure 25.4
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
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
Staphylococcal Food Poisoning
• S. aureus is present on
skin, in nasal secretions
─ Contaminated hands
• Best prevention strategy:
adequate refrigeration
Figure 25.6
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: <100 bacteria
• Attach to intestinal mucosa and release toxin into
lumen
─ Infection
Escherichia coli Gastroenteritis
• Enterohemorrhagic E. coli (EHEC): produce Shiga toxin
─ ~50% of feedlot cattle may have enterohemorrhagic
strains in their intestines (asymptomatic)
─ E. coli O157:H7 serotype most common
cause of outbreaks in US
◦ O = cell wall antigen
◦ H = flagellar antigen
www.sciencenews.org
─ Severe cases (~6%): severe colon inflammation with
bleeding (hemorrhagic colitis)
◦ Can progress to affect kidneys (hemolytic uremic
syndrome)
Helicobacter
Peptic ulcer disease
• Helicobacter pylori
─ Cause of majority (70-95%) of
peptic ulcer disease cases
◦ Not identified until ~1983
◦ B. Marshall and Koch’s 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
Helicobacter Peptic ulcer disease
Figure 25.13
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
Microbial Diseases of the Urinary
System:
Cystitis
Normal Microbiota of the Urinary
System
• Urinary bladder and upper urinary tract sterile
─ >1,000 bacteria/ml or 100 coliforms/ml of urine
indicates urinary tract infection
Urinary Organs
Valves to
prevent backflow
from bladder
(shields kidneys
from infections)
Figure 26.1
Diseases of the Urinary System:
Cystitis & 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 that’s 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