Principles and Types of Epidemiology

Principles and Tools of Epidemiology

• John Snow is known as the Father of Epidemiology (1813–1858)
• In 1854, Snow tracked a London cholera outbreak to water from a specific well
• The cholera outbreak ended by breaking the chain of transmission

Types of Epidemiology

• Descriptive epidemiology involves collecting data to track disease occurrence based on person, place, and time
• Analytical epidemiology uses surveillance data to form hypotheses about the cause and risk factors of a disease
• Analytical epidemiology includes observational, cohort, and case-control studies

Endemic, Epidemic, Pandemic

• Endemic, epidemic, and pandemic describe the number of disease cases observed in a specific region (place) over a time period
• A disease outbreak refers to an increase in the number of disease cases above the endemic level
• Local disease outbreaks can develop into an epidemic, when cases increase rapidly and the affected area widens
• Epidemics may occur if the disease reservoir increases or the infectious agent evolves to no longer need a reservoir
• Pandemics are out-of-control epidemics that spread across continents
• Bubonic plague, influenza, and COVID-19 are examples of pandemics

Disease Prevalence vs Incidence

• Prevalence tracks active cases of a disease in a population
• Incidence tracks new cases of a disease in a population
• Incidence rate = (number of new cases/population size) × 100
• Prevalence rate = (total number of active cases/population size) × 100
• For the entire month of March, at Happy Valley Rest Home (HVRH), 10 new cases of pneumococcal pneumonia occurred, a total of 23 cases were recorded out of 200 residents
• The incidence rate of pneumococcal pneumonia at HVRH in March = (10/200) × 100 = 5%
• The prevalence rate of pneumococcal pneumonia at HVRH in March = (23/200) × 100 = 11.5%

Health Care-Associated Infections

• Stephanie contracted a health care-associated infection (HAI)
• To identify the source of an HAI, determine if each patient is infected with an identical isolate, if staff contacted all patients, or if patients contacted the same supplies
• Additional steps to identify a source include: determine if affected patients contacted each other, test hospital surfaces for the organism, and check if standard infection control measures were maintained

Infection Control Measures

• Hand sanitation by using foam hand sanitizers upon entry to and exit from patient rooms
• Use of disposable paper gowns and latex gloves when entering the rooms of immunocompromised patients or patients with dangerous infectious diseases, such as MRSA
• Aseptic technique during procedures (e.g., inserting a catheter)

Global Disease Trends

• Methods to recognize global disease trends should be discussed
• The importance of finding the index case (patient zero) of an outbreak should be explained
• Online sources should be used to track worldwide disease trends
• Health organizations should be notified by local physicians
• Disease tracking during epidemics involves finding the index case and identifying all contacts
• Global surveillance may be limited because some countries lack modern labs and efficient case reporting or effective political means to recognize and limit infectious outbreaks
• Developing countries may lack resources for public health surveillance
• The CDC and WHO mobilize scientists and medical personnel when global health is threatened

Detecting Emerging Microbial Diseases

• COVID-19 is a global pandemic caused by SARS-CoV-2
• As of October 2020, COVID-19 had 32 million cases and 1 million deaths
• R number: the number of individuals potentially infected by one infected individual
• Global travel increases the spread of infectious diseases
• Air travel spreads influenza, Ebola, and Zika
• Blood banks spread HIV, hepatitis C, and Babesia
• Suburban sprawl causes a loss of habitat and species diversity, which spreads Lyme disease
• With global spread of HIV/AIDS, the increasing number of immunocompromised persons has allowed for reemergence of some infectious diseases once thought to be “under control.”
• Immunocompromised AIDS patients are highly susceptible to infection by many organisms, including Mycobacterium tuberculosis
• Drug-resistant strains have caused a reemergence of M. tuberculosis among non-AIDS patients

Bioterrorism and Biodefense

• Microorganisms can be used as bioweapons
• Biowarfare: aims to inflict massive casualties
• Bioterrorism: aims for few casualties but widespread psychological trauma
• Selected agents are highly virulent, contagious infectious agents that can’t be prevented by a protective vaccine, and are not treatable with pharmaceuticals

Vaccines and Immunizations

• Active immunization: involves an injection of antigen
• The goal of active immunization is to stimulate the immune system to produce antigen-specific antibodies and T cells
• Passive immunization: protective antibodies are administered
• Methods of passive immunization: injection of immunoglobulin, antitoxins, and breastfeeding
• Effective vaccines should not harm the person being vaccinated
• Effective vaccines should stimulate B-cell and T-cell responses, result in long-term memory, not require many boosters, and protect against the natural pathogen.
• Four basic types of vaccines: killed whole cells/inactivated viruses, live attenuated bacteria/viruses, purified components of an infectious agent, and DNA/RNA vaccines
• Killed vaccines use inactivated organisms, retaining antigenicity (ex: cholera and rabies)
• Live, attenuated vaccines use mutated bacteria/viruses that mimic infection and generate stronger immunity (ex: MMR)

Herd Immunity

• Herd immunity occurs when a large portion of the population is immunized
• Heard immunity is only possible for contagious diseases transmitted between humans
• Herd immunity varies by pathogen, but requires at least three-fourths of the population be immunized to reduce disease spread

Opposition to Vaccines

• The data surrounding vaccines are indisputable and millions of lives have been saved
• Vaccines are extremely safe, but allergic reactions can occur (rare)
• Vaccines have no link to autism or diabetes

Layers of the Skin and Microbiota

• Major layers of human skin: epidermis, dermis, and hypodermis
• Epidermis: outermost, relatively thin layer made of keratinocytes with an outer stratum corneum of dead cells to limit contact between the outside world and live tissues
• Desquamation is the shedding/peeling of skin
• Dermis: contains blood vessels, nerves, hair follicles, sebaceous glands (sebum), sudoriferous (sweat) glands
• Hypodermis: also called subcutaneous tissue or superficial fascia, connects skin to the underlying fascia of bones/muscles
• The skin is where normal microbiota consists of commensal organisms deriving nutrition from skin cells and secretions such as sweat and sebum
• Normal microbiota of skin tends to inhibit transient-microbes by producing antimicrobial substances
• Normal microbiota varies on different regions of the skin, especially in dry vs moist areas

Skin Rashes

• Skin rash: change in color/texture of the skin
• Exanthem: widespread skin rash with systemic symptoms (fever, malaise, headache)
• Enanthem: rash on mucous membranes
• Skin rashes can be caused by an infectious agent or a reaction to a toxin produced by the organism, or damage to the skin by the organism, and/or an immune response

Types of Skin Rashes

• Macular: flat and red, less than 1 cm in diameter
• Vesicular: small blisters are formed
• Papular: small, solid, and elevated
• Pustular: a papule filled with pus
• Maculopapular: a papule that is reddened

Skin Lesions

• Abscess: localized collection of pus
• Furuncle: (boil) pus-filled abscess due to infection of a hair follicle
• Ulcer: break in the skin; open sore
• Skin lesions: have numerous causes and may look similar

Viral Infections of the Skin

• Viruses That Produce Macular Rashes include Measles and German measles
• Viruses That Produce Papular and Pustular Rashes include Chicken pox, Cold sores and genital herpes, Warts, and Small Pox

Measles (Rubeola)

• Measles is a negative-sense, single-stranded RNA virus
• Measles is very contagious (8–10 day incubation period)
• Portal of entry is respiratory or conjunctiva
• Measles replicates in the lungs and moves to regional lymph nodes
• Viremia spreads measles throughout the body
• Measles prodromal period starts with cold/flu-like symptoms and High fever (40°C/104°F)
• Koplik’s spots (white spots on the buccal mucosa/inner cheeks) are a sign of measles
• Immunocompromised patients can develop Death, Blindness (ulceration of the cornea), Myocarditis or pericarditis, and a Variety of GI maladies

Serious Complications of Measles:

• Acute disseminated encephalomyelitis (ADEM) and subacute sclerosing panencephalitis (SSPE)
• German Measles (Rubella/Third Disease) was first described in the mid-eighteenth century by German physician and chemist, Friedrich Hoffmann
• In 1814, George de Maton suggested that it be considered a disease distinct from both measles and scarlet fever

German Measles (Rubella)

• German measles is also called 3-day measles and has a rash similar to measles
• German measles was eliminated from the United States in 2004
• German measles is acquired by inhalation of aerosolized respiratory particles replicates in the cytoplasm of cells lining the nasopharynx, and is spread to nearby lymph nodes
• Viremia ensues during the 12–23-day incubation period
• Characterized by a pinpoint maculopapular pink rash that spreads fast from on head the body and extremities, is immune-related, and does not darken or scab
• German measles has Short duration of 1–3 days, Low-grade fever, Enlargement of head and neck lymph nodes, and is Mild, subclinical, and self-limiting
• German measles is more difficult in adults and can lead to joint pain and/or Bacterial superinfections

Chicken Pox and Shingles

• Can cause birth defects
• Chickenpox is in the Herpesviridae family from the Varicella-Zoster virus (VZV)
• The initial exposure equals chickenpox, and Shingles occurs more frequently in older individuals as Cell-mediated immunity decreases
• Chickenpox and shingles can be diagnosed clinically, but antibody and DNA tests can also be used
• Chickenpox is contracted via Inhalation of infected particles from skin lesions with Virus replicates in the nasopharynx and infects the regional lymph nodes, leading to viremia
• The second round of viral replication takes place in the liver and spleen followed by a secondary viremia 14–16 days postinfection
• VZV invades capillary endothelial cells and the deepest layer of the epidermis which Produces fluid accumulation and vesicle formation
• Children do not usually have prodromal symptoms and first come down with itchy rash on the face, back, chest, and belly that becomes maculopapules, vesicles, pustules, and scabs

Chickenpox: Latency

• Latency occurs, and Chickenpox Can be life-threatening in immunocompromised patients as Chickenpox Is established when viral DNA integrates into host DNA
• VZV Virus remains latent in the dorsal root ganglia, and Re-emerges later in life in about 20% of patients, which causes shingles

Chickenpox

• Virus infects the nerve endings of the skin and Travel along nerves to ganglia where they lie in a dormant state leading to Latent virus reactivation
• Latent virus reactivation causes Virus particles travel along the sensory nerves of the skin to produce a localized, painful, dermatomal rash known as shingles
• Chickenpox treatment involves anti itch medication and pain medication
• Acyclovir is used to treat shingles in only severe or complicated cases
• Varicella vaccination contains live attenuated VZV and is part of the childhood routine immunization schedule
• Persons 60 years and older receive zoster vaccine to prevent shingles

Cold Sores and Genital Herpes

• Cold sores is caused by herpes simplex viruses 1 and 2 (HSV-1 and HSV-2)
• Cold sores Infects skin and mucous membranes including the central nervous system and occasionally the visceral organs
• Cold sores are Transmitted by direct contact and replicates in mucosal surfaces or epidermis
• Cold Sore The final destination is the neuronal cell in the ganglia where the virus becomes latent at Primary infection
• Cold Sore Infections: may be subclinical or symptomatic while Reactivation always results in symptoms
• Severity and recurrence of infection with the Cold Sore Virus is dictated by the immune status of the person infected.
• Fever blisters/ herpes labialis
• Herpes Labialis is Primarily caused by HSV-1 virus which leads to virus being Contagious and Is present in the active or latent form in 60‒90% of older adults
• There is No vaccine against HSV-1 so virus is Spread from person to person by contact which can lead to: Fever, sore throat, muscle aches, and cervical lymphadenopathy, with vesicular lesions, lasting up to 2 weeks

Herpes

• Some patients experience prodromal symptoms such as pain, tingling, or burning before an outbreak
• Vesicles commonly form at the outer border of the lips
• The Virus is present in lesions and can infect other parts of the body where the skin is disrupted
• In children and some health care professionals, abrasions of skin of fingers result in herpetic whitlow
• Rugby players and wrestlers get outbreaks of HSV-1 on the neck, face, and arm called herpes gladiatorum
• HSV-1 can set up a chronic infection that involves deeper parts of the skin in immunocompromised patients and cause Herpetic keratitis
• Cold Sore treatment: Acyclovir, valacyclovir, and famciclovir can be used during primary infections to Reduce pain and duration of lesions and Decrease viral shedding and Reactivation can be treated with a topical antiviral
• HSV-2 causes primarily genital herpes, which is a Sexually transmitted disease
• Tissue distribution of HSV-1/2 is not absolute but HSV-1 can infect the genital skin and mucosa and for HSV-2 infects the oral tissue

Warts

• Warts are caused by human papilloma virus (HPV) of the family Papillomaviridae through contact and Enters cell via an endosome by a receptor-mediated mechanism
• HPV DNA leaves the endosome, enters the nucleus and Virals proteins interfere with cell cell proliferation controls
• The Infected cell replicates uncontrollably, producing warts may be removed through freezing, burning, and surgical removal or treated with vaccines
• HPV-6/11 infect mucous membranes of the ano-genital region and cause 90% of genital warts (condyloma acuminata)

Smallpox

• Smallpox is caused by HPV as the only known reservoir in humans but the agent has been Eradicated from population in 1979
• The Small Pox comes from the Poxviridae family and is divided into two variants: Variola major and Variola minor and Small Pox Is Transmitted by direct or indirect contact
• A person who inhales small aerosolized particles or handles fomites containing the virus can contract Small Pox
• Small Pox has sequential viremias which infect the lymph nodes, lymphoid organs, bone marrow manifesting as Small pox spots on the oral mucosa (enanthem) and Smallpox pustules on the skin (exanthem)
• Smalls Pox has No FDA approved treatments so patients do not get it and but Government officials have stockpiled vaccine in strategic centers

Staphylococcal Skin Infections

• Staphylococcal skin infections may be from Staphylococcus epidermidis and or Staphylococcus aureus
• Staphylococcus aureus is a Normal inhabitant of the nares (nose) that Can infect a cut and gain access to dermis via hair follicle and/or lead to diseases

Exotoxins

• S. aureus possesses enzymes that contribute to disease such as coagulase, exfoliative toxin, and Toxic shock syndrome toxin (TSST)
• Coagulase Coats the bacteria with fibrin and walls off infection from the immune system and antibiotics, promoting abscess formation
• Staph infections routinely require surgical drainage and antibiotic therapy/ Exotoxins damage host tissue and weaken host defense
• Toxic shock syndrome toxin leads superantigen causes toxic shock syndrome and Exfoliative toxin leads to superantigen cause a blistering condition in children called scalded-skin syndrome

Staphylococcal Infections Continued

• A S. aureus infection of hair follicles can be superficial or deep and cause Folliculitis/Carbuncles and MRSA
• MRSA is a Methicillin-resistant S. aureus Strain that has emerged over the past decade that is Resistant to the antibiotic methicillin by Interfering with cell wall synthesis which have now evolved to resist methicillin (~60%)
• Treatment choice is Vancomycin which has gone from First appeared as nosocomial infections to been today being no longer confined to the hospital and existing as "community acquired infections”
• Impetigo is caused by S. aureus and group A strep and includes Bullous and Nonbullous types Impentigo:
• Nonbullous: Starts as a superficial bump and becomes a papule and vesicle that forms the characteristic pustules on erythematous skin and becomes weepy
• Bullous: Vesicles grow larger and become bullae that are full of clear yellow fluid

Streptococcal Skin Infections

• Caused by Streptococcus pyogenes whic hUses the human nasopharynx and parts of the skin as it's natural reservoir
• Necrotizing fasciitis is also known as flesh-eating disease and as Type 1 (polymicrobial) and Type 2 (1 microorganism) and is treated in general with clindamycin, metronidazole, and gentamicin
• An increase in the use of NSAIDs increases and accentuates a persons susceptibility to S. pyogenes and Necrotizing fasciitis

S. Pyogenes Virulence factors

• Capsule: inhibits phagocytosis
• Pilus-like M protein: binds complement regulatory protein (factor H)
• Lipoteichoic acid: facilitates adherence to host cells
• Streptolysins: lyse blood cells
• Enzymes that Degrade DNA (DNAses), fibrin (streptokinase), and connective tissu and Peptiglycan makes pus less viscous
• Exotoxins: Streptococcal pyogenic exotoxins (SPEs) superantigens massive amounts of cytokines released that leads to scarlet fever, streptococcal toxic shock syndrome, and necrotizing fasciitis

Other Bacterial Infections

• Rheumatic fever can develop after the resolution of a primary GAS infection
• Sequela: result of immunological cross reactivity between specific GAS protein antigens and the host
• Autoreactive B cells activated by the bacterial M protein antigen create antibodies against cardiac antigen and damages those tissues
• Erysipelas: acute infection caused by S. pyogenes that leads to small erythematous patch that becomes a fiery-red shiny plaque
• Erysipelas can also involve is upper layer of dermis spreads to the superficial lymphatics and include symptoms like swollen lymph nodes, fever, and systemic symptoms
• Erysipelas rash can be found face but is most commonly seen on the lower extremities and present as butterfly appearance
• Cellulitis an uncomplicated non-necrotizing inflammation of the dermis related to acute infections that is localized, characterized by localized pain, swelling, tenderness, erythema, and warmth
• acne bacteria

Acne

• Acne vulgaris: Affects 60–70% of Americans 20% having severe acne
• Results from blocked hair follicles/pores called comedones that
• Factors the contribute: genetic, hormonal or gram + Propionibacterium acnes (feeds on triglycerides) P. acnes that binds to macrophages causes inflmmation

Fungal Skin Infections

• Includes molds and yeasts Eukaryotic microbes Filamentous or single

The Dermatophytes “love” skin. •Cool, moist, keratinized tissues (skin, hair follicles, nails) •Epidermophyton, Trichophyton, and Microsporum cause infections based on body location: Tinea capitis (scalp) Tinea corporis (body) Tinea cruris (jock itch) Tinea pedis (foot) Tinea unguium (nails)

• Tinea versicolor = a Chronic infection mostly located in the warm climates

• Pathogenesis: round yeast converts to hyphal (damage to melanocytes)

• Candida includes Dimorphic yeasts Which normally reside in GT vag tract in certain times infections are prone Candida

More Fungal Infections

• More located Candida affects where skin touches (underarms ,fingers: intertrigo Fungal skin infections are: •Clinical appearance •Microscopic examination of potassium hydroxide (KOH) preparations of , so it can be viewed through a microscope

More Treatments

•Antifungal medications used to treat these diseases. •Imidazole compounds like clotrimazole are common and purchased

Deep Tissue Special Circumstances

Skin is primary layer against infection and is compromised,

• Burns cover 10 % body = serious infection Burns = affect and alter the immune system T- cells

• Cell structures: staphyylococci and then colonized

• Microbes: from paient, GI , respiratory, hospital Cullulitis, necrosis , even

Methane resistant

Candida = high risk peseudo

Q:

• Endotoxins
• Dry + wetgangrene Gangree Clostricium
• Conjuctivitis The body may have a reaction