Malaria

The Role of International Agencies in Conquering Malaria

Merozoite Surface Protein 1 Protects Aotus Monkeys Against Malaria

Immuno-epidemiology of malaria

Modeling vaccination strategies for developing countries

Vaccine Development and Recommendations

Malaria in Pregnancy

VACCINES: TECHNOLOGY TRANSFER TO THE DEVELOPING WORLD

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Infection

Infection

General points: A general listing of different viral diseases that affect different organs of the body.
Viruses infect specific Organisms Tissues. Effects can range from Unnoticeable Deadly

Routes of viral entry

Respiratory tract diseases
Virus induced respiratory infections kill about 1 million children each year as well as a significant number of older adults.

* Many of the viruses that infect only the respiratory tract do not induce a strong immune response and hence reinfection with the same or a similar strain is common.
* Children get about 6 colds a year and adults get 2-3 per year.
* Deaths from respiratory infections: approx. 4.4 x 106/yr for Bact. and viruses world wide.
* Influenza- 20,000 deaths/yr in US during epidemic years (most years), Spanish flu of 1918, 500,000 in US 20 x 106 worlwide, Hong Kong outbreak 68-69, 34,000 in US.
* Human Respiratory Syncytial Virus- 4,500 deaths/yr (children) in US.

Respiratory tract diseases
* Rhinitis (Common Cold)-watery nasal discharge and obstruction, sneezing, mild sore throat and coughing but little or no fever. Infection based in upper respiratory. Sometimes complicated by superinfection with bacteria.

* Pharyngitis (most are viral)-sore throat, malaise, fever, sometimes cough. Infection based in pharynx. Can be caused by many of the same agents that cause common colds. RSV and adenovirus are prominent causes in young children and Herpes type viruses in young adults.

* Laryngotracheobronchitis (Croup)-fever, barking or metallic cough, respiratory distress, sometimes complete laryngeal obstruction. Most common causes are influenza and parainfluenza virus.

Respiratory tract diseases

* Bronchiolitis-Rapid and labored breathing, persistent cough, wheezing, cyanosis, variable amount of atelectasis, marked emphysema. Major causes are Influenza, parainfluenza, and RSV especially in young children. RSV can develop virtually overnight causing SIDS in young children.

* Pneumonia-often develops following upper resp. tract infection. Febrile, some cough, degree of dyspnea, wheezing, moist rales. X-rays often show only scattered areas of consolidation and diffuse lesions unlike pronounced lesions and consolidated areas in bacterial pneumonia. RSV, Influenza, parainfluenza, adenoviruses are major causes. A major cause of death to older people and young children. RSV is the major respiratory pathogen in young children and kills 4,500 children a year in the U.S. alone.

Viral Gastroenteritis

* Inflammation of the stomach and intestines
* Usually manifested as diarrhea which is watery but not bloody in the case of viral infection.
* Fever and Vomiting common with some infectious agents.
* Diarrheal diseases kill 3 million children each year mostly in developing countries.
* Rotaviruses are the main culprits and are responsible for most of the deaths.
* Astroviruses and Caliciviruses (Norwalk virus) can also cause diarrhea.

Central Nervous system diseases
* Most result as rare complication of primary infections elsewhere in the body.
* Viruses may be
o neuroinvasive (able to enter the nervous system) and/or
o neurovirulent (cause nerve damage).
o e.g. Mumps is highly neuroinvasive but not very neurovirulent while herpes is just the opposite.
* Viruses cause disease in a variety of ways
o infection of a specific area (Ammon's horn with rabies, and temporal lobes with HSV)
o Broad infection.
* Some lyse neurons while some cause demyelination of axons.

Central Nervous system diseases
* Deaths - Measles which can cause a variety of brain infections kills about 1 million/yr worldwide, mostly in area without vaccination.

* Meningitis-Infection of meningeal cells. Viruses are major cause but viral infection is much less severe than bacterial with full recovery likely. Headache, Fever, and neck stiffness with/or without vomiting and photophobia are symptoms. Mumps and Enteroviruses are most common agents.

* Paralysis-Mostly from poliovirus in countries where the virus has not been eradicated. Poliomyelitis involving demyelination of nerve cells.

* Encephalitis-Fever, headache, neck stiffness, vomiting, alterations in state of consciousness indicating involvement of brain parenchymal tissue. Patient is lethargic and confused and seizures, or paralysis may develop before coma and death. Postinfectious Encephalitis- Occurs a few days after infection of children with measles, mumps, or varicella. Severe demyelination is observed and prognosis is grim.

Central Nervous system diseases
* Guillain-Barre syndrome- Demyelination is common finding. Most frequently caused by EBV infection and appearing 1-4 weeks after mononucleosis infection. Most recover completely but 15% have residual nerve damage.

* Reye's syndrome - Cerebral edema without inflammation is common symptom. 25% of cases are fatal. Follow influenza or chickenpox infection in children and seems to be an association between syndrome and aspirin administration.

* AIDS Dementia Complex - Results from destruction of nerve cells often late in AIDS syndrome. Direct destruction of nerve cells and demyelination are involved.

Skin Rashes
* Macular-Flat colored spots;
* Papular-Slightly raised containing no expressible fluid;
* Vesicles-blister with clear fluid from which virus can be isolated;
* Pustular- Blisters containing puss;
* Nodular- Generally warts.

Hemorrhagic fever
* A variety of diseases that share the common feature of widespread hemorrhages from the bodies epithelial tissue including internal mucosa such as the gastrointestinal tract and the skin.
* A variety of internal damage is often associated with the different diseases.
* Hanta virus for example causes severe renal necrosis.
* Other agents (Ebola and Yellow fever virus) cause severe liver damage.
* Many have high fatality rates.

Genitourinary infections
* Herpes simplex virus 2 and Papillomaviruses are the major viruses infecting the genital area.
* Sexual transmission is the main way of acquiring the agent.
* Herpes manifests as painful itchy ulcerated vesicular lesions occasionally accompanied by fever and malaise especially in woman. Spread to the central nervous system occurs in 10% of cases with mild meningitis resulting. Recurrences are common although generally less severe than the initial infection.
* Papillomaviruses: Genital warts. Warts appear as external condyloma and usually disappear without treatment within a couple of years. Certain types of HPV may progress over several years through stages of cervical intraepithelial neoplasia (CIN) to invasive squamous cell carcinoma.
* HIV: Deaths by HIV-about 1 million/yr worldwide, 20,000/yr in US although was much higher before triple drug therapy

Eye diseases
* A number of common childhood viral diseases can involve conjunctivitis
o Inflammation of the conjunctiva which is the transparent membrane covering the sclera i.e. white of the eye and the inner eyelid).
o Results in redness, discomfort and discharge and is commonly called pink eye. Some types are particularly dangerous, especially those involving the cornea (keratoconjunctivitis).
* HSV is the commonest infectious agent that causes blindness in the Western world.
* A number of eye diseases, e.g. cataracts, glaucoma, and retinopathy are associated with congenital rubella syndrome and cytomegalic inclusion disease of infants.

Viral arthritis
* Stiff and painful joints.
* Usually accompanied by fever and myositis (inflammation of muscle tissue causing pain tenderness and weakness)
* Can occur with or without rash.
* Rarely persists for more than a few weeks.
* Major causative agents are certain toga-, flavi-, and bunyaviruses (arboviruses).
* It has been hypothesized that rheumatoid arthritis may have a viral origin.

Viral Carditis
* Myocarditis = inflammation of the heart muscle
* Pericarditis = inflammation of pericardium membrane that encloses he heart
* Cardiomyopathy = diseases causing reduction in the force of the heart
* Associated with certain enteroviruses (family of picornaviruses), most notably coxsackie B virus.
* Infections often reoccur, leading to permanent myocardial damage, cardiomegaly (enlarged heart), or congestive cardiac failure.

Viral Hepatitis
* Inflammation of the liver with accompanying liver cell damage.
* 20-30 cases per 100,000 people per year in the U.S.
* Symptoms :jaundice often proceeded by flu-like illness.
* Liver failure can occurs.
* Can become chronic depending on the infectious agent and cirrhosis
* Transmission:
o parenteral (needle infection usually),
o perinatal (occurring just before or after birth),
o sexual, or enteric (via gut cells).
* 5 viruses known to infect the liver as the primary organ. Other viruses can also cause hepatitis e.g. Herpes viruses and some viruses causing hemorrhagic fever.
* Deaths- Hepatitis B is the most common killer killing 2 million/yr worldwide and 5000/yr in US.

Viral pancreatitis and diabetes
* Mumps infection can be complicated by severe pancreatitis (inflammation of the pancreas).
* Can also be caused by certain other enteroviruses.
* There is some evidence that viral infections triggers insulin-dependent juvenile diabetes mellitus.

Chronic fatigue syndrome
* Characterized by extreme fatigue.
* EBV, Coxsackie B, CMV, and HTLV are among the many viruses to be isolated from such patients
* Importantly, no cause-effect relationship has been established

Congenital and Perinatal Infections
* Include a variety of diseases acquired
o Prenatally,
o Intrapartum (during birth process) or
o Postnatally within the first few weeks.
* Can be particularly dangerous since the newborn is not protected by the mothers antibodies

Infection.ppt

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Bacterial Diseases

Bacterial Diseases

A. Airborne Bacterial Diseases
B. Foodborne & Waterborne Bacterial Diseases
C. Soilborne Bacterial Diseases
D. Arthropodborne Bacterial Diseases
E. Sexually Transmitted Bacterial Diseases
F. Miscellaneous Bacterial Diseases

V. A. Airborne Bacterial Diseases

1. Streptococcal Diseases
2. Diphtheria
3. Pertussis
4. Meningococcal Infections
5. Haemophilus influenzae Infections
6. Tuberculosis
7. Pneumococcal Pneumonia
8. Primary Atypical Pneumonia
9. Legionellosis

Foodborne & Waterborne Bacterial Diseases

1. Foodborne Intoxications vs Infections
2. Botulism
3. Staphylococcal Food Poisoning
4. Clostridial Food Poisoning
5. Typhoid Fever
6. Salmonellosis
7. Shigellosis
8. Cholera
9. Diseases associated with Escherichia coli
10. Camphylobacteriosis and Helicobacteriosis

Soilborne Bacterial Diseases

1. Anthrax
2. Tetanus
3. Gas Gangrene
4. Leptospirosis
5. Listeriosis

Arthropodborne Bacterial Diseases

1. Plague
2. Lyme Disease
3. Rocky Mt. Spotted Fever
4. Epidemic Typhus
5. Endemic Typhus

Sexually Transmitted Bacterial Diseases

1. Syphilis
2. Gonorrhea
3. Chlamydia
4. Chanchroid

Miscellaneous Bacterial Diseases

1. Leprosy
2. Staphylococcal Infections
3. Pseudomonas aeruginosa Infections

Bacterial Diseases .ppt

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Infectious Diseases of the Skin and Eyes

Infectious Diseases of the Skin and Eyes

Skin Structure

Natural Defenses of the Skin
* Keratin
* Skin sloughing
* Sebum: low pH, high lipid
* Sweat: low pH, high salt, and Lysozyme, which digests peptidoglycan

Normal Skin Flora
* Propionibacterium acnes
* Corynebacterium sp.
* Staphylococci
o Staphylococcus epidermidis
o Staphylococcus aureus
* Streptococci sp.
* Candida albicans (yeast)
* Many others

The Eye
* Normal flora sparse
* Similar to skin flora
* Tears have lysozyme, IgA

Bacterial eye infection resulting from injury is a medical emergency!

Bacterial Skin Infections
* Acne
* Necrotizing fasciitis
* Leprosy

Acne
* Propionibacterium acnes: Gram + rod
* Digests sebum
* Attracts neutrophils
* Neutrophil digestive enzymes cause lesions, “pus pockets”

Microscopy
Acne
* Most common skin disease in humans
* Oil-based cosmetics worsen disease
* No effects of diet

Acne Treatments
* Benzoyl peroxide dries plugged follicles, kills microbes
* Tetracycline (antibiotic)
* Accutane – inhibits sebum formation

Necrotizing Fasciitis “Flesh Eating Strep”
Streptococcus pyogenes (Group A Strep)
* Tissue digesting enzymes
o Hyaluronidase
o Streptokinase
o Streptolysins
* Rapidly spreading cellulitis may lead to loss of limb

Necrotizing Fasciitis
* Disease starts as localized infection
* Pain in area, flu-like symptoms
* Invasive and spreading
* May lead to toxic shock (drop in blood pressure)
* Incidence 1-20/100,000
* 30-70% mortality
* Surgical removal, antibiotics

Hansen’s Disease: Leprosy
Mycobacterium leprae
* Disease of skin and nerves
* Change of pigmentation, loss of sensation
* Slow progressing
* Transmits poorly
* Droplet or skin contact?

Hansen’s Disease: Leprosy
* Mycobacterium leprae
* Acid fast bacterium
* Slow growth
* Strict parasite
* Multiplies in macrophages
* Prefers cool areas of body
* Long course, drug cocktail


Virus Infections of the Skin: Rashes
Maculo-papular rashes
(flat to slightly raised colored bump)
Measles virus (Rubeola)
Rubella virus (German Measles)
Roseola (Human Herpesvirus-6)
Fifth Disease (Human Parvovirus B19)

Measles
* Viral infection through aerosol droplet: One of the MOST communicable viruses
* Initial infection of the oro-pharynx

 local infection lymph node(s) (of the neck)
 lymphocyte associated viremia
Fever, malaise
 Spread throughout the body
 Shed in respiratory tract secretions
Koplik’s spots
Skin Rash
 Recovery; life long immunity

* Effective childhood vaccine (2-3 doses): MMR (measles, mumps, rubella), but disease still exists worldwide

An example of the rash of measles.
Note flat, reddened areas

Measles World Wide
* Measles is the leading cause of vaccine-preventable death among children
* Millions of children still remain at risk from measles.
* In developed, measles death rates range from 1-5%, but among malnourished children, the death rate reaches 10-30%
* Over 500,000 children under the age of five die each year.
* Measles causes health complications, including pneumonia, diarrhea, encephalitis, and corneal scarring.
* The primary reason for ongoing high childhood deaths is the failure to deliver at least one dose of measles vaccine to all infants.

The Measles Vaccine Initiative 2001
American Red Cross
United Nations Foundation (UN Foundation)
United States Centers for Disease Control and Prevention (CDC)
World Health Organization (WHO)
United Nations Children's Fund (UNICEF)

Measles World Wide

Rubella
* Viral infection through aerosol droplet; systemic infection
* A ~Mild~ rash
* Serious for a fetus when contracted in the first trimester of pregnancy
* Disrupts fetus development of the CNS and/or other organs: Congenital Rubella Syndrome
+ Small birth weight, blindness, hearing loss, mental retardation, heart problems
+ Infection lasts for months-years in the newborn
* Vaccine highly effective (MMR)

Features for Measles and Rubella
Virus Infections of the Skin: Vesicles
Vesicular or pustular rash
(elevated lesions filled with fluid)
Smallpox (Human Pox virus)
Cold Sores (Human simplex 1 and 2)
Chickenpox (Human Herpesvirus-3)

Chickenpox “Varicella – Zoster”
* Common virus; decreasing disease in the USA due to effective childhood vaccine
* Benign disease with life long immunity
* Life-threatening for immunocompromised individuals
* Recuperation can result in life long benign Varicella-zoster virus latency
* May re-emerge as shingles (skin lesion): Should we vaccinate adults?

Chickenpox virus in the body
* Viral infection through aerosol droplet; systemic infection

 local infection in lymph node(s) (of the neck)
 lymphocyte associated viremia
Fever, malaise
 Spread throughout the body
 Shed in respiratory tract secretions and
Skin Vesicles (small blisters of clear fluid)
 Recovery with virus latency in neurons
 Life long immunity
* May re-emerge as shingles and spread to others (skin vesicular lesions):






Chicken pox reemerges as Shingles
Causes: stress, X-ray treatments, drug therapy, or a developing malignancy, or ?
Varicella-zoster virus reemergence as shingles

Smallpox
* A disease with an interesting history
* Very infectious viral disease (epidemic)
* The disease has been eliminated due to world-wide vaccine program:
+ Vaccinia: a Jennerian vaccine

Named for Edward Jenner, 1796
* The virus has been preserved in government labs by agreement, at CDC in Atlanta, and in Russia
* Considered a bioterrorism agent

Features of Chickenpox and Smallpox.

Virus Infections of the Eye
Herpesvirus Keratitis (Human simplex 1)
Chlamydial infection of the eye
Chlamydia trachomatis causes trachoma
and can lead to blindness

Warts and Papillomas
* Mostly a benign viral infection
* Nearly everyone is infected!
* Contact transmission; fomite transmission
* Different virus types
o Plantar warts (HPV-1)
o Flat warts (HPV-3,10,28,49)
o Genital Warts (HPV 6,16,18,31)

Common warts
Infectious Diseases of the Skin and Eyes.ppt

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Differential diagnosis of the flu-like illness

The sepsis syndrome: Differential diagnosis of the flu-like illness
By:Divya Ahuja, M.D.

Med Micro 2008 Clinical Correlations #5
Traditional definitions

* Bacteremia (or fungemia): presence of microorganisms in the blood
* Sepsis: Harmful consequences of microbes or their toxins in blood or tissues
* Septicemia (or bloodstream infection): bacteremia with clinical manifestations
* Septic shock: shock due to sepsis, often with bloodstream infection

Revised definitions
* Systemic inflammatory response syndrome (SIRS)
* Sepsis
* Severe sepsis
* Septic shock

Systemic Inflammatory Response Syndrome (SIRS)
* Two or more of the following
o temperature > 38 degrees C (100.4 F)
o respirations > 20/minute
o Heart rate > 90 beats per minute
o leukocyte count > 12,000/cmm or < 4000/cmm or with > 10% band forms

Sepsis and Severe Sepsis
* Sepsis: SIRS plus a documented infection (culture proven or identified by visual inspection)
* Severe sepsis: Sepsis associated with organ dysfunction, abnormalities due to hypoperfusion (such as lactic acidosis, oliguria, or acute alteration in mental status), ARDS, DIC, low platelets

Septic shock
* Definition: Sepsis-induced hypotension despite fluid resuscitation and/or inotropic support, plus hypoperfusion abnormalities
* The hallmark of septic shock is low systemic vascular resistance, which distinguishes it from hemorrhagic shock and cardiogenic shock.

Multiple Organ Failure
* Some physiologic descriptors
o Serum creatinine
o Platelet count
o pO2/FiO2 ratio
o Serum bilirubin
o Glasgow coma score

Sepsis
* Sepsis has a 20-50% mortality
* Severity has increased recently
* Hospital case-fatality has declined
* Incidence is greatest in winter
* Risk factors for sepsis
o Bacteremia
o Advanced age
o Impaired immune system
o Community acquired pneumonia

Continuum of severity
* Incidence of positive blood cultures increases along the continuum
* Increased mortality rate
* Severe organ dysfunction manifested as
o Acute respiratory distress syndrome
o Acute renal failure
o Disseminated intravascular coagulation

Disseminated intravascular coagulopathy
Case #1
* 20-year-old college student in ER
* General malaise, low-grade fever, and rapid development of purplish discoloration on his face. (from when he left his house to the time he arrived at the emergency room).
* Blood cultures were drawn and he was admitted to the intensive care unit

Presentation
* Febrile, tachycardic, systolic BP-70
* Creatinine- 3.6, poor urine output
* Platelets-46000
* INR- 2.6
* Obtunded mental status
* Needing maximum ventilatory support
* Meningococcemia with Waterhouse-Friderichsen Syndrome and DIC
* Treat with penicillin, ceftriaxone or chloramphenicol.
* Family members and hospital employees in contact with respiratory secretions should receive prophylaxis. Attack rates for household contacts is 0.3-1%, 300-1000 times the rate in the general population (rifampin x 4 doses or cipro x 1 dose)

Epidemiology of meningococcal disease

Evaluation of blood cultures
* True-positive versus false-positive (contamination; pseudobacteremia)
* Transient versus intermittent versus continuous
* Polymicrobial versus unimicrobial
* Primary versus secondary

Clues to contamination
* Microorganisms that are usually not pathogenic, unless isolated from multiple cultures (e.g., coagulase-negative staphylococci; Bacillus species)
* < 2 positive cultures and/or delayed growth and/or < 1 cfu/ml
* Doesn’t “fit” the clinical picture

Patterns of bacteremia
* Transient: caused by manipulation of a flora-containing body surface
* Intermittent: typical of most infections giving rise to positive blood cultures
* Sustained (or continuous): characteristic of intravascular infections--endocarditis, endarteritis, suppurative thrombophlebitis, infected AV fistula

Number of microorganisms
* Unimicrobial (or “monomicrobial”) bacteremia: one isolate
* Polymicrobial bacteremia: more than one microorganism; typical of complicated situations often with surgical implications

Epidemiology of sepsis
* Contributes to > 100,000 deaths in the United States each year.
* Annual incidence is probably between 300,000 and 500,000 cases.
* About 2/3rds of cases occur in patients hospitalized for another illness (nosocomial infection).

Risk factors for nosocomial sepsis
* Gram-negative bacilli: diabetes mellitus; tumors; cirrhosis; burns; invasive procedures; neutropenia
* Gram-positive cocci: vascular access lines, devices
* Fungi: immunosuppression; broad-spectrum antibiotic therapy

Host factors in sepsis
* Mortality is directly related to severity of underlying disease: rapidly-fatal> ultimately fatal (i.e., within 5 years)>nonfatal.
* Elderly have increased mortality.
* Mortality is higher in patients with subnormal temperatures than in those with fever.

Clinical findings in sepsis
* Early: apprehension, hyperventilation, altered mental status
* Complications: hypotension, bleeding, leukopenia, thrombocytopenia, organ failure
* Lungs: cyanosis, acidosis, full-blown ARDS
* Kidneys: oliguria, anuria, tubular necrosis
* Liver: jaundice and transaminitis
* Heart: heart failure, stunned myocardium
* Gastrointestinal: nausea, vomiting, diarrhea, stress ulceration
* Systemic: lactic acidosis
* Petechiae early in course: suspect especially meningococcemia, RMSF
* Ecthyma gangrenosum: Ps. aeruginosa
* Generalized erythroderma: Toxic Shock Syndrome

Petechiae
Ecthyema gangrenosum

Skin lesions in septicemias (1)
* Neisseria meningitidis: erythematous macules or petechiae and purpura
* Rocky Mountain spotted fever: petechiae, purpura
* Staphylococcus aureus: “purulent purpura”
* Pseudomonas aeruginosa: ecthyma gangrenosum
* Salmonella typhi: “Rose spots”
* Hemophilus influenzae: cellulitis
* Endocarditis: petechiae; Osler’s nodes (painful lesions of finger and toe pads); Janeway lesions (painless lesions of palms or soles)
* Anthrax: papules-->vesicles-->eschar
* Fungemias

A 50 yo man presents to emergency room with severe pain and swelling of LLE. On exam, temperature is 40.0 ºC, pulse rate is 135/min, respiration rate is 35/min, and blood pressure is 80/40

Which of the following is the most appropriate initial therapy?
* LLE elevation
* X-ray of LLE
* Surgical consultation
* Oral antibiotics

Necrotizing fasciitis
* Necrotizing fasciitis usually results from an initial break in skin (trauma or surgery)
* It is deep: may involve the fascial and/or muscle compartments
* The initial presentation is that of cellulitis

Necrotizing fasciitis: Red flags
* Severe pain (out of proportion of skin findings)
* Bullae (due to occlusion of deep blood vessels)
* Skin necrosis or ecchymosis
* Gas in soft tissue (palpation or imaging)
* Systemic toxicity
* Rapid spread during antibiotic therapy

Necrotizing fasciitis
* Monomicrobial: S. pyogenes, S. aureus, anaerobic streptococci,…. Most are community acquired and present in the limbs in patients with DM or vascular insufficiency

* Polymicrobial: aerobic and anaerobic (bowel flora), Usually associated with abdominal surgical procedures, decubitus ulcer, perianal ulcer, bartholin abscess, IV drug injection

Staphylococcal bacteremia
* Complications: endocarditis; metastatic infection; sepsis syndrome
* Staphylococci adhere avidly to endothelial cells and bind through adhesin-receptor interactions
* Fulminant onset; high fever, erythematous rash with subsequent desquamation, and multiorgan damage
* DDx: Rocky Mountain spotted fever, streptococcal scarlet fever, leptospirosis

Streptococcal toxic shock syndrome
* Early onset of shock and organ failure associated with isolation of group A streptococci
* Necrotizing fasciitis present in about 50% of cases
* Early symptoms: Myalgias, malaise, chills, fever, nausea, vomiting, diarrhea
* Pain at minor trauma site may be first symptom

Sepsis in the asplenic patient

* Frequently fulminant with massive bacteremia
* Streptococcus pneumoniae accounts for 50% to 90% of infections and 60% of deaths
* Other pathogens: Haemophilus influenzae, Neisseria meningitidis, Capnocytophaga canimorsus (after dog bites),
Babesia microti (babesiosis)

64 year old WM
* Presents with fever, hypotension, cellulitis with bullous skin lesions
* PMH: cirrhosis
* SH: recently returned from New Orleans, likes oysters

Vibrio vulnificus sepsis
* Organism found in warm seawater and in shellfish (90% of deaths due to seafood in U.S.)
* Cirrhosis a major risk factor to sepsis, with rapid onset
* Chills, fever, characteristic skin lesions (bullae with hemorrhagic fluid; necrotizing fasciitis, other)
* Also causes wound infection after exposure to salt water

41 year old WM
* Fever, “worst headache ever,” myalgias, rash
* Returned from family camping trip in Smoky Mountain National Park 1 week PTA

Rocky Mountain spotted fever
* Generalized infection of vascular endothelium
* Headache typically severe. Fever may be low-grade and rash may be absent (“spotless fever”) when patient first seen
* Suspect with flu-like illness and severe headache in endemic areas!

65 year old woman
* PMH diabetes
* During influenza epidemic, presents with fever, chills, aching all over (myalgia)
* PE: bibasilar rales; no murmur
* Admitted to hospital for treatment of heart failure

Infective endocarditis: definitions

* Septic vegetations of the endocardium usually involving the heart valves or other areas of turbulent flow
* Acute endocarditis occurs on normal heart valves, is caused by highly virulent bacteria and leads to death in < 6 weeks
* Subacute endocarditis is caused by less virulent bacteria and has a more indolent course.

Pathogenesis of endocarditis
* Sterile vegetations arise downstream of high-flow areas of the heart
* Damaged endothelium and foreign bodies increase turbulent flow
* Microorganisms implant on the sterile vegetations during transient bacteremia
* Septic vegetations become a source of infection elsewhere

Diagnosis of endocarditis
* Revised Duke Criteria : positive blood cultures plus echocardiography with or without minor criteria
* Heart murmurs (especially regurgitant)
* Splinter hemorrhages (nail beds)
* Osler nodes (finger pulps; painful)
* Petechiae; “pustular purpura” (Staph)
* Roth spots (fundi)

Etiologies of endocarditis
* Viridans streptococci most common (30-40%)
* Other streptococci include enterococci and Streptococcus bovis
* Staphylococci cause 20-30%)
* Less common: aerobic gram-negative rods; HACEK organisms; fungi; anaerobic bacteria; Brucella; Coxiella burnetti; Chlamydia psittaci
* “Culture-negative” (<5% to 24%)

Case
* 42 year male
* Previously healthy, non smoker
* 2 week history of progressive cough, dyspnea, fever
* Intubated within 48 hours of admission

Case
Hamman-Rich syndrome
* Also known as acute interstitial pneumonia, is a rare, severe lung disease which usually affects otherwise healthy individuals
* Cough, fever, dyspnea
* Hamman-Rich syndrome progresses rapidly, with hospitalization and mechanical ventilation within days to weeks after initial symptoms

Sepsis-summary
* Look at the host (age, immunedeficiency,-HIV, cancer, steroids, cirrhosis, dialysis,
* Clinical assessment for MOD (vitals, perfusion, mental status, urine output)
* Lab parameters-platelets, creatinine, coags, leukocytosis vs. leukopenia
* Hemodyanamic, ventilatory support, antibiotics
* Hit hard and hit early and then deescalate based on emerging microbiological data

The sepsis syndrome: Differential diagnosis of the flu-like illness.ppt

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Update on Infections

Update on Infections
By:Mark A. Lassoff, MD, MBA, MPH
September 18, 2007

Malacoplakia
* “malako” – soft, “plakos” – plaque
* Rare granulomatous disease
* Michaelis – Gutmann bodies: basophilic lamellar inclusion bodies
* Associated with other autoimmune diseases
o Sarcoidosis, Chedak-Higashi syndrome
* Incidence: 1 in 10,000
* Female: Male – 4:1
* Peak incidence is in patients ≥ 50 yrs old
* 75% of cases occur in GU system, most commonly in the bladder (2nd – kidney)
* Predilection for those with immunodeficiency, systemic dz, carcinoma or chronic UTI with coliform organisms (E Coli – up to 75%, Enterobacter, Klebsiella, Proteus and Pseudomonas)
* Etiology – unknown
o Theory: acquired immunodeficiency interfering with normal intracellular function of the monocyte’s phagolysosome. Residual undigested bacterial components become mineralized by Ca++ & Fe
o Cause appears to be related to imbalance in the intracellular cGMP/cAMP
* Dx made by biopsy
o Lesion: large histiocytes  von Hansemann cells and small intracytoplasmic calculospherules  Michaelis-Gutmann bodies
o Immunohistochemical staining for α1-antitrypsin useful for early and accurate differential dx
* Clinical findings
o Bladder
+ Irritability and hematuria
+ Mucosal plaques or nodules  fungating, firm, sessile masses
o Renal
+ Bilaterality in up to 50%; multifocal is more common
+ Fever, flank pain or mass on PE
+ Cause loss of function via direct invasion or obstruction
+ E Coli infxn in up to 93%
+ Bilateral dz  mortality rate approaches 100% w/i 6 mos of dx w/o intervention
+ IVP: unifocal – may displace calyces vs. multifocal – nephromegaly and poor renal fxn; multiple filling defects
* Management
o Lower tract:
+ Initial treatment with medications
# Bethanecol (↑ cGMP), Ascorbic acid (↓ cAMP)
# Fluoroquinolones (DOC)
# Others: Bactrim, Rifampin, Cipro
+ TUR prn for plaque removal
o Upper tract:
+ Unilateral renal dz: most often requires nephrectomy
o In immunodeficient pts and those with multifocal dz, surgical tx is essential to survival

Sexually Transmitted Infections
Syphilis
* Treponema pallidum (spirochete)
* Spread: infectious lesions, body fluids, in utero, blood transfusions
* Primary
o Single painless, indurated ulcer appearing 3 wks after inoculation (@ site of inoculation) and remains for 4 – 6 wks
o Often with bilateral, non-tender inguinal or regional lymphadenopathy
o Can heal w/o treatment; often goes unnoticed
o Presence of chancres increases risk of HIV acquisition 2-5x
* Latent
o Seroreactivity w/o clinical evidence of dz
o Early: within the last year
o Late latent vs. latent syphilis of unknown duration
* Secondary
o Begins 4 – 10 wks after the appearance of the ulcer but may present up to 24 mos after initial infection
o Mucocutaneous, constitutional and parenchymal signs and symptoms
+ Maculopapular rash (trunk and arms)
+ Generalized non-tender lymphadenopathy
+ Papular rash (may accompany first rash)
# Becomes necrotic and pustular
# Affects palms and soles
# Intertriginous areas: enlarge and erode  condyloma lata (infectious)
+ Less commonly: hepatitis and immune-complexed glomerulonephritis
* Tertiary
o One third of untreated pts
o Rare in industrialized countries, except for pts w/ HIV
o Cardiovascular, skeletal, CNS, skin
+ Aortitis, meningitis, uveitis, optic neuritis, general paresis, tabe dorsalis, gummas of skin/skeleton
* Screening
o Rapid Plasma Reagin (RPR) & Venereal Disease Research Laboratory (VDRL)
+ Correlate with disease activity
+ Become negative one year after treatment
o T. pallidum particle agglutination (TP-PA) or Fluorescent Treponemal Antibody Absorbed (FTA-ABS)
+ Antibody tests remain positive for life; do not correlate w/ active disease
o HIV can cause FN results by treponemal & non-treponemal methods
* Treatment
o Benzthiazide penicillin G (2.4 million units IM x 1)
o Jarisch – Herxheimer rxn
+ Headaches, myalgia, fever, tachycardia, increased resp rate within first 24 hrs after tx w/ PCN
+ Managed with bed rest and NSAIDs
o PCN allergy: Doxycycline (100mg BID x 14d)
o Latent: PCN IM weekly x 3 doses or doxycycline for a total of 4 wks
o Tertiary: Aqueous crystalline PCN G (IV q4h) x 10-14 d or PCN G procaine IM + probenecid (po QID) x 10-14 d
o Pregnancy: desensitization to PCN

Herpes Simplex Virus
* Genital herpes: HSV-2 (85-90%), HSV-1 (10-15%)
* Silent infection may account for >75% of transmission
* Primary
o Painful ulcers of genitalia or anus
+ Group of vesicles on an erythematous base that does not follow a neural distribution is pathognomonic
o Bilateral painful inguinal adenopathy
o Often associated with constitutional flu-like symptoms
o Urethral lesions may cause transient urinary retention in women
o Asx viral shedding can happen up to 3 mos after clinical presentation
* Recurrent episodes are usually less severe
* Severe dz and complications:
o Pneumonitis, disseminated infxn, hepatitis, meningitis, encephalitis
* Dx: viral culture with subtyping (gold standard)
o Not on clinical suspicion alone, classic presentation occurs in a small percentage of pts
o Can see abrasions, fissures or itching
o Subtyping is important for prognosis and counseling
+ HSV-2: ave of 4 recurrences in 1st yr vs. 1 for HSV-1
o Sensitivity: 30 – 95% depending on stage of lesion and whether it is primary or recurrence
* Treatment
o Oral acyclovir, valacyclovir and famciclovir
o Topical meds are not effective
o Recurrences: episodic or suppressive approach
+ Suppressive: decreases frequency/duration and viral shedding
Chancroid
* Haemophilus ducreyi
* Men: Women – 3:1
* Painful, non-indurated ulcer on penis or vulvovaginal area
o Friable base covered with a gray or yellow purulent exudate and a shaggy border
* Inguinal adenopathy is typically unilateral and tender with tendency to become suppurative and fistulize
* Dx: culture media not widely available so gram stain often helpful (short, fine, GN streptobacilli in short, parallel chains)
* Approximately 10% are co-infected w/ HSV or syphilis
* Treatment
o Single dose
+ Azithromycin 1gm po or Ceftriaxone 250mg IM
o Other tx: Cipro x 3d or Erythromycin x 7d

Lymphogranuloma Venereum
* Chlamydia trachomatis – L1, L2, L3
* Single, painless ulcer on the penis, anus or vulvovaginal area that goes unnoticed
* Painful unilateral suppurative inguinal adenopathy and constitutional symptoms that occur 2 – 6 wks after resolution of ulcer
* Significant tissue injury and scarring can occur leading to labial fenestration, urethral destruction, anorectal fistulas and elephantiasis of penis, scrotum or labia
* Dx: mainly clinical
o Complement fixation or indirect fluorescence antibody titers can confirm
* Tx: Doxycycline BID or erythromycin QID x 3 wks

Genital Warts
* Condylomata acuminata
* Human papillomavirus (HPV) – DNA virus
* Types 6 and 11 are most often responsible for visible external genital warts
o Cervix, vagina, urethra, anus, mucous membranes
* Types 16, 18, 31, 33, 35, 39, 45 and 51: associated with cervical dysplasia and neoplasm in women and squamous intraepithelial neoplasia in men
o >99% of cervical cancers and 84% of anal cancers are associated with HPV (16 & 18)
o Cervical cancer is considered an AIDS defining illness
* Most are subclinical and asx
* In women HPV may be associated with nonspecific symptoms such as vulvodynia or pruritis; malodorous vaginal discharge
* Dx: usually inspection or palpation
* Bx: not routinely needed
o Atypical, pigmented, indurated, fixed or ulcerated
o Lesions persist/worsen after tx; immunocompromised pts
* Treatment
o Depends on size, number, location, and patient and physician preference
o Observation (spontaneously resolve with time)
o Patient applied (less expensive)
+ Podofilox 0.5% solution or gel (3d on, 4d off, may repeat x 4)
+ Imiquod 5% cream (3/wk qhs for up to 16 wks)
# Needs to be washed off, can cause ulceration
o Provider applied
+ Cryotherapy with liquid nitrogen
+ Electrosurgery
+ Laser therapy (CO2)
+ Podophyllin resin (20 – 25%)
+ Trichloracetic acid (TCA) or bichloracetic acid (BCA)
+ Surgical excision
* Lesions around the meatus may herald presence of urethral or bladder condyloma
* Urethral or bladder lesions should be cystoscopically excised
* Intraurethral 5% FU cream 2/wk
* Vaccine containing 8 of the most common HPV types associated with cancer could potentially prevent 95% of cervical cancer
* Topical BCG: promising preliminary results

Sexually Transmitted Infections
Chlamydia
* Chlamydia trachomatis: most common bacterial STD in the US and worldwide
* Majority of men and women are asx
* 50% of men experience LUTS attributed to urethritis, epididymitis or prostatitis; may see clear or white urethral discharge
* 75% of women are asx and 40% of those untreated will have PID
* May be transmitted during vaginal birth
o Ocular, oropharyngeal, respiratory, urogenital or rectal infxn
Chlamydia
* Women should be screened annually until 25 yo or if risk factors such as new sexual partner are present
o Nucleic acid amplification test (NAAT) on endocervical swab or urine specimen
o Unamplified nucleic acid hybridization test, enzyme immunoassay or direct fluorescence antibody test
o Culture
* Treatment
o Azithromycin 1gm po x 1 or Doxy BID x 7d
o Refrain from sex until treatment completed or 7d after single dose therapy
o Re-culture recommended 3 wks later if treated with erythromycin, in pregnant women or if symptoms persist
o Re-screened 3 – 4 mos after tx as are high risk for re-infxn

Gonorrhea
* Neisseria gonorrhoeae (GN diplococcus)
* Men usually experience LUTS attributed to urethritis, epididymitis, proctitis or prostatitis w/ associated mucopurulent urethral discharge
* Women may have vaginal and pelvic discomfort, dysuria or abnormal vaginal discharge but are usually asx
* Same screening recs as for Chlamydia
* Treatment
o Ceftriaxone 125mg IM x 1
o Single dose oral regimen
+ Cipro, Levaquin, Ofloxacin (growing resistance to FQs)
o Simultaneous treatment for Chlamydia






Trichomoniasis

* Trichomonas vaginalis (flagellated protozoan)
* Increased incidence in developing countries and those with multiple sexual partners
* Can inhabit the vagina, urethra, Bartholin glands, Skene’s glands and prostate (not rectum/mouth)
* Men: usually asx but can produce short-term urethral discharge, dysuria and urgency
* Women: asx in 50%, otherwise can see sudden onset of frothy white or green, foul-smelling vaginal discharge, pruritis, and erythema
o Dyspareunia, suprapubic discomfort, urgency
Trichomoniasis
* Examination: frothy discharge and “strawberry vulva” or “strawberry cervix”
* Vaginal discharge has increased pH
* Motile protozoa on vaginal wet-mount smear or microscopic examination of urine
* Men: urethral cx or microscopic exam of urine
* Treatment
o Metronidazole 2gm po x 1 (ok in 2nd trimester)
+ GI side effects common
o Abstain from Etoh consumption
o Prolonged Metronidazole for failure

Vaginitides / Urethritides
* Ureaplasma urealyticum, Mycoplasma hominis, Mycoplasma genitalium
o Implicated in chronic prostatitis and urgency frequency symptoms in women and in up to 40% of NGU
o Tx: Azithromycin po x 1 or doxycycline x 2 wks
* Bacterial vaginosis
o Gardnerella vaginalis, anaerobic orgs, Mycoplasma and/or inhibition of normal vaginal flora
o 10% KOH with vag secretions  fishy odor secondary to release of amines
o Microscopic exam (3 of 4 necessary): (1) thin, white vag d/c (2) vag pH >4.5 (3) clue cells (4) pos whiff test
o Tx: Metro po BID x 7d, Clinda cream x 7d, Metro gel x 5d
* Candida albicans
o Thick, cheesy vaginal discharge usually associated with vulvar irritation and itching
+ Vaginal discomfort, burning, dyspareunia and external dysuria
o Dx: yeast or pseudohyphae on wet prep or gram stain
o Tx: single oral dose of fluconazole (150mg) or OTC antifungal vaginal creams, tablets or suppositories x 1-7 days (butoconazole, clotrimazole, miconazole and terconazole)
References

Update on Infections .ppt

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VASCULITIS SYNDROMES

VASCULITIS SYNDROMES
By:Emily B. Martin, MD
Rheumatology Board Review

KAWASAKI SYNDROME
Mucocutaneous lymph node syndrome
KAWASAKI DISEASE
* Diagnostic criteria:
CLINICAL MANIFESTIONS
* Arthritis and arthralgia
* Urethritis
* CNS involvement
* GI symptoms

DIFFERENTIAL DIAGNOSIS
* Viral infections
* Toxin mediated illnesses
* Rickettsial or spirochete infections
* Drug reactions
* JRA
* Mercury hypersensitivity reaction

LABORATORY EVALUATION
* Markers of systemic inflammation
* Anemia (normocytic, normochromic)
* Sterile pyuria (urethral origin, don’t do a cath)
* Transaminase elevation (mild to moderate)
* CSF findings
* Synovial fluid inflammation
* Hyponatremia (increased risk for coronary aneurysms)

TREATMENT
* Mainstay of treatment is IVIG 2 gram/kg over 8-12 hours.
* IVIG may need to be repeated in refractory cases.
* Several studies have shown that IVIG + aspirin decreases the risk of coronary aneurysms compared to aspirin alone.
* High dose aspirin during acute illness then low dose for about 2 months.

FOR THE BOARDS…
* Know the clinical manifestations of Kawasaki syndrome.
* Know the differential diagnosis of KD.
* Know the laboratory abnormalities seen in KD.
* Recognize the value of high-dose IVIG in treatment of KD.

QUESTIONS
HENOCH-SCHONLEIN PURPURA

* Most common systemic vasculitis in children.
* Immune mediated
* Often a self-limited disease.
* Occurs more often in fall, winter, and spring.
* About 50% of cases are preceded by URI’s.

CLINICAL PRESENTATION
* Classic tetrad
GI SYMPTOMS
* HSP can cause edema and submucosal hemorrhage of GI tract.
* May be the presenting symptom of HSP.
* Symptoms typically develop within 8 days of the rash.
* Intussusception is the most common GI complication.

RENAL DISEASE
* Occurs in up to 50% of patients.
* Ranges from hematuria to end-stage renal disease (<1% of patients).
* Usually presents within four weeks of onset of HSP.
* Overall prognosis is very good, but there is some long-term risk of progressive renal impairment.

LABORATORY FINDINGS
* There is NO definitive diagnostic test.
* IgA levels may be elevated in 50-70% of patients.
* Platelet counts and coag studies should be normal.
* Inflammatory markers may be elevated.
* Urinalysis
* Negative RF and ANA.
* Recognize the typical presentation of HSP.
* Recognize that HSP may present initially with ABDOMINAL PAIN OR JOINT COMPLAINTS.
* Know the typical laboratory findings in HSP.

MOST likely diagnosis is
* Henoch-Schonlein purpura
* Immune thrombocytopenic purpura
* Juvenile rheumatoid arthritis
* Parvoviral infection
* Post-streptococcal arthritis

VASCULITIS SYNDROMES.ppt

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Influenza A (H1N1) guidance documents from WHO

Influenza A(H1N1) guidance documents from WHO

A

Advice on the use of masks in the community setting in Influenza A(H1N1) outbreaks

C

CDC protocol of realtime RTPCR for swine influenza A(H1N1)
Clean hands protect against infection
Considerations of influenza A(H1N1) and HIV infection
Countries able to perform PCR to diagnose influenza A (H1N1) virus infection in humans

G

Global surveillance during an influenza pandemic
Guidance to influenza laboratories: diagnosing swine influenza A/H1N1 infections of current concern

I

Infection prevention and control in health care in providing care for confirmed or suspected A(H1N1) swine influenza patients
Infection prevention and control of epidemic- and pandemic-prone acute respiratory diseases in health care
Instruction on how to obtain CDC realtime RT-PCR kits for detection of influenza A(H1N1)
Instructions for shipments of swine influenza A(H1N1) specimens and virus isolates to WHO Collaborating Centres for influenza
Interim WHO guidance for the surveillance of human infection with swine influenza A(H1N1) virus

L

Laboratory biorisk management for laboratories handling human specimens suspected or confirmed to contain influenza A (H1N1) causing the current international epidemics

P

Pandemic influenza preparedness and mitigation in refugee and displaced populations. WHO guidelines for humanitarian agencies.
Pandemic influenza preparedness and response
Pandemic influenza prevention and mitigation in low resource communities
Protocol for antiviral susceptibility testing by pyrosequencing

R

Reducing excess mortality from common illnesses during an influenza pandemic.

S

Sequencing primers and protocol
Status of candidate vaccine virus development for the current Influenza A(H1N1) virus

V

Viral gene sequences to assist update diagnostics for swine influenza A(H1N1)
Viral gene sequences to assist update diagnostics for swine influenza A(H1N1) - GenBank accession numbers

W

WHO ad hoc scientific teleconference on the current influenza A(H1N1) situation
WHO Technical Consultation on the Severity of Disease Caused by the new influenza A (H1N1) virus infections

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Infections of the Labyrinth

Infections of the Labyrinth
Presentation lecture by:Elizabeth J. Rosen, M.D. & Jeffery T. Vrabec, M.D.

Labyrinthitis
* Inflammatory process involving the inner ear
o infectious vs. non-infectious
o generalized vs. circumscribed
o acquired vs. congenital
o isolated vs. systemic

Pathogenesis

* Meningogenic
o spread through IAC or cochlear aqueduct
* Tympanogenic
o spread through round or oval windows
* Hematogenic
o spread through vascular channels

Bacterial Infections
* Toxic Labyrinthitis
o sterile inflammation
o bacterial toxins penetrate perilymphatic spaces
o mild hearing loss or mild vestibular loss
o usually resolves without sequelae
* Suppurative Labyrinthitis
o bacterial invasion of the inner ear
o intense inflammatory reaction
o progresses along four pathologic stages
o medical emergency

Suppurative Labyrinthitis
Bacterial Labyrinthitis
Bacterial Meningitis
Audiologic Diagnosis and Follow Up
Syphilis
Viral Infections
Cytomegalovirus
Rubella
Mumps
Measles
Varicella-Zoster
Herpes Simplex
Human Immunodeficiency Virus
Protozoal Infections
Toxoplasmosis
Fungal Infections
Acute Cochlear Labyrinthitis
ISSNHL
Acute Vestibular Labyrinthitis
Conclusion
Case Presentation

Infections of the Labyrinth.ppt

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Hematuria

Hematuria

Gross hematuria:
Suspected if a red or brown color change of urine
Intermittent red or brown color urine a/w variety of clinical setting
Medications (phenazopyridine, microbid, NSAID)
Ingestion of beets or certain dyes
Metabolities
Myoglobinuria or hemoglobinuria

Work up
Centrifuge the specimen, Supernatant be tested for heme (hemoglobin or myoglobin) with a urine dipstick.

Causes of heme-negative red urine
Medications
Food dyes
Metabolities
Doxorubicin
Beets (in selected patients)
Bile pigments
Chloroquine
Blackberries
Homogentisic acid
Deferoxamine
Food coloring
Melanin
Ibuprofen
Methemoglobin
Iron sorbitol
Porphyrin
Nitrofurantoin
Tyrosinosis
Phenazopyridine
Urates
Phenolphthalein
Rifampin

Approach to the patient with red or brown urine
Microscopic hematuria:
Major causes of hematuria by age and duration
The evaluation should address the following three questions

1. Are there any clues from the history or physical examination that suggest a particular diagnosis?
2. Does the hematuria represent glomerular or extraglomerular bleeding?
3. Is the hematuria transient or persistent?

Goal is to quickly identify
* Infection
* Kidney stone
* Malignant

History and Physical
Mechanisms by Which Selected Drugs May Cause Hematuria
Hemorrhagic cystitis
Urolithiasis
Carbonic anhydrase inhibitors
Vital sign: BP, T, HR
Abdomen for masses, tenderness (flank, suprapubics), bruits
CVS: irregular irregular
Edema (especially periorbital)
Joint erythema, swelling, warmth
Paleness, jaundice
Careful inspection of external genitalia
Physical Examination Findings and Associated Causes of Hematuria

Physical examination finding
Cause of hematuria
General (systemic) examination
Severe dehydration
Renal vein thrombosis
Peripheral edema
Nephrotic syndrome, vasculitis
Cardiovascular system
Myocardial infarction
Renal artery embolus or thrombus
Atrial fibrillation
Renal artery embolus or thrombus
Hypertension
Glomerulosclerosis with or without proteinuria
Abdomen
Bruit
Arteriovenous fistula
Genitourinary system
Enlarged prostate
Urinary tract infection
Phimosis
Urinary tract infection
Meatal stenosis
Urinary tract infection
Glomerular or Extra Glomerular bleeding?
Microscopic hematuria DDx
Microscopic hematuria DDx
Rare cause of Microscopic Hematuria
Arteriovenous malformations and fistulas
Nutcracker syndrome
Loin pain-hematuria syndrome
Proteinuria
Extraglomerular vs Glomerular in UA
Findings on Microscopy
Transient or persistent hematuria
Exception:
Persistent hematuria
Laboratory Tests (initial work up)
Further Work up
Renal Biopsy
Radiologic and other tests for the evaluation of hematuria
Initial Evaluation of Asymptomatic Microscopic Hematuria
Reference

Hematuria.ppt

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Infections of the Central Nervous System

Infections of the Central Nervous System
Presentation by:Charles S. Bryan, M.D.

* Pleocytosis: increased WBCs in the CSF
* Hypoglycorrhachia: low CSF glucose
* Meningitis: inflammation of meninges
* Encephalitis: inflammation of the brain
* Meningoencephalitis: both of the above
* Myelitis: inflammation of the spinal cord
* Encephalomyelitis: encephalitis + myelitis
* Parameningeal infection: localized infection “beside the meninges”, e.g. brain abscess, subdural empyema, epidural abscess,suppurative intracranial thrombophlebitis, mycotic aneurysm

The CSF formula
* Red cells (normally 0)
* WBCs (normally < 5/cmm)
* Differential (normally all mononuclear cells)
* Protein (normally 15 to 45 mg/dL)
* Glucose (normally 40 to 70 mg/dL or about 2/3 of simultaneous blood glucose)

Some pointers on the LP
* If you think of it, it’s generally best to do it!
* In chronic problems, rule out localized intracranial pathology; for acute problems, don’t delay if there are no localizing signs!
* Save an extra tube (the Golden Rule)!

Acute bacterial meningitis
* A MEDICAL EMERGENCY
* Consider in every patient with a history of URI interrupted by one of the “meningeal symptoms”: vomiting, headache, lethargy, confusion, stiff neck
* Clinical picture is often unimpressive when the patient is first seen

Triad of acute bacterial meningitis
* Fever (bacterial invasion of blood & CSF)
* Stiff neck (nuchal rigidity due to protective reflexes from inflammation of the subarachnoid space)
* Brain dysfunction (nausea/vomiting, headache, irritability/excitability; obtundation)

Kernig’ sign
Brudzinski’s sign
LP in acute bacterial meningitis
Gram’s stain of CSF in meningitis
Pathogenesis of meningitis
* Mucosal colonization
* Mucosal invasion
* Bacteremia
* Meningeal invasion
* Bacterial replication in CSF
* Host response to bacterial antigens
* Subarachnoid space inflammation

Pathogen offensive strategies in acute bacterial meningitis
* IgA protease secretion
* Ciliostasis
* Adhesive pili
* Evasion of alternative complement pathway by polysaccharide capsule

Host defensive strategies in acute bacterial meningitis
* Secretory IgA
* Ciliary activity
* Mucosal epithelium
* Complement (serum bactericidal system)
* Cerebral endothelium: Blood-brain barrier

The blood-brain barrier in meningitis
* 99% of bacteremic adults do not develop meningitis
* However, 1/3 of bacteremic infants develop meningitis suggesting immaturity of blood-brain barrier
* Barrier seems to function unidirectionally (inoculation of subarachnoid space causes bacteremia 1/3 of the time)
* Normal functions: active transport, facilitated diffusion, aqueous secretion of CSF, homeostasis
* Major sites: arachnoid membrane, choroid plexus, and endothelial cells of cerebral microvascular
* Meningitis: cytokines (especially interleukin-1) increase permeability

Cytokines in meningitis
Why is bacterial meningitis so devastating?
Complications of meningitis
Causes of bacterial meningitis by age
“The big three” of bacterial meningitis
Haemophilus influenzae meningitis
H. influenzae meningitis: current issues
Invasive meningococcal disease
Epidemiology of meningococcal disease
Meningococcal disease: indications for preventive
Pneumococcal meningitis
Neonatal meningitis due to gram-negative bacilli
Listeria monocytogenes meningitis
Epidemiology of bacterial meningitis: some associations
Aseptic meningitis: etiology of the term
Aseptic meningitis: current operational definition
Causes of viral meningitis
Pearls on viral meningitis
Other causes of aseptic meningitis syndrome
* Partially-treated bacterial meningitis
* Tuberculous or fungal meningitis
* Parameningeal infection
* Syphilis or leptospirosis
* Toxoplasmosis, amebiasis
* Sarcoidosis
* Drug reactions
The syndrome of chronic meningitis
Causes of chronic meningitis
Tuberculous meningitis
Cryptococcal meningitis
Syphilitic meningitis
Herpes simplex encephalitis
Brain abscess
Subdural empyema
Cavernous sinus thrombosis
Spinal epidural abscess

Infections of the Central Nervous System.ppt

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Lemierre’s Disease

Lemierre’s Disease
Presentation by:by Brandy Harkins

Patient Presentation
* 20 year old female
* Diagnosed with infectious mononucleosis 2 days prior to admission
* No remarkable previous medical history
* Blood pressure – 101/72
* Pulse – 167 beats/min
* Respiratory rate – 52/min
* Shortness of breath and chest pain with shallow breathing
* Sore throat
* Headache
* Fever
* Decreased appetite
* Abdominal pain (no nausea, vomiting, diarrhea or constipation)
* Pale
* Initial diagnosis was pneumonia

Laboratory Findings
* Blood culture positive at 24hrs (Fusobacterium necrophorum)
* Monospot negative
* EBV-VCA IgG positive
* Increased fibrinogen, PT & PTT
* Increased bilirubin
* Liver enzymes – AST 74 (19-45), ALT 44 (8-37)
* WBC’s – 15.3 (4.0-10.9)
* Plts – 106 (150-400)

Fusobacterium necrophorum
* Normal flora in oral cavity, female genital tract, and gastrointestinal tract
* Pleomorphic gram negative bacillus (GNB)
* Non-motile
* Non-spore forming
* Strict anaerobe

Disease Association
* Can cause parotitis, otitis media, sinusitis, odontogenic infection, mastoiditis and Lemierre’s syndrome (necrobacillosis)
* Produces lipopolysaccharide endotoxin, hemagglutinin, leukocidin, and hemolysin
* Invasion usually from intra-oral disease (bacterial tonsillitis, EBV, dental disease)

Questions to Consider
* What organism is usually responsible for Lemierre’s sydrome?
* Why has Lemierre’s become the “forgotten disease?”
* What are the symptoms of the syndrome?
* What age group is most commonly affected?
* What are the stages commonly seen with Lemierre’s and at which stage does the red flag appear?

Lemierre’s Syndrome
* Thrombophlebitis of the internal jugular vein (IJV) due to anaerobic infection (usually F. necrophorum)
* Virulent toxin production with platelet aggregation IJV thrombosis
* Causes severe disease as primary pathogen in healthy individuals
* Generally affects young adults 16-29 y/o
* 1 in 1,000,000 infected per year
* Common in the early 20th century, but disappeared with antibiotics
* Used to have 100% mortality rate…today’s rate is 6-20%

Disease Presentation
* Sore throat
* Tender/swollen lymph nodes
* Prolonged fever
* May experience abdominal pain, nausea or vomitting
* Bacteremia
* Increased WBC’s or left shift
* Hyperbilirubinemia and slight increase in liver enzymes

Classical Characterization
* Primary infection in oropharynx
* Septicemia documented by at least one positive blood culture bottle
* Evidence of internal jugular vein thrombosis
* At least one metastatic focus (usually pulmonary)

Stages
* Patient generally exhibits three stages
1. Pharyngitis – sore throat (< 1 week)
2. Local invasion of lateral pharyngeal space and IJV septic thrombophlebitis swollen/tender neck = red flag
3. Metastatic complications – fever, pulmonary infiltrates or possible joint involvement

Treatment
* Fatal if untreated
* 1-2 weeks IV antibiotics and 2-4 weeks oral antibiotics
* Aggressive approach when patient has pharyngitis and tender/swollen neck
o Get blood culture
o Look for evidence of IJV thrombophlebitis with CT, MRI, ultrasound
o Use antibiotics affective against anaerobes (clindamycin, metronidazole, etc.)
* Anticoagulant therapy controversial
* May require surgery to remove the IJV because of continuing sepsis, localized collection of pus, or embolism

So why’s it so hard to diagnose?
* Rarely seen in the antibiotic-era…most physicians have never seen it
* Can present with pneumonia-like or meningitis-like clinical picture
* Many sore throats have a viral etiology and are not treated with antiobiotics, therefore a patient can be misdiagnosed and untreated for long periods of time before clinicians suspect Lemierre’s
* More severe with longer duration of symptoms than viral sore throat!

Summary
* Lemierre’s syndrome is usually caused by Fusobacterium necrophorum
* Affects healthy young adults
* Patient presents with fever, sore throat, swollen/tender neck (red flag)
* 3 stages – pharyngitis, IJV thrombosis, and metastatic complications
* Disease severity is often underestimated and left untreated or is treated as a case of pneumonia or meningitis


References
Credits:This case study was created by Brandy Harkins, MT(ASCP) while she was a Medical Technology student in the 2004 Medical Technology Class at William Beaumont Hospital, Royal Oak, MI.

Lemierre’s Disease.ppt

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Infectious Diseases Conference

Infectious Diseases Conference
Presentation by:Charles de Comarmond MD

History of present illness
Past medical Hx, FHx, SHx, ROS
* Multiple sclerosis
* Seizure disorder
* Pernicious anemia
* Chronic back syndrome
* Migraine headache
* Depression

Medications
* Betaseron
* Ampicillin-sulbactam
* Vancomycin
* Tegretol
* Librium
* Paxil
* Risperidal
* Trazodone
* Vicodin
* Phenergan
* FHx: Non-contributory
* SHx: 20 pack/year smoker, occasional ETOH
* ROS: chronic low grade temp, repeated admission for hyponatremia

Physical exam
* Vitals: Tmax. 101.5° F, HR:86, RR:20, BP: 111/79.
* Appeared comfortable at time of exam.
* Skin: no rash or jaundice
* HEENT: PERLA, ears, nose, mouth normal
* Neck: supple
* Chest: Clear
* Heart: S1S2 regular rate and rhythm
* Abdomen: Soft, no hepatosplenomegaly
* Extremities: Grossly erythematous swelling of the cubital fossa, with erythema extending to the palmar aspect of left wrist. No evidence of drainage.
* Neuro: AAOx3

Labs

* WBC: 5.3 segs; 84%
* bands; 5%
* lymphs; 7%
* monos; 4%
* Hemoglobin; 12.2 mg/dL
* MCV; 102.8 FL
* Platelets;
* Na 130
* K 4.2
* Cl 9.2
* BUN 8
* Creatinine 0.8
* Glucose 107
* Calcium 8.4
* UA: normal
* 12/25/02 BC: gram +ve cocci (1 of 1)
* Cardiac echo;
* Overall normal valvular appearance and function with mild mitral regurgitation and tricuspid regurgitation. No pericardial effusion.

Differential diagnosis

* Op note; The cephalic vein was dissected out and was noted to be thrombosed. There was an abscess cavity right at the antecubital fossa. The vein was tied off distally, and the entire cephalic vein and a portion of the basilic vein were completely excised.
* Pathology; Acute phlebitis with necrosis and organizing thrombus. There is focal necrosis of the intima. Neutrophils infiltrate the wall of the vessel.
Follow-up cultures
Differential Diagnosis

* Infectious
* Multiple abscesses —Bacteremic patients may develop multiple lung abscesses, which are more common in dependent areas of the lungs. Typically the lesions are between 0.5 and 3 cm in diameter, round, and well-defined.
* Septic emboli — Septic thrombophlebitis may generate septic emboli which produce multiple 0.5 to 3 cm round or wedge-shaped nodules with a predilection for peripheral areas of the lower lobes Cavitation is common, usually producing thin-walled lesions. On CT, subpleural lesions can display a feeding vessel.

* Fungi
* Histoplasmosis
* Coccidioidomycosis
* Aspergillosis
* Cryptococcus
* In these cases, the lesions tend to range from 0.5 to 3 cm in diameter without a clear predilection for a specific area of the lungs
* Neoplastic
* Metastatic solid organ malignancies
* the most common cause of multiple pulmonary nodules and account for 80 percent of such cases.
* The lesions are variable in size and location, with a proclivity for the better perfused lung bases
* The lesions are usually round with sharply demarcated borders
* Cavitation of metastatic lesions occurs in less than 5 percent of cases.
* Non-Hodgkin's lymphoma: These are more common in the lower lobes.
* Intrapulmonary lymphoma nodules usually originate from the bronchial-associated lymphoid tissue (BALT), and occasionally exhibit a halo of ground glass attenuation
* HIV: Kaposi's sarcoma can present with multiple pulmonary nodules in a peribronchovascular distribution.
* The size of these nodules tends to exceed 1 cm at the time of diagnosis
* Noninfectious
* Inflammatory conditions;
* Wegener's granulomatosis: Can produce multiple round, sharply or poorly demarcated lesions varying in size from 0.5 to 10 cm.
* Areas of consolidation may be associated with nodules, and cavitation occurs in slightly less than one-half of patients, generally producing a thick wall with an irregular inner lining
* Lymphomatoid granulomatosis
* Sarcoidosis
* PULMONARY ARTERIOVENOUS MALFORMATIONS
* Present radiographically as either solitary or, in 30 percent of cases, multiple pulmonary nodules.
* Lesions are usually well-defined, round or oval opacities ranging from 1 to 5 cm in diameter
* The presence of a shunt fraction of >5 percent when breathing 100 percent oxygen in the absence of an intracardiac shunt strongly favors the diagnosis of pulmonary arteriovenous malformations.
* PNEUMOCONIOSES
* Coal workers' pneumoconiosis
* Silicosis
* May evolve to progressive massive fibrosis or conglomerate masses, yielding a radiographic appearance of multiple pulmonary nodules
* These may range in size from 1 to 10 cm and usually are located in the upper lobes
* Calcification and cavitation are unusual, but can occur and raise the possibility of superimposed tuberculosis.

Thrombophlebitis
* Thrombophlebitis represents a spectrum of disease processes and includes:
* Nonspecific, nonsuppurative thrombophlebitis or "bland phlebitis" manifested by pain, tenderness and redness over the vein course
* Nonsuppurative thrombophlebitis caused by infection of an intraluminal thrombus
* Suppurative thrombophlebitis with intraluminal purulent exudate, necrosis of the vein and periphlebitic abscess

Suppurative superficial thrombophlebitis
Epidemiology
Pathogenesis
Pathology
Microbiology
Clinical Manifestations
Diagnosis
Treatment

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Infectious Disease Presentation

Infectious Disease Presentation
Presentation by:Jennifer Coleman
T & C II

Comparison of 20th Century Annual Morbidity and Current Morbidity, Vaccine-Preventable Diseases (pre-1990 Vaccines)
Congenital Rubella Syndrome
Polio (paralytic)
Mumps
Measles
Diphtheria
Smallpox
Annual Morbidity
Comparison of Pre-Vaccine Era
Estimated Annual Morbidity and Current Morbidity,
Vaccine-Preventable Diseases (post-1990 Vaccines)
Meningococcus (invasive)
Influenza (<5 years)
Pneumococcus (invasive)
Hib (invasive)
Hepatitis B (acute)
Hepatitis A
Pre-Vaccine Era Estimated Annual Morbidity
Invalid Contraindications to Vaccination

* Minor illness
* Mild/moderate local reaction or fever following a prior dose
* Antimicrobial therapy
* Disease exposure or convalescence
* Pregnancy or immunosuppression in the household
* Premature birth
* Breastfeeding
* Allergies to products not in vaccine
* Family history (unrelated to immunosuppression)
Varicella
* Chickenpox
* 10-21 day incubation
* Contagious 1-6 days prior to rash until all vesicles are crusted over
o Causes fluid-filled vesicles with elevated temp. and intense itching
* Tx: Antihistamine, antipyretic, ?Acyclovir
* Vaccine – Live virus, 12 months and 4-6 yrs.
Coxsackievirus Infections
* Herpangina – virus
* S/Sx: High temp to 105 for 1-4 days, difficulty swallowing, very sore throat, cough, vomiting, HA, abdominal pain, small, grayish vesicles on tonsils, soft palate and uvula, disappear after temp
* Tx: Analgesics, antipyretics, soft foods, cool liquids

Diptheria
Erythemis Infectiosum
Haemophilus Influenza, Type B
Influenza
Rubeola
* Measles
* Contagious 4 day prior to rash to 4 days after rash starts
o High fever, cough, red rash
o Recognized by presence of Koplik spots on buccal mucosa
* MMR - Live viral vaccine at 12 months and 4-6 yrs.
Epstein Barr virus

* Mononucleosis – Incubation 2-8 wks
* S/Sx: chills, high fever (6 days), HA anorexia, malaise, lymphadenopathy, severe sore throat, petechiae on palate, spleen and liver may enlarge, rash
* Tx: Bedrest with acute stage, force fluids, no contact soports until spleen normal, fatigue up to 6 weeks

Mumps
Pertussis
Pneumococcal infection
Poliomyelitis
Roseola Infantum
Rubella

Streptococcus A
Helpful Websites

* www.vaccinesafety.edu/
* www.vaccineinformation.org/
* www.cdc.gov/nip/default.htm
* www.immunizationed.org/
* www.hibdisease.com
* www.pertussis.com

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Management of the Febrile Infant

Management of the Febrile Infant
Theodore C. Sectish, MD
Director, Residency Training Program in Pediatrics
Assistant Professor in Pediatrics
Stanford University School of Medicine

Fever in Infants
Learning Objectives:

* Fever in infants and outcomes of fever
* Evaluation of the febrile infant
* Modified Clinical Practice Guideline
* Guidelines and Practice
* New considerations
* Management of Fever without Source - 2001

Historical Perspective

* 1967 Occult bacteremia
* 1970s Hospitalization of febrile infants
* 1980s Outpatient management
* 1985 HIB Vaccine
* 1993 Clinical Practice Guideline
* 2000 PCV7 Vaccine
Fever in Practice

Diagnoses: Febrile Infants < 3 months

* URI 35.0%
* Otitis media 16.1%
* Bronchiolitis 8.4%
* Gastroenteritis 7.8%
* Urinary tract infection 4.7%
* Viral meningitis 2.7%
* Bacteremia 1.5%
* Bacterial meningitis 0.3%
* Cellulitis 0.2%
* Osteomyelitis 0.04%

Fever without Source (FWS)

* 20% of all infants <3 years with fever have FWS
* 3% have occult pneumococcal bacteremia
o Of bacteremic infants, 3% have meningitis
o 1 out of 1000!
* Risks of pneumococcal bacteremia in a PCV7 immunized infant is unknown
* Risk reduction estimate once immunized: 90%

Definition of Fever

* 38.00 C
* Rectal measurement
* Unbundled infant
* No recent antipyretics
* No recent immunizations

Bundling and Fever

* Experimental design with controls
* Bundling = 5 blankets and a hat
* 20 bundled infants: mean change + 0.560 C
* 20 infant controls: mean change - 0.040 C
* 2 infants reached 38.0 C, not higher

Febrile Infants: Outcomes of Interest
Serious Bacterial Infection (SBI)

* Urinary tract infection
* Sepsis or bacteremia
* Meningitis
* Bacterial enteritis
* Bone and joint infections
* Pneumonia
Probability of Bacterial Infection in Febrile Infants, <90 Days of Age
Probability of Occult Bacteremia: Febrile Infants, 3 - 36 months
Outcomes of Occult Bacteremia in the Age of Hemophilus
Occult Bacteremia in the Post-HIB Vaccine Era: 3-36 months
* Streptococcus pneumoniae 92%
* Others: 8%
o Salmonella sp
o N meningitidis
o Group A Streptococcus
o Group B Streptococcus
Outcomes of Outpatients with Pneumococcal Bacteremia

* 548 episodes in an ER population
* Treatment strategies varied:
o No antibiotics (N = 73)
o Oral antibiotics (N = 239)
o Parenteral antibiotics (N = 236)

Reevaluation of Outpatients with Pneumococcal Bacteremia
Conclusions
How Do Clinicians Evaluate Febrile Infants?
Evaluation of the Febrile Infant
* Careful history
* Physical examination
* Selected laboratory tests

Evaluation of the Febrile Infant

* Age
* Toxicity
* Decisions to test, to treat, to admit
* Evaluate:
o Vital signs
o Skin color
o Behavior
o State of hydration
* Document carefully and convey a clear picture of the overall clinical appearance of the patient.
* Perform a complete physical exam with particular attention to:
o Skin: for petechiae / purpura, rashes
o Oropharynx: for signs of gingivostomatitis/herpangina
o Pulmonary examination: for occult pneumonia
o Bones, joints and soft tissues: for infection
* Consider the history of fever as correct in all reported measured temperatures

What is “Toxic”?
It is a very difficult task to define “toxic”; the closest I can come to a definition is to say that if to an experienced physician he looks and acts damned sick, he’s toxic.

Definition: “Toxic” Infant
* Lethargy
o poor or absent eye contact
o failure to recognize parents
o poor interaction with persons / environment
* Signs of poor perfusion
* Marked hypoventilation / apnea
* Hyperventilation
* Cyanosis

1993 Clinical Practice Guideline
* Review of literature
* Evidence based
* Outcomes driven
* Consensus opinion

Important Clinical Questions

* Which young infants are at low risk for serious bacterial infection?
* Which older infants deserve empiric antibiotic therapy?

Clinical Practice Guideline
Low Risk Criteria: Clinical Appearance

* Nontoxic appearance
* Previously healthy
* No focal bacterial infection on exam
Otitis media is not considered a focal infection

Clinical Practice Guideline Low Risk Criteria: Laboratory Tests
Guideline: 0 - 28 days
Guideline: 29 - 90 days
Follow-up
Modified Guideline: 3 - 36 months
Modifications to the Guideline
Modified Guideline: 3 - 36 months Options

* Urinalysis or Urine leukocyte esterase + nitrite
* Send urine culture:
o All males <6 months + uncircumcised males <1yr
o Females <1 yr
* Send urine culture if positive urine screening
o Circumcised males 6-12 months
o Females 1-2 yrs

Modified Guideline: 3 - 36 months Options
Follow-up
Guidelines and Practice
Data Support Departures from the Guideline
Adherence Rates with Guideline
Otitis Media Influences Management
Data from Pediatric Practice:the PROS Fever Study
PROS Fever Study: Laboratory Tests
PROS Fever Study: Management
Adherence Rates to Guideline
New Considerations

* Automated Blood Culture Systems
* Band counts - out?
* Importance of UTI
* Fever with Source
o Recognizable Viral Syndromes
Automated Blood Culture Systems
Band Count: Not Discriminatory
Importance of UTI
Recognizable Viral Syndromes
Why Do Clinicians not Adhere to the Clinical Practice Guideline?
Many clinicians disagree with:

* Definition of fever
* Age thresholds
* Applying study data to their practices in which there is better compliance and follow-up
Caveat
Management of Fever Without Source

* Guideline is a place to start
* Need to know IZ status
* UTI: most frequent infection
* Recognize the “toxic” infant
* If you treat, obtain cultures
* Document carefully
* Arrange follow-up
Charles Prober’s Golden Rules

* The younger the infant, the greater the uncertainty
* A toxic appearance demands immediate action
* A non-toxic appearance fuels controversy
* Careful follow-up must be assured
* Recommendations continue to evolve
* No rules are golden

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Fever and Rash

Fever and Rash
Presentation by:Marcellina Mian
Professor of Pediatrics

* Macule: discolored spot (often, but not necessarily red; often, but not necessarily round); blanches
* Papule: raised spot
* Maculopapular: a papule rising from a macule, often red
* Petechia: pinpoint purple/red bruise; does NOT blanch, often in clusters
* Ecchymosis: red/purple bruise, variable size & shape

Definitions
Case #1
Maculopapular rash
Measles
* “Stepwise” high fever
* Cough, coryza, and conjunctivitis
* Rash (exanthem) starts on head & spreads to rest of body
* Koplick spots (enanthem) prior to or at very beginning of rash
* Complications: OM, diarrhea, encephalitis, pneumonia

Koplick Spots
Measles (Rubeola)
* Highly contagious
* Most deadly of all childhood rash/fever illnesses
* Spread by droplets or direct contact with nasal or throat secretions of infected persons
* Incubation period: 8 -12 days
* Prevention: immunization (MMR) just past one year & before kindergarden

Case #2

13-year-old male with:
* fever x two days
* generalized rash
On PE:

* Well & comfortable
* Maculopapular rash
* Postauricular lymphadenopathy

Rubella (German Measles)
* Low grade fever
* Rash:
o starts on face & spreads down body, clearing in same pattern
o Light red spots, fainter than measles
o Lasts 1 - 3 days
* Mild illness, may be missed
* Adults & adolescents may have arthritis or arthralgia
* Complications: encephalitis, neuritis & in pregnancy  Congenital Rubella Syndrome in baby

Congenital Rubella

* Rash
* Cataracts
* CHD (PDA)
* Blindness
* Neurosensory deafness
* Microcephaly & mental retardation

Rubella

* Droplet transmission
* Incubation period: 2 - 3 weeks
* Prevention: Vaccination (MMR)

Case #3

* 15-month-old presents with several days of fever, & rash that looks like this:

Fifth Disease, Erythema Infectiosum
* Parvovirus B19
* Fever, malaise & headache may precede rash by up to 10 days
* “Slapped cheeks” and “lacy, reticular” rash over body that may itch
* No longer infectious once rash develops
* Virus may also cause polyarthropathy syndrome, aplastic crisis, or hydrops fetalis

Hydrops Fetalis

Case #4

* 8-month-old female with fever to 40C for past 5 days
* Baby does not look unwell
* PE reveals no source of fever
* U/A negative
* WBC mildly elevated; mostly lymphocytes
* D/C on acetaminophen
* Next day mother calls to say baby has a rash

Roseola (Sixth disease, Exanthem subitum)
* Peak incidence 6-24 months
* 20% of HHV-6 infections
* Also HHV-7
* Self-limited disease:
o 3-7 days of fever
o Rash follows defervescence
* Febrile seizures in 10-15%
* Occasionally, bulging fontanelle & encephalopathy

Case #5

* 3-year-old boy with fever & irritability x 6 days.
* PE:
o maculopapular rash
o red eyes
o strawberry tongue
o cervical lymphadenopathy

Scarlet Fever

* Group A Strep
* Generalized rash:
o Sandpapery
o Circumoral pallor
o Pastia’s lines

Pastia’s lines
Circumoral pallor
Kawasaki Syndrome Mucocutaneous Lymph Node Syndrome 3 phases:

* Acute: 1-2 wks, fever, etc
* Subacute: 2-4 wks
o After acute signs
* Convalescent: 6-8 wks
o about 4th wk; when clinical signs disappear
o Until ESR returns to normal

Kawasaki Syndrome Mucocutaneous Lymph Node Syndrome
Acute Phase:
Subacute phase
Associated findings:
Kawasaki Syndrome: Coronary aneurysm
Kawasaki Syndrome: Treatment

Case #6
Lyme disease in
Erythema chronicum migrans
* Borrelia burgdorferi transmitted by:
* Ixodes tick
o Ehrlichia, babesia
Lyme Disease: early localized
* Erythema migrans:
Lyme Disease: early disseminated
Lyme Disease: late disseminated

Case #7
Epstein Barr Virus
Infectious Mononucleosis

Case #8
Scarlet Fever
Case #9
Neisseria meningococcemia
Case #10
HSV Stomatitis
Whitlow
Case #11
Hand-Foot-and-Mouth Disease
* Coxsackie A16 & Enterovirus 71
* Oral lesions only: herpangina
* Vesicles on an erythematous base, at posterior pharynx/soft palate
* Commonly presents in spring & summer
* Supportive care

Case #12
* 2-year-old child presents with fever for four days & rash for two days.
* His father, who is visiting from Mexico to harvest strawberries, brought him to a walk-in clinic.

Varicella
* Herpes virus, vaccine preventable
* Incubation period: 14-16 days Prodrome: fever, constitutional symptoms, then rash starting on trunk & spreading to limbs (centrifugal)
* “Dewdrop on a rose petal”
* Vesicles in various states of evolution
* Contagious until all lesions crust over

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Infectious Disorders

Infectious Disorders
Presentation from: Chipola College

Stages of infectious disease
* Incubation period
o Time between the invasion of an organism & the onset of S/S
o 7-10 days (maybe longer depending upon pathogen)
* Prodromal period
o Time between the beginning of nonspecific symptoms & specific symptoms
o Hours to a few days
* Illness
o Specific symptoms are evident
* Convalescent period
o Time between when the S/S begin to fade and a return to full wellness

Chain of infection
* Reservoir
o Place in which organisms grow & reproduce
* Portal of exit
o Method by which organisms leave an infected person’s body to be spread to another individual
o Table 43-1 (blood, respiratory secretions, feces, & exudate from lesions)
* Means of transmission
o Direct contact, indirect contact, fomites (inanimate objects, ex. food, bedding, towels, combs, drinking glasses, etc), insects, or vermin
* Portal of entry
o Means by which a pathogen can enter an individual’s body
o Inhalation, ingestions, breaks in the skin (ex. bites, abrasions, burns)
* Susceptible host

VIRAL INFECTIONS
* Viral exanthems (rashes)
o Exanthem subitum (Roseola Infantum)
+ Rash following a high fever
o Rubella (German measles)
+ Rarely seen because of MMR
+ Important because it can cause serious birth defects
o Measles (Rubeola)
+ Rarely seen because of MMR
+ Occurs with Coryza (rhinitis and sore throat), cough, and conjunctiva
+ Koplik’s spots-whitish spots on the buccal membranes
* Viral exanthems (rashes)
o Chickenpox (Varicella zoster)
+ Will become rare because of mandatory immunization
+ Fluid filled vesicles that crust over, occur in different stages
+ Highly contagious, spread by respiratory droplets as well as contact
o Herpes zoster
+ Same virus as chicken pox but usually occurs in older children/adults
+ Causes painful vesicles along a dermatome
+ May be treated with acyclovir
o Erythema infectiosum (Fifth disease)
+ “slapped cheeks” appearance and a lacy rash
+ Important because it can cause birth defects
o Smallpox (Variola)
+ Important because of bioterrorism
+ People with this are really sick with fever, chills, vomiting, then rash
+ Rash progresses from macule to papule to vesicle to pustule.

VIRAL INFECTIONS
* Enteroviruses
o Coxsackievirus infections
+ Herpangina
o Poliovirus infections: Poliomyelitis
+ Occurs in other parts of the world
+ IPV used now instead of OPV because of immunocompromised people contracting disease shed in stool

Cytomegalovirus

* Common cause of congenital infection in infants
* Some children are asymptomatic for years and then manifest with
o Mental retardation/learning disabilities
o Hearing loss/blindness
* Symptoms evident at birth can include
o Jaundice
o Seizures
o Respiratory distress
o microcephaly
* Therapy is experimental
* Viruses causing central nervous system diseases
o Rabies
* Other viral infections
o Mumps
+ Rarely seen because of MMR
+ Mumps in a teenage or adult man can lead to sterility
o Infectious mononucleosis
+ S/S similar to tonsillitis with sore throat, lymphadenopathy, and fever
+ Spleen is enlarged and fatigue can last ~6 weeks
+ Treat symptoms only

OTHER INFECTIONS
* Scarlet fever
o Group A beta-hemolytic strept
o Often seen with Strept throat
o Usually not seen with “cold” symptoms
o Treated for 10-14 days with antibiotics
* Eye infections/inflammations
o Conjunctivitis (viral or bacterial)
+ Starts in one eye and moves to the other
+ Bacterial…purulent discharge
+ Viral…watery discharge
+ Schools or day care will only believe it is bacterial so treat with antibiotic ointment
+ Highly contagious, can be spread by gnats

OTHER BACTERIAL INFECTIONS

* Anthrax
o Important because of bioterrorism
o Three types, inhalation, cutaneous, & gastro
o Inhalation
+ Most serious, >90% mortality
+ Begins with flu like symptoms
o Cutaneous
+ Begins as a papule and progresses to a painless depressed black eschar
+ Mortality 1% with antibiotic therapy
o Gastrointestinal
+ Acquired by eating undercooked meat infected with anthrax
+ Develops abd. pain, diarrhea; mortality is 25%
o Management
+ Cipro for >18 years, Doxycycline for <18.

* Diphtheria
o S/S
+ Foul nasal discharge, low-grade fever
+ Gray membranes on tonsils and pharynx
+ Neck edema
o Therapeutic management
+ DTaP…rarely seen due to immunization
* Pertussis
o S/S
+ See Box 40-1 pg. 1034
o Therapeutic management
+ DTaP…rarely seen due to immunization
* Lyme disease
o Transmitted by the deer tick
o S/S
+ Papule at the site of the tick progressing to a large swollen ring
+ Systemic involvement
o Therapeutic Management
+ Amoxicillin or PCN V or doxycycline
+ Prevention is the most important tool
* Rickettsial diseases
o Rocky mountain spotted fever
+ Transmitted by the wood, dog, or rabbit tick
+ S/S
# A reddened area develops at the site of the tick bite
# Afterwards, rash, headache, fever, and mental confusion
# CNS involvement
+ Management
# Tetracycline for 7-10 days
# Prevention

OTHER INFECTIOUS PATHOGENS

* Helminthic infections
o Roundworms (Ascariasis)
o Hookworms
o Pinworms

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