Microbiology Lecture 10 Review: Chapter 22, 23

Lecture Review

Chapter 22 - Skin Infections

1.    [22-01] Describe four types of lesions. Describe three types of skin diseases based on pathogen’s entry. Give example for each type – Lecture 10, Slide 10 –

Lesion = Any damage/change in the tissue of an organism, caused by disease/trauma. 4 types of Lesions

Vesicle: Less than 1 cm, fluid-filled lesion (Ex: Chicken pox)
Bulla:Over 1 cm, fluid-filled lesion (Ex: Bullous impetigo)
Pustule:Pus-filled lesion (Ex: Smallpox)
Macule:flat and reddened lesion (Ex: Rubella)

3 types of skin diseases

Exogenous: Pathogen enters via breaks in the integrity of the skin (Ex: Folliculitis, Impetigo, Necrotizing fasciitis).

Endogenous: Pathogen enters the skin from underlying tissue or carried by blood or lymph (Ex: viral infections – rashes caused by measles, varicella, rubella).

Toxin-induced: Pathogen infects place distant from skin, toxin produced is delivered to the skin (Ex: scalded skin syndrome, toxic shock syndrome).

2.    [22-02] Staphylococcal scalded skin syndrome (SSSS) – Describe signs and symptoms. Describe etiological agent – Lecture 10, Slide 17 –

Signs & Symptoms: Nose, mouth, genitalia tenderness → Skin becomes red and wrinkled (sandpaper like) → Large blisters with fluid appear everywhere on body

*** Characteristic Nikolsky’s sign = epidermis is detaching if skin slightly rubbed with finger.

Etiological agent: Staphylococcus aureus (strains that produce exfoliative toxin)
Gram +, grows in clusters, facultative halophilic, mannitol positive anaerobe, catalase +
Strain w/ exfoliative toxin that targets desmoglein I (desmosomes)

3.    [22-03] Staphylococcal scalded skin syndrome – Describe pathogenesis. Describe epidemiology – Lecture 10, Slide 18 –

Pathogenesis: Exfoliative toxin produced by S. aureus → toxin enters blood stream & is delivered to skin → toxin activity causes epidermis to split from dermis just below dead keratinized outer layer → Loss of epidermis causes infected to lose fluids and at risk for secondary infections (Pseudomonas aeruginosa).

Epidemiology: Contagious, Notifiable disease
Reservoir – Infected humans(w/ S. aureus strain containing exfoliative toxin)

Transmission – Direct OR indirect contacts

Number of cases reported – Usually isolated cases, some epidemics occur in nurseries

Mortality rate – 40%, if untreated → outcome depends on prompt treatment

4.     [22-04] Staphylococcal scalded skin syndrome – Describe prevention and treatment – Lecture 10, Slide 19 –

Prevention: No vaccine, quarantine of patient (reduces spread + decrease chance of 2^nd infection)

Treatment: Fluid replacement → Antibiotic treatment – semi-synthetic/modified penicillin (resistant to penicillases) AND/OR ß-lactam antibiotics w/ ß-lactamase inhibitors AND/OR clindamycin (lincomycin derivative w/ anti-exotoxin activity).

5.    [22-05] Lyme disease – Describe signs and symptoms. Describe etiological agent – Lecture 10, Slides 22, 23 –
Signs & symptoms: Early localized infection – Tick bite, erythema migrans (red bulls eye) → Early disseminated infection – 2-8 weeks post rash, flu-like symptoms, painful eye movement, enlargement of lymph nodes, fainting, irregular heart beat, enlargement of lymph nodes, paralysis of facial muscles, emotional instability, impaired concentration → Late persistent infection – 6months after rash, slowly disappears over years, arthritis of large joints, chronic nervous system impairment (nerve pain, numbness/tingling, short term memory, inflammation of brain/spinal cord, paralysis, depression)

Etiological agent: Borrelia burgdorferi – Microaerophilic spirochete, very large can reach up to 25µm in length, slow generation time 24-48 hours, diderm (double membrane), axillary filament (11 endoflagella → corkscrew movement), can growth w/o iron.

6.    [22-06] Lyme disease – Describe pathogenesis – Lecture 10, Slide 24 –
Pathogenesis: Tick bite, immune suppression with tick saliva → bacterial spread from original bite site, erythema migrans → spreads to blood stream and other parts of body → early signs & symptoms → later persistent infection b/c intense immune response →  development of autoimmune disease over time

7.    [22-07] Lyme disease – Describe epidemiology – Lecture 10, Slide 24 –

Epidemiology: Communicable, reportable zoonic disease.

Reservoir: White-footed mouse
Pathogen does NOT cross placenta.
Transmission – Tick bites infected mouse → bites human
Number of cases reported – Over 28,000 cases (2015) in all states except Montana, Oklahoma, and Hawaii.
Mortality rate – Rare cause of death, only 23 deaths attributed (2011 reuters)

8.    [22-08] Lyme disease – Describe prevention and treatment – Lecture 10, Slide 25 –
Prevention: Avoid tick infested areas (tall grass often have ticks), DEET repellents, Wear protective clothing (light colored clothing less likely to attract ticks), carefully inspect body (ticks take time to find appropriate place on body, remove w/o crushing).

Treatment: Antibiotics effective first stage only (doxycycline, amoxicillin), patients w/ neurological & cardiac conditions (advanced stage) may required IV ampicillin or ceftriaxone.
Antibiotics less effective in late 2^nd and 3^rd stage of disease.

9.    [22-09] Viral infections of skin – Compare Varicella (chickenpox), Rubeola (measles) and Rubella (German measles) by describing their signs and symptoms – Lecture 10, Slides 26, 27 –
Signs & symptoms: Varicella has incubation period up to 2 weeks. First red spots appear on head’s back then spread to rest of body → Spots turn to vesicular lesions that are mainly located on torso → Vesicles may turn pustules due to secondary bacterial infections. Lesions disappear in 1-2 weeks. Disease may be reactivated years after resulting in shingles (very painful rash around waist).  
Signs & symptoms: Measles begins with running nose, cough, red weepy eyes and fever → Macular rash appears first on forehead and then spread to rest of body. Highly specific Koplik spots resembling grain of salt appear on mucous membrane opposite to molars → Rash disappears in 1 week.
*Secondary infections caused by Gram-positive cocci are common.
Signs & symptoms: Rubella has incubation period up to 3 weeks and begins with slight fever and mild cold → Faint rosy macular rash appears on face, then spreads to rest of body → Lymph nodes behind ears and on neck become swollen → Rash disappears within 3 days.
*Small red papules develop on soft palate (Forchheimer’s sign) develop in 20% of the cases. Adults are likely to experience joint pain that can last for 3 weeks. The child will be born with congenital rubella syndrome if pregnant mother with no immunity will be exposed to Rubella.

10. [22-10] Viral infections of skin – Compare Varicella (chickenpox), Rubeola (measles) and Rubella (German measles) by describing their etiological agents – Lecture 10, Slide 28 –
Etiological agents:
Chickenpox is caused by varicella zoster virus. It is an enveloped virus whose genome is double-stranded linear DNA. The virus is related to herpes virus and can turn into provirus and, thus, can cause latent viral infection.
Measles is caused by rubeola virus – an enveloped virus whose genome is single-stranded linear “minus” RNA. One of the viral antigens, M antigen, forces the fusion of adjacent infected cells forming characteristic giant multinuclear cells that become visible as Koplik spots.
Rubella is caused by rubella virus – an enveloped virus whose genome is single-stranded linear “positive” RNA. It can not become provirus and is causing active viral infection only.

11. [22-11] Viral infections of skin – Compare Varicella (chickenpox), Rubeola (measles) and Rubella (German measles) by describing their pathogenesis – Lecture 10, Slides 29, 30, 31 –
Pathogenesis:
ALL three diseases at starting with infection of upper respiratory tract and replication of these viruses in epithelial cells → ALL three viruses enter circulatory system – blood (varicella and rubella viruses) and lymph (measles virus).

For varicella & rubella, starting infection occurs without signs and symptoms, while measles is forming Koplik spots in mucous membrane against molars (result of fusion of infected cells into giant multinuclear cells caused by M protein of measles virus).

Varicella-Zoster virus infects & replicates in epithelial cells of mucous membrane in respiratory system → replicating virus enters bloodstream → virus delivered to the skin is lysing the cells causing vesicular skin rush due to inflammation reaction → enters peripheral neurons causing latent viral infection → when immunity wanes, varicella virus re-activated causing shingles.
***Complications from secondary infections are common. Virus CAN cross placenta → causes congenital varicella syndrome.

Measles virus infects & replicates in epithelial cells of mucous membrane of upper respiratory system + mouth → Viral M protein causes Koplik spots → virus enters lymph and spreads → virus delivered to skin is causing inflammation reaction and development of macular skin rash that lasts for about 1 week.
***Complications from secondary infections are common.

Rubella virus infects & replicates in epithelial cells of mucous membrane of upper respiratory system → virus enters bloodstream causing sustained viremia (virus presence in blood, systemic) → Produced antibody forms complexes with rubella virus that are deposited in skin and joints leading to faint skin rush and joint pain that lasts for 3 days.
***If pregnant mother becomes infected, rubella virus is causing congenital rubella syndrome with severe birth defects.

12. [22-12] Viral infections of skin – Compare Varicella (chickenpox), Rubeola (measles) and Rubella (German measles) by describing their epidemiology – Lecture 10, Slide 32
*ALL contagious, notifiable, human reservoir, transmitted via respiratory droplets OR fomites

Epidemiology of Varicella: Contagious, notifiable
Reservoir – Humans
Transmission – Respiratory droplets, direct contact w/ skin lesions, fomites
Number of cases reported – From 1995-2008 varicella among infants decreased 90%.
Mortality rate – 30% possible liver and brain damage.

Epidemiology of Measles (Rubeola): Contagious, notifiable
Reservoir - Humans
Transmission – Respiratory droplets, and fomites
Number of cases reported – Present: 100,000 cases reported global annually, 2014 measles outbreak in California involving 200 people.
Mortality rate – Malnutrition + inadequate healthcare 10%, w/ complications 20-30%.

Epidemiology of Rubella (German measles): Contagious, notifiable
Reservoir - Humans
Transmission - Respiratory droplets, and fomites
Number of cases reported – 121,432 cases globally, 3 in US (2009)
Mortality rate – Very low, more serious concern is congenital defects during pregnancy.

13. [22-13] Viral infections of skin – Compare Varicella (chickenpox), Rubeola (measles) and Rubella (German measles) by describing their prevention and treatment – Lecture 10, Slide 33 –
ALL 3 can be prevented by MMRV vaccine (MMR + varicella zoster vaccine).
Prevention: MMRV vaccine

Treatment: NO treatment, antibiotics for preventing secondary infections only

Chapter 23 - Wound infections

14. [23-01] Tetanus – Describe signs and symptoms. Describe etiological agent Describe pathogenesis – Lecture 12, Slides 49, 50, 51 –

Signs & symptoms: Starts with difficulty swallowing, spasm of jaw muscles (Lock jaw) → develops into convulsions, difficulties breathing, risus sardonicus (rigid smile b/c spasm of facial muscles) → Severe cases – opisthotonus (rigid arched back b/c spasms of back muscles, can lead to regurgitation of stomach into respiratory system → pneumonia).

Etiological agent: Clostridium tetani – Gram +, obligate anaerobic bacillus, in anaerobic conditions forms terminal endospores.

Virulence factors – Tetanolysin (binds to cholesterol membranes to form pores to lyse cells), Tetanospasmin (A-B neurotoxin, A-part is zinc dependent protease that interrupts vesicle membrane transport between neurons, blocks release of GABA between inhibitory and motor neurons causing spasm/paralysis of muscles)

Pathogenesis: C. tetani enters via deep puncture/wound → grow under anaerobic conditions → microbe produces toxins (tetanolysin, tetanospasmin) → Generalized skeletal muscle spasm (paralysis) develops → 60% of cases cardiac failure, death

15. [23-02] Tetanus – describe epidemiology, prevention and treatment – Lecture 12, Slides 52, 53,  –
Epidemiology: Non-communicable, notifiable disease
Reservoir: Soil
Transmission – Deep wounds or unhealed umbilical stump
Number of Cases reported –9397 cases reported globally (2010), 50% neonatal tetanus.
Mortality rate – 60%experience cardiac failure

Prevention: TDaP vaccine (tetanus toxoid, diphtheria toxoid, acellular pertussis)

Treatment: Anti-toxin, tetanus immune globulin (TIG), used to neutralize tetanospasmin, and antimicrobial treatment given to kill vegetative bacteria.

16. [23-Additional_1] Pseudomonas aeruginosa infection – Describe signs and symptoms. Describe etiological agent and its virulence factors – Lecture 10, Slides 47,48 –
Signs & symptoms: Starts with skin lesions, chills, fever → change in tissue color (pseudomonas spp. Produce water-soluble pigments pyocyanin (blue) and pyocerdine (yellow) creating green color → shock (caused by bacteremia)

Etiological agent: Pseudomonas aeruginosa – Gram-negative facultative anaerobe, motile, bacillus of γ-proteobacteria

Virulence factors: Produces enzymes = collagenase (digesting collagen in human tissues) and elastase (digesting elastin in human tissues), multiple enzymes to break down various antibiotics.
Toxins = Exotoxin A (type III secretion system – stops protein synthesis), Exoenzyme S (most strains produce – interferes with phagocytosis + causes death of host cells), Phospholipase C (damages plasma membrane of host cells by digesting lecithin).
Biofilm formation.

17. [23-Additional_2] Pseudomonas aeruginosa infection – Describe pathogenesis – Lecture 10, Slide 48 –
Pseudomonas aeruginosa is causing secondary and nosocomial infections.
Continuous contact with human tissue causes inflammation reaction → produced enzymes (proteases) that cause additional damage and delay healing → some strains have toxins that increase virulence → COMPLICATION if bacteria enters bloodstream: Infections in heart, bone infection, kidney infections, septic shock

18. [23-Additional_2] Pseudomonas aeruginosa infection – Describe epidemiology – Lecture 10, Slide 48 –
Epidemiology: Communicable, notifiable disease (?)
Reservoir – Soil, water, Humans
Transmission – Direct contact and fomites
Number of cases reported – ubiquitous in nature, may enter hospitals (on soles of shoes, flowers, produce, or ornamental plants) ~51,000 cases/year (CDC).
Mortality rate – About 400 deaths/year (CDC).

19. [23-Additional_2] Pseudomonas aeruginosa infection – Describe prevention and treatment – Lecture 10, Slide 48 –
Prevention: Elimination of bacterial sources. Prompt wound care and treatment (removal of dead tissue from burns, application of antibacterial silver cream)

Treatment: Microbe is multi-drug resistant. Some antibiotics are still effective: ciprofloxacin, gentamicin, imipenem (ß-lactam class)