Inflammation and Infection

Objectives

• Identify and describe cellular adaptive changes, etiological factors that cause maladaptive changes and describe cardinal signs of inflammation

• Describe the phases of the inflammatory process, mediators, and cells involved in the reaction

• Identify laboratory tests that are involved in the diagnosis of inflammation and infection

• Distinguish between the stages of wound healing and identify factors that affect the process of wound healing

• Describe infectious disease processes and identify common bacteria and viruses that produce disease

• Differentiate between innate, adaptive, humoral, and cell-mediated immune responses to infection

• Identify clinical presentation of HIV, define laboratory tests involved in diagnosis, and mechanisms that help treat and prevent HIV

Human Immunodeficiency Virus

HIV is a retrovirus and is a slow and progressive disease

Two strains:

• HIV-1 - Most commonly seen in the US

  • Transits more easily than 2 and progresses more rapidly into AIDS

• HIV-2 - Limited to west africa

Transmission routes:

• Blood

• Semen

• Vaginal fluids

• Transplacenta

• Breast fluids

• Saliva (into open mouth wounds)

• Can also get in through cuts or needles

• The HIV has to get into the bloodstream through a mucous membranes

  • EX: Anus, vagina, mouth, tip of dih

Pathophysiology:

• Attacks CD4 cells and macrophages

  • Hallmark sign: progressive depletion of CD4 T-Cells

• CD4 cells are involved in both humoral and cell-mediated immune reactions

• HIV slowly debilitates body immune systems, both T cells and B cell immunity

• Macrophages act as a reservoir for the virus

  • This allows the virus to go undetected

  • Also helps disseminates/spreads the virus

  • Macrophages are found at mucous membranes

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Enzymes are what allow the virus to spread and occur

• HIV attaches to the CD4 receptor cell

• Reverse transcriptase changes viral RNA into viral DNA

• Integrase allows viral DNA to be in integrated into host DNA

• Protease helps assemble protein component to build new viruses

• Host becomes a factory for manufacturing new viruses

• Virus then destroys the host (CD4 cell) after using it, weakening immune response

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Risk Factors

Unprotected sex

• Heterosexual females more at risk than heterosexual males

• Men who have sex with men

  • Most at risk

  • Receptive partner is at higher risk than insertive partner

IV drug abusers or anyone who frequently inserts needles into themselves

African American Males

Hispanic Males

History of STDs

Offspring of infected mothers

Stages of HIV

Acute Phase:

• Highly infectious stage since the virus is multiplying rapidly

• Present flu-like symptoms, similar to mononucleosis

  • Fever, headache, fatigue, swelling of lymph nodes (lymphadenopathy), pharyngitis, muscle pain (myalgia)

• Occurs within 28 days of contracting the virus

• Lasts a couple of weeks and then resolves. Virus then goes dormant in CD4 cells and patient becomes asymptomatic

  • This period of dormancy is what makes HIV difficult to treat. Symptoms are also usually disregarded since pt goes asymptomatic after a few weeks

Chronic phase:

• This is known as the latent stage

• Can last from 6 months to 10 years

• Symptoms can be:

  • Coughing

  • shortness of breath

  • weight loss

  • diarrhea

  • Fatigue

• Viral load is slowly increasing while CD4 count continues to decrease

AIDS:

• Acquired Immune Deficiency Syndrome

• CD4 count diminishes to 200 or less

• Symptoms:

  • Rapid weight loss

  • Recurring fever or profuse night sweats

  • Red rash that doesn’t itch, usually on torso

  • Prolonged swelling of the lymph glands in the armpits, groin, or neck

Complications:

• Kaposi sarcoma - cancer cells found in the skin and/or mucous membrane that line the GI tract from mouth to anus

• Pneumocystis jiroveci Pneumonia (PJP) - Fungal infection of the lungs

• Other opportunistic infections due to immune deficiency

Lab Studies and Diagnostics:

Screening of HIV is highly recommended

• Those exposed are recommended to get tested every year

• HIV RNA blood test (done 1st)

  • Checks presence of virus in the bloodstream

  • Virus is detectable 4-11 days after infection

  • <10,000 = low risk for AIDS

  • >10,000 = high risk for AIDS

• Presence of HIV antibodies:

  • It can take 2 weeks and 6 months for immune system to make antibodies

• CD4 count is used to monitor the course of the disease - most accurate measurement of immune system impairment

  • Normal CD4 count: 800-1,200 cells/mm3

  • Impaired: below 500 cells/mm3

  • If it drops below 200 cells/mm3 and there’s an opportunistic infection, the diagnosis of AIDS is made

Treatment and Management of HIV:

• Treatment can be challenging:

  • Latency of the disease

    • Pts do not seek treatment until infected by opportunistic disease which is late enough that their immune system is compromised

  • Immunocompromised

  • Highly mutable virus

• Antiretroviral Therapy (ART) - only long term successful treatment

  • Medication works by attacking the virus at various stages

  • EX: Protease inhibitor, transcriptase inhibitor, integrase inhibitor, fusion inhibitor

• Treatment need to be started as soon as possible

• Pt can live a long life if complaint with medication

Preventative treatment:

• PREP - pre-exposure prophylaxis

  • uses antiviral medications in highly susceptible, uninfected individuals

  • Used when one partner is HIV positive and the other is not

  • Must take the medication everyday and pts should still use protection

  • Follow up w/ healthcare provider every 3 months

  • Significantly decreases chances of contracting HIV by 92%

• PEP - Post-exposure prophylaxis

  • uses antiviral medication after a single high-risk event to prevent contraction of HIV

  • Must be started within 72 hours to be effective

  • Includes a 28-course of triple ART

  • Only to be used in emergency situations

Complications:

• Opportunistic infections → usually the cause of death of the pt

  • Tuberculosis

  • Candida (thrush)

  • PJP

  • Toxoplasmosis

  • Histoplasmosis

  • Hep A, B, C

• Malignancies

  • Kaposi sarcoma

  • Non-Hodgkin’s lymphoma

  • Cervical cancer

  • Anal cancer

Immune System Function

Innate:

• First line of defense

• Natural mechanisms

• Acts quicker, but not specific

Adaptive:

• Occurs after innate

• More specific defense

• Uses memory for specific antigens - creates antibodies

• Does not react as quickly as innate, but lasts longer

Goal:

• recognize self from nonself

• recognize and target specific antigen

• limit response

• create antibodies (memory) for future exposures

Memory response allows it to act quicker in future exposures

Driven by lymphocytes that originate in bone marrow

• these lymphocytes cannot initiate immunity until mature

2 types:

• Humoral - B lymphocytes

• Cell-mediated - T lymphocytes

Humoral:

• B - cell immunity

  • Plasma cells

  • Memory B cells

• Mature in the bone marrow, spleen, and lymph nodes

• Protects against extracellular pathogens

  • Pathogens that multiply outside of the host cells like the skin, mucous membranes, etc

Immunity is developed by B cell lymphocytes producing antibodies

B cells are immature until they meet a pathogen. After exposure to a pathogen, they mature into plasma cells which create the antibodies/immunoglobulins (Igs)

Antibodies:

• IgG, IgA, IgE, IgM, IgD

• specifically recognize and bind to particular antigens

Support is provided by helper T cells to help promote/escalate immune response

Cell-mediated:

• T cell immunity

• Mature in the thymus gland → found in the bloodstream and lymph nodes

• Protects against intracellular pathogens

  • things wrong inside the body/cells

  • Cancer, infected cells, transplant tissues, etc

This is the immune response without the use of antibodies

• Uses macrophages, t-lymphocytes, and cytotoxic cells for a direct approach at pathogen destruction

When an antigen is captured by antigen presenting cell (APC), such as macrophages or dendritic cells, it’s processed inside the cell before presenting the antigen to t cells. The t cells activates cytotoxic t cells to destroy the cell alongside the virus.

Passive V. Active Immunity:

Active Acquired:

• Obtained through exposure of the antigen or through immunization (vaccine)

• The pt’s body has to synthesize the specific immunoglobulin against the antigen

• Endows longer term immunity

Passive Acquired:

• Premanufactured immunoglobulins are given or passed down

• Body passively accepts immunoglobulins and the body does not have to manufacture them

• Short term immunity

• Administered when pt needs immunity NOW

Immunizations and Boosters:

• A vaccine is a weakened and inactivated virus

• Cannot cause disease, genes for the disease has been removed

• Body builds specific Igs against it when given

• Sometimes more than one dose needed

Booster:

• repeated vaccine administered some time after the initial vaccine in order to remind the body to create antibodies for it

Antibody titer:

• Antibody screening tests, referred to antibody titers, confirm adequate immune protection by measuring IgM and IgG immunoglobulin

• If pt has negative titer = no antibody in immune system

  • has not been exposed to disease

  • never developed immunity

  • need vaccination/booster

Immunity, Inflammation, and Infectious Disorders

Homeostasis

• Body needs to maintain itself at a relative constant composition

• When cells have challenges, stress, or injuries, they must:

  • adapt with compensatory changes → positive changes

  • Develop maladaptive changes → negative changes

• Can result in cell death or injury if it’s too damaging

Atrophy:

• results in needing less resources and energy

• Results from:

  • disuse or diminished workload

  • lack of nerve stimulation (paralysis)

  • loss of hormonal stimulation

  • inadequate nutrition

  • Decreased blood flow (ischemia)

  • Aging

Hypertrophy:

• Require more energy/resources

• increase in individual cell size that result in the enlargement of functioning tissue mass

• EX: hypertrophy of the heart due to increased workload from hypertension

Hyperplasia:

• Driven by hormones or compensatory

• Increased mitotic activity resulting in increased number of cells → increased tissue or organ mass

• EX: driven by hormones → increased breast tissue due to pregnancy and its demand for breast milk, causing hyperplasia of breast milk glands and tissue mass

• EX: compensatory → scars or keloids

Metaplasia:

• Cells replaced by another cell

• Results from chronic inflammation

• cell genetics reprogramming in response to environmental conditions

  • EX: GERD causing chronic inflammation in esophagus, causing the cells to change from normal squamous epithelial cells to columnar like cells

Dysplasia:

• Deranged cellular growth

• A change in size, shape, or order

• Often caused by precancerous conditions or chronic inflammation

• Will often develop into neoplasia

• Can be acquired or born with

Neoplasia:

• Uncontrolled new growth

• Usually disorganized and lack normal cell function

• Usually cancerous, causing tumors that are either benign or malignant

• Can break away

• Neoplasm = tumor

Causes of cellular injury/damage:

• Hypoxic cells = oxygen deprivation

• Free radicals = oxidative stress → unpaired electrons

• Physical agents = shearing against endothelium in HTN

• Chemical - high glucose causing glycosylation of endothelium

• Infectious agents

• Injurious immunoglobulin reactions - allergic reactions

• Genetic defects

• Nutritional imbalances

Apoptosis:

• Programmed cell death

• can be genetically programmed or triggered by injury

  • injury: cancer

  • genetic: ovaries undergo apoptosis after age 55

• Cells that fail to undergo apoptosis can cause cancer, tumors, and detrimental hyperplastic cell changes

• Necrosis - uncontrolled cell death

  • cells can burst and explode onto other cells which can stress them out, causing a cycle

Inflammation and the Inflammatory Response

• Protective, coordinated response of the agent to injurious agents

• Acute or chronic

• “itis”

• Aims of inflammation:

  • Wall off or isolate the pathogen

  • Minimize damage or spread

  • Activate immune response

Cardinal Signs:

• Rubor (redness) - blood flow to the area

• Tumor (swelling) - caused by interstitial fluids

• Calor (heat) - caused from the increased blood flow to the site

• Dolor (pain) - nerve involvement. histamine, prostaglandin stimulate nerves which signal pain

• Loss of function

3 Stages of Acute:

• Vascular permeability → Vessels open up to allow WBCs, platelets, etc., to enter and exit the sire

  • Blood vessels dilate at the site of the injury due to inflammatory mediators that are released during injury

  • Permeability permits:

    • WBCs and platelets to enter the site

    • fluid to travel out of the blood vessels and into the site which causes the swelling

• Cellular chemotaxis → chemicals are released by WBCs to signal for more help and activate immune system

  • Cytokines are inflammatory mediators that are released by WBCs to amplify or deactivate inflammation

  • Acute Phase Proteins are released to the liver under the direction of the cytokines

    • Influence the process by stimulating, modulating, and deactivating the reactions

  • Cytokine signals the liver that it needs helps, causing the liver to release the acute phase proteins

  • Acute phase proteins can be measured to show presence of inflammation (inflammatory markers)

• Systemic responses → Cardinal signs

  • Can cause fevers, pain, general malaise, lymphadenopathy, anorexia, sleepiness, lathergy, anemia, weight loss, etc

  • Systemic response caused by the inflammatory mediators released by the WBCs

Clinical Manifestations: Fever

• Protective mechanisms

• Pyrogens → substances that cause fevers

  • EX: microbial organisms, bacterial products, cytokines

• Pyrogens activate prostaglandins to reset hypothalamic temperature - regulation center in the brain to higher level

• Recommend to keep fevers below 102º to prevent seizures and brain damage

  • Use antipyretic medication that inhibit prostaglandin formation, thus decreasing fever

Reye’s Syndrome

• Caused by the use of aspirin in those 18 and younger after vital illness

• Affects liver and neurological symptoms

• causes:

  • nausea and vomiting

  • changes in mental status

  • weakness

  • vision and hearing changes

  • agitation/seizures

• Treatment: supportive measures

  • No cure → brain has swelled

Assessment of the Immune System:

• CBC via venipuncture

• Examines amount leukocytes and other white blood cells

• Normal range = 4,000 - 10,000 cells/ml

  • Leukocytes = less than 4,000 cells/ml → not enough

  • Leukocytosis = greater than 10,000 cells/ml → typically seen in infections

    • Typically between 15,000-20,000 during infections

  • Leukemoid = greater than 50,000 cells/ml → Too much WBC, seen in leukemia

Types of WBCS:

Granulocytes - give immediate immunity and created in the bone marrow. Released as needed. Has vesicles

• Neutrophils

  • First responders (within 24-48 hours)

  • die within 12 hr and become pus 

  • Most abundant (80%) 

  • Destroy pathogens

  • Immature neutrophils = bands

• Eosinophils

  • Seen in allergies or parasitic infections

  • 1-5%

• Basophils

  • less than 2%

  • in inflammatory 

  • filled w/ histamine

Agranulocytes - long term immunity. Uses memory to fight pathogens. Has no vesicles 

• Monocytes (macrophages)

  • Go into tissue and eat pathogens

  • Comes later than neutrophils

  • Activated after 24-48 hours

  • Longer lifespan, weeks to months

• Lymphocytes

  • B & T cells

  • create the antibodies from infections and vaccines

Interpreting CBC:

• ratio of neutrophils, lymphocytes, monocytes, Eosinophils, Basophils have to equal 100

Wound Healing

Divided into multiple phases:

• Hemostasis - stop bleeding

• Inflammation

• Proliferation, granulation tissue formation, and epithelialization - rebuilding, new cells are created

• Wound contraction and remodeling - scar tissue created. Blood vessels regrow if damaged 

Could last 1-2 months depending on depth of injury

Factors that affect wound healing:

• Nutrition - take in enough protein

• Oxygenation

• Circulation - needs good blood flow

• Immune strength

• Diabetes - weakens healing

• use of corticosteroids, diminishes healing

• Use of immunosuppressants agents

• Contamination

• Surgically inserted devices

• Obesity - heavier you are, the harder to heal

• Age - the older you are, the harder to heal 

Nurse’s role in wound healing:

• Keep area clean and change dressing

• Lab values - albumin, pre-albumin → check these protein levels

• Tight glycerin control → avoid high blood glucose levels

• Nutrition - encourage high protein diet and supplementation of zinc and vitamin c which is good for healing skin 

• Ambulation - to increase circulation and perfusion

• Turning bed bound patients every 2 hours

• Off loading weight - prevent ulcers

• Heat can delay healing

Complications of Wound Healing:

• Keloid - hyperplasia of scar tissue

  • African American are more at risk 

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• Evisceration - opening of wound with extrusion of tissue and organs

• Contractures - inflexible shrinkage of wound tissue that pulls the edges toward the center of the wound 

  • Makes it difficult to move area of injury

• Dehiscence - opening of a wound’s suture line

  • Seen post surgery

• Stricture - an abnormal narrowing of a tubular body passage from the formation of scar tissue 

• Adhesions - internal scar tissue between tissues and organs

• Fistula - an abnormal connection between two epithelium-lined organs or vessels

  • Most commonly seen in genitals

Infectious Diseases

Normal Flora vs. Pathogens

• Normal flora do not cause diseases. Can aid in protecting against pathogens. 

• Only becomes an issue when they travel to areas they’re not supposed to be in

  • EX: E.coli in the urethra/bladder

Opportunistic vs. Nosocomial

Opportunistic infection - caused by pathogen or microorganism that flourishes due to host’s compromised immune system

Nosocomial infection - Caused by microorganisms inherent to the health-care facility environment; hospital acquired infection

• difficult to treat because they are often caused by antibiotic resistant bacteria

• Commonly caused by Staph a.

Portals of entry:

• Skin

• Respiratory tract

• GI tract - vomiting or stool

• GU tract - urine

• Blood-blood transmission

• Maternal-Fetal Transmission

Pathogens often exit the body of the host the same way they entered it

5 Stages of Infection:

• Incubation 

  • Host is asymptomatic but highly contagious

  • beginning active replication

• Prodromal Stage

  • Immune response start

  • Initial appearance of symptoms, but vague such as malaise, headache, fatigue

  • Highly contagious

• Acute stage

  • Peak replication; immune system is fighting back full force

  • experiences fill infectious disease with rapid proliferation of pathogen

  • Symptoms are heightened; still contagious

• Convalescent Stage

  • body’s attempt to rid of the pathogen

  • Resolution of symptoms begin

• Resolution Stage

  • Total elimination of the pathogen; no signs or symptoms

  • No longer contagious

Infection can still cause permanent damage even after resolution stage

Lab Tests:

• CBC with differential

• Gram stain - used for bacteria

• Culture - used for urine, stool, sputum, wound

• Biopsy

• Antibody titer 

• Polymerase chain reaction (PCR) - detects genetic material

Immunizations:

• Vaccines are the most effective form of prevention for contagious diseases

• Stimulates the immune system by injecting a weakened version of the disease with genetic material removed, causing it to create antibodies against that disease.

• Takes about 30 days for the body to create the antibodies from vaccines

  • Usually life long immunity

Staphylococcus

• Found on the skin, nares, vagina, oropharynx

• results in cellulitis

• Can cause endocarditis in IV drug users

• resistant to antibiotics:

  • MRSA - Methicillin resistant staphylococcus

  • VRSA - Vancomycin resistant staphylococcus 

  • Some bacteria develop ability to secrete beta lactamase enzyme

• spread through contact, resistant to a lot of medications

Streptococcus

• Release endotoxin causing rash and fever

• Have capsules that prevent phagocytosis 

• Spread by contact and respiratory droplets

• Causes:

  • streptococcal pharyngitis

  • scarlet fever

  • rheumatic fever

  • glomerulonephritis

  • necrotizing fasciitis 

  • toxic shock syndrome

• S. pneumoniae - common community acquired pneumonia → can cause meningitis

• S. faecalis - source of UTI, nosocomial and endocarditis

Meningitis

• Inflammation of the meningeal layers that surround brain and spinal cord

• Can be bacterial or viral:

  • S. pneumoniae/N.meningitides/H. influenza 

  • Bacteria worse than viral → less likely to die to viral

• Signs and symptoms:

  • Kernig’s sign: Extending leg causes pain to neck and leg

  • Brudzinski sign: pt flexes knee and hip when you flex neck

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• Lumbar puncture is the diagnostic tool

• Complications: seizures, hearing and vision loss, brain damage, ischemia of extremities

• Vaccines: H. influenza, meningococcal, pneumococcal

• Spread via contact/droplets

Diphtheria

• Corynebacterium diphtheriae

• Infects the mucous membranes of the respiratory tract

• Causes sore throat, fever, tonsillar, excaudate, and inflammation that can obstruct the airway

Pertussis

• Bordetella Pertussis (whooping cough)

• Infects the upper respiratory tract by airborne droplets and direct contact with throat or nasal fluids

• Binds to ciliated cells and causes forceful coughing with an audible whoop

Tetanus

• Clostridium tetani

• Infection occurs after bacteria enter penetrating wound such as a puncture wound or laceration

• C. Tetani toxin blocks inhibitory neurotransmitters causing muscles spasms (tetany), particularly in the masseter muscles (lock jaw)

Tdap vaccinations should be done every 10 years

Clostridium Difficile

• C. Diff

• found in soil, water, gut, stool

• a spore forming, toxin secreting anaerobic bacteria

  • Emits toxins that disrupts the intestinal mucosa and erode the epithelial cells → destroys colon

• Forms pseudomembranes that contain necrotic tissue, WBC, and mucus in intestines

• Symptoms:

  • Watery, bloody diarrhea (10-15/day)

  • Abdominal pain/cramping

  • Dehydration

  • Fever

  • Weight loss

  • BP goes up while HR goes down

• Predisposing factor is long term antibiotic use, older age, and low immunity

• Source of nosocomial infection

• Alcohol based sanitizer is not effective against the spores → need hot water and soap

• Diagnosis: stool testing

Influenza

• Major strains: A (most severe), B, and C

• Invades upper then moves to lower respiratory tract

• Occurs through droplet infection and aerosols generated by coughs and sneezes of individuals

• Clinical manifestations:

  • Chills, fever, headache, malaise, cough, sore throat

• Treatment: supportive care

  • Amantadine, Rimantadine, Zanamivir, and Oseltamivir are antiviral medications that can be used to shorten the course of the disease

  • Typically resolves in 7 days

• Prevention:

  • Influenza vaccine is recommended annually for all persons older than age 6 months

Epstein Barr Virus (EBV)

• Infectious mononucleosis or kissing disease

• Spread through spit or sexual contact

• Infects B lymphocytes in the tonsil area

  • Infects the cells of the orthopharynx → invades the bloodstream → inciets an immune response that causes proliferation of B lymphocytes within lymphoid tissue, resulting in lymphadenopathy

• Clinical manifestations:

  • Pharyngitis, fatigue, headache, fever, chills, abdominal pain, nausea, and vomiting are usually presenting symptoms

  • Pharyngitis is often the most prominent sign with tonsillar enlargement and exudate

• Diagnostic: test for antibodies against the virus → titer

• Disease can spread to liver or spleen

• Potential complication: Splenomegaly

  • Avoid strenuous activities or contact sports for at least 3 weeks or until the spleen returns to normal size

Measles

• Spread with coughing/droplets

  • Incubation period: 7-14 days

  • Prodromal stage: 4-7 days

• Active on surfaces for up to two hours

• Clinical manifestations: high fever, cough, upper respiratory illness, conjunctivitis with periorbital edema and photophobia 

• Hallmark sign: Unique white areas in the oral buccal mucosa called Koplik spots

  • After, the characteristic tiny, maculopapular, mildly pruritic rash appears on the body → starts on the face and travels down to feet, fades after 5-7 days

• Diagnostic: Specific measles IgM and IgG immunoglobulin can be found in the blood

• Treatments: supportive measures such as rest, fluids, and isolation from others

Mumps

• Transmission: Direct contact and/or respiratory droplets

  • Incubation: 14-25 days

  • Prodromal: 3-5 days

• Symptoms: Inflammation of the parotid salivary gland, sore throat, fever, joint pain

  • Loves the parotid gland, causes swelling

• Males can develop orchitis (swelling of the genitals), can lead to sterility

• Diagnostic: mump specific IgG and PCR testing of virus

• Typically lasts 5 days; supportive care

• Vaccination administered at 12-15 months and 4-6 yo

Rubella:

• Transmission: respiratory droplets; salivary, direct contact

  • Incubation: 14-19 days

• Most contagious when rash is erupting and are non contagious after 7 days of rash

  • Starts on face and travels down

• Symptoms: fever, sore throat, and rhinitis, Forchheimer spots (1st sign seen in soft palate), which are pinpoint red macules, and petechiae over the soft palate and the uvula

• Diagnostic: Specific IgM and IgG immunoglobulin and PCR testing

• Treatment: supportive care

• Immune issues are seen later on when recovered from as children

Varicella Zoster (chickenpox)

• Mostly impacts children

  • Mainly 8 and under

• Transmission: droplet inhalation or contact

  • Incubation: 10-21 days

• Traid: rash, malaise, and low grade fever are signs

• Characteristic chickenpox vesicle is described as a “dewdrop on a rose petal”

• first appears on upper body: scalp, face, trunk, and proximal limbs

• Rapid progression over 12-14 hours to papules, clear vesicles, and pustules, with subsequent central umbilication and crust and scab formation

• Diagnostic: PCR testing of skin lesions

• Treatment: supportive measures, antipyretic, hydration, oatmeal baths, and antihistamines

• Vaccination is recommended

Herpes Zoster (Shingles)

• A reactivation of the varicella roster virus that remains dormant in the sensory spinal neurons

• Can re-emerge due to immunosuppression/cancer or stress

• usually along a dermatome (one side)

• Symptoms:

  • painful, fluid filled vesicles (protect these), skin sensitivity, tingling, burning, itching

• Treatment: acyclovir (medication) can lessen severity

• Prevention: immunization 50 years or older

Herpes Simplex Virus (HSV), HSV-1 and HSV-2

• HSV-1 is the common cold herpes, affecting the mouth but can still affect the genitals

  • Spread through saliva

• HSV-2 is the genital herpes infection, but can also affect the mouth

  • Spread through sexual contact

• Can cause acute and latent infection

  • Acute infection - abrupt onset of vesicular lesions within the epidermis and mucous membranes. The fluid-filled vesicles contain active viral particles

• Acute phase ceases and is followed by a period of dormancy when the virus is inactive

• Herpes viral DNA remains dormant within the neurons and evades immune destruction

  • Once you have it, you always have it

• Reactivation of HSV occurs during times of stress, illness, or immunosuppression

• Acyclovir - antiviral medication can help lessen severity

• Creates vesicles with fluid

  • These vesicles or lesions have to be present to spread it

Fungal infections

• Mild to severe infections

• reproduce through spores in the air

• Affect those with weakened immune system (HIV/AIDS patients)

• Hard to treat

Candida Albicans

• Most common fungal infection

• Part of normal flora of the gastrointestinal and vaginal tracts - in mouth, skin, etc

  • Becomes pathogenic when overgrowth occurs

• Weakened immune system can develop widespread dissemination of Candida within the body, which can then progress to overwhelming sepsis

• Risk factors: antibiotic use, diabetes, HIV, steroids, oral contraceptives

  • fungus loves sugar → high blood sugar can help it thrive

• Treatment: antifungal medication (EX: Nystatin)

• Presents as:

  • Thrush - mouth

  • Esophageal infection

  • Vulvovaginitis - in vagina

  • Balanitis - head of penis

Malaria

• Caused by plasmodium, a parasite that lives in anopheles mosquito

• Mosquito bites human → plasmodium enters body and red blood cells → plasmodium degrades RBC by poking holes in red blood cells → degradation of RBCs cause hemoglobin to be released 

  • Accumulation of bilirubin from hemoglobin breakdown results in jaundice

  • Deformation of the RBCs causes obstruction of small blood vessels and accumulate within the spleen

• Clinical manifestation: fever, chills, headache, myalgia, nausea, vomiting, and orthostatic hypertension are common

• Treatment: Chloroquine (medication), there is some resistance

• Prevention: Mefloquine is a prophylactic med that can be taken if travel is planned