Infectious Disease

Front 1

This organism commonly causes pneumonia, meningitis, & bacteremia?

Back 1

Streptococcus pneumoniae

Front 2

What rarely causes endocarditis?

Back 2

Streptococcus pneumoniae

Front 3

This organism is a common cause of GI & urinary tract infections?

Back 3

Escherichia coli

Front 4

Plasmodium species infections?

Back 4

infect RBC & liver cells to cause malaria

Front 5

What organism causes amebic dysentery, liver abscesses?

Back 5

Entamoeba histolytica

Front 6

In order to survive and propagate, a pathogen must do what?

Back 6

1. colonize the host
2. find a nutritionally compatible niche in the host’s body
3. avoid, subvert, or circumvent the host’s innate and adaptive immune responses
4. replicate, using host resources
5. exit and spread to a new host

Front 7

Common Routes of Infectious Disease

Back 7

1. Through the air
2. Through contaminated food or water
3. Through body fluids
4. By direct contact with contaminated surfaces
5. By animal vectors such as insects, bats

Front 8

Agents that cause infectious diseases can be transmitted in several ways:
Through the air – (sneezing, coughing)

Back 8

mycobacterium tuberculosis (pulmonary TB)
Measles
Influenza
Legionnaires Disease

Front 9

Through contaminated food or water –

Back 9

Hepatitis A
E. Coli
Clostridium Botulinum
… and many more

Front 10

Through body fluids

Back 10

HIV, HepB, many others

Front 11

By direct contact with contaminated objects

Back 11

many viruses and bacteria

Front 12

By animal vectors such as insects, bats

Back 12

malaria, rabies, etc.

Front 13

Normal flora

Back 13

organisms that live symbiotically on or in human host but rarely cause disease
Skin – staphylococci, diphtheroids
Oropharynx – streptococci, anaerobes
Large intestine – enterococci, enteric bacilli
Vagina - lactobacilli

Front 14

Host defense mechanisms that serve to inhibit colonization by pathogenic organisms include:

Back 14

mechanical clearance (cilia, mucus, fluid movement, etc.)
phagocytic killing (innate immune system cells)
Colonization (competition) by nonpathogenic organisms

Front 15

Pathogens adapt to evade or overcome these inhibition defenses:

Back 15

Gonococci →avoid urine excretion: adhere to mucosa lining
Pneumococci →resist phagocytosis: encapsulation
Staphylococci →elaborate enzymes (hemolysins): destroys RBC, gaining access to iron

Front 16

Colonization of pathogen? And example?

Back 16

replacement of normal flora with colony of pathogenic bacteria
i.e. Broad-spectrum antibiotic destroying normal GI flora-overgrowth of Clostridium difficile

Front 17

Nosocomially acquired, example?

Back 17

replacement of normal flora occurring in hospital environment
-Often resistant to multiple antibiotics
-Colonization may progress to symptomatic infection
EX: Pseudomonas – life-threatening pneumonia

Front 18

Obligate pathogen

Back 18

isolation from any site is diagnostic

Front 19

Carrier

Back 19

asymptomatic host – transfers infection

Front 20

Opportunistic infections

Back 20

ubiquitous organisms that are not considered human pathogens
-Infects immunocompromised hosts
-Rarely cause disease in an immunocompetent host

Front 21

Emerging Infectious Diseases

Back 21

“Diseases that have recently appeared within a
population, or whose incidence or geographic range is increasing rapidly”

Front 22

For emerging disease to become established, at least 2 events must occur:

Back 22

1. Be introduced into a vulnerable population
2. Must have the ability to spread readily from person to person, cause disease & sustain itself w/in the population

Front 23

Disease can emerge or re-emerge due to:

Back 23

Appearance of a previously unknown agent
(SARS)
Evolution (mutation) of a new infectious agent that cause human disease
(H5N1, H1N1)
Resurgence of endemic diseases
(Malaria, TB)
Acquisition of resistance to anti-microbial drugs
(TB, Gonorrhea)
Deliberate introduction into a population
(Anthrax, Small pox)

Front 24

Factors for Emerging Infections

Back 24

Ecological changes
Dams/irrigation, deforestation/reforestation, flood/drought, climate changes
Human demographic changes and behavior
Population growth & migration, war conflicts, sexual behavior, IVDU
Travel and commerce;
Worldwide movement of people & goods
Technology and industry;
Globalization of food supplies, changes in food packing & processing, tissue/organ transplantation, drugs, overuse of antibiotics
Microbial adaptation and change;
Microbial evolution
& Breakdown of public health measures
Reduction in prevention programs, inadequate sanitation & vector control

Front 25

CDC Recommends a 2-tiered approach:

Back 25

1st tier = standard precautions
Recommended for the delivery of care to all pts

2nd tier = transmission-based precautions
Designed for the mgt of pts known/suspected to be infected

Front 26

1st tier = standard precautions

Back 26

-Recommended for the delivery of care to all pts
-Routine hand hygiene (washing, antimicrobial products)
-Use of appropriate protective apparel
- masks, eye protection, gloves

Front 27

2nd tier = transmission-based precautions

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-Designed for the mgt of pts known/suspected to be infected
-3 defined types of transmission-based precautions:
1) Airborne-organism precautions
2) Droplet precautions
3) Contact precautions

Front 28

Airborne-organisms: “Airborne Transmission occurs by

Back 28

dissemination of either airborne droplet nuclei (small-particle residue {5 um or smaller in size} of evaporated droplets containing microorganisms that remain suspended in the air for long periods of time) or dust particles containing the infectious agent.” CDC.gov

Front 29

Droplet precautions – “Droplet transmission involves

Back 29

involves contact of the conjunctivae or the mucous membranes of the nose or mouth of a susceptible person with large-particle droplets (larger than 5 um in size) containing microorganisms generated from a person who has a clinical disease or who is a carrier of the microorganism. Droplets are generated from the source person primarily during coughing, sneezing, or talking and during the performance of certain procedures such as suctioning and bronchoscopy.” – CDC.gov

Front 30

Contact precautions – “Contact Precautions are

Back 30

designed to reduce the risk of transmission of epidemiologically important microorganisms by direct or indirect contact.”

Front 31

What makes you sick? The pathogen or the host immune response?

Back 31

Normal flora only cause disease if the immune system is weak

With some pathogens like paramyxovirus the immune response damages the tissue (mumps)

For many pathogens like Mycobacterium tuberculosis, if the immune system is too strong or too weak suffer damage whereas those with normal immune responses can be colonized but remain asymptomatic

Front 32

Initial infection

Back 32

-Innate immunity
-Adaptive immunity

Front 33

Innate immunity

Back 33

nonspecific mediators predominate
allowing immediate response to foreign material
Complement, phagocytes

Front 34

Adaptive immunity

Back 34

production of antibodies & stimulation of lymphocytes
Take days

Front 35

Re-infection

Back 35

Protective adaptive immunity

Front 36

Protective adaptive immunity

Back 36

(via initial infection or vaccination):
occurs after initial exposure through memory lymphocytes
& pathogen-specific antibody
More rapid response to re-infection

Front 37

Humoral immunity

Back 37

immunity mediated by monoclonal antibodies that are secreted by B cells

Front 38

Cell-mediated immuninity

Back 38

immunity mediated by CD4 T cells that secrete cytokines and CD8 T cells that directly kill infected cells

Front 39

Innate immunity

Back 39

the rapid less specific response that is mostly mediated by phagocytic cells like macrophages and neutrophils

Front 40

Nonspecific Host Defenses

Back 40

(Innate)
Mechanical: motor activity for movement of mucus and air (peristalsis and ciliary action), protective barrier provided by tight junctions

Chemical: lysozyme, gastric acid, bile salts, defensins, etc

Microbiological: Normal flora in nose, mouth, gut

Front 41

Ex. of mechanical non specific host defense?

Back 41

The transmembrane proteins claudin and occludin form strands that band the epithelial plasma membranes together. This forms a tight seal that completely encircles the endothelial cells and provides a barrier against passive diffusion.

Front 42

Entering and Colonizing the Host

Back 42

- Bacteria that infect the urinary tract resist the washing action of urine by adhering tightly to the epithelium lining the tract via specific adhesins.

Front 43

What happens when microbes get through the physical and chemical defenses?

Back 43

Inflammation initially mediated by the innate immune system in response to microbes usually clears the infection and stimulates the adaptive immune response to guard against future infections.

Bacterial or viral products alert the innate immune system.
-These include bacterial cell wall components (for example: LPS) or bacterial or viral DNA

Front 44

What is inflammation? Is it good or bad?

Back 44

It is a reaction to infection or injury that initiates defense and repair. It results in an accumulation of fluid and leukocytes in the extravascular spaces.

It is good when it eradicates the cause of injury and promotes healing. (examples: neutralization of toxins and microbes, clearance of necrotic cells and debris, promotion of wound healing)

It is bad when it becomes a chronic condition that leads to damage of healthy tissues or when it is so acute that it leads to permanent damage or death.

Front 45

What medication inhibits inflammation?

Back 45

ibuprofen NOT tylenol

Front 46

Signs of Inflammation

Back 46

Redness
Swelling
Heat
Pain
Loss of function

Front 47

Stages of Inflammation

Back 47

1. Initiation
2. Amplification
3. Termination

Front 48

1. Initiation

Back 48

-Increased blood supply to the damaged area.
-Increased vascular permeability and exudation of serum proteins.
-Migration of leukocytes out of the capillaries into the damaged area.

Front 49

2. Amplification

Back 49

Activated immune system cells secrete cytokines and chemokines that amplify the response.

Front 50

3. Termination

Back 50

As toxins, microbes, debris are cleared the response wanes. Direct inhibitory mechanisms are also in place to shut down response.

Front 51

Principal Mediators of Acute Inflammation

Back 51

1. Circulating
2. Soluble Factors
3. Tissue Resident

Front 52

Circulating:

Back 52

Neutrophils
Eosinophils
Basophils
Monocytes

Front 53

Soluble Factors:

Back 53

Cytokines/Chemokines
Complement (lyses cells)
Vasoactive amines (histamine)
Acute phase proteins
Platelet Activating Factor
Arachidonic Acid Metabolites

Front 54

Tissue Resident:

Back 54

Mast cells (release histamine)
Macrophages (release chemokines, phagocytosis)

Front 55

Innate Immunity – Neutrophils

Back 55

Usually first leukocytes that leave circulation and infiltrate site of injury or infection.

Important for phagocytosis of microbes (a process that also usually kills the neutrophil).

Front 56

Neutrophils eject

Back 56

their chromatin to trap bacteria in a sticky web.
-The sticky chromatin can
entrap many different kinds of bacteria,
including (left to right) Staphylococcus
aureus, Salmonella enterica, and Shigella
flexneri.

Front 57

Innate Immunity – Macrophages

Back 57

-Phagocytose microbes.

-Secrete factors that are important in regulating fibroblasts and endothelial cells.

-Secrete inflammatory factors and cytokines that activate other leukocytes.

Front 58

Innate Immunity – Macrophage Killing of Microbes

Back 58

Macrophages engulf bacteria into “phagosomes” that fuse with granules that contain toxins that kill the bacteria. These toxins include hypochlorite (active ingredient in bleach), defensins, hydrogen peroxide, and other toxins.

Front 59

Leukocytes Home to Sites of Infection

Back 59

Release of bacterial peptides (N-FMLP), chemokines from endothelium and resident macrophages, and lipid mediators cause vasodilation, vascular permeability, and expression of adhesion molecules on nearby endothelium

Front 60

Adaptive Immunity

Back 60

Stem cells begin in the bone marrow and are constantly producing T cells and B cells that further differentiate as needed. The memory cells are important for quick eradication of infections the next time the host encounters the same pathogen. A high titer of specific antibodies along with a pool of memory B and T cells will allow for such a quick response that the individual will not even be aware he/she was infected.

Front 61

Adaptive Immunity – CD4 T “Helper” Cells

Back 61

After virus infection, CD4 T cells are activated down different “helper” pathways.

The TH2 cells make cytokines that promote B cells to become plasma cells and secret antibodies.

The TH1 cells make cytokines that promote CD8 T cells to become cytotoxic T cells and directly kill virus-infected cells.

Front 62

Adaptive Immunity – CD8 T Cell Killing

Back 62

CD8 T cells that differentiate into cytotoxic cells (CTLs) kill infected cells by injecting toxic granzymes and other toxic chemicals directly into them. This leaves uninfected tissue intact.

Front 63

Adaptive Immunity – CD8 T Cell Killing

Back 63

CD8 T cells that differentiate into cytotoxic cells (CTLs) kill infected cells by injecting toxic granzymes and other toxic chemicals directly into them. This leaves uninfected tissue intact.

Front 64

Adaptive Immunity – Antibodies

Back 64

Antibodies bind to bacteria, viruses, toxins and neutralize in a variety of ways. Antibodies can prevent colonizaiton, kill bacteria through complement activation or induce phagocytosis by macrophages. They can cause release of histamines and other active compounds from mast cells and eosinophils.

Front 65

B Cells Need Antigen Boosts for Robust Protection

Back 65

This is the principle behind multiple booster shots for many vaccines. Not only is there a higher titer of specific antibody after each round of vaccination but the quality of the antibody also increases and gives much better protection from infection.

Front 66

Adaptive Immunity – Newborn Antibodies

Back 66

Newborns are initially protected by IgG antibodies from their mother that cross the placental barrier.

Breastfeeding allows for IgM and IgA antibodies to help protect the infant until they get their own full protection.

Front 67

Delayed Type Hypersensitivity (DTH)

Back 67

Takes approximately 24 to 48 hours for effector T cells to home to site of microbial challenge, activate macrophages at the site, and induce a detectable reaction.

DTH responses in skin show edema and fibrin deposition, T cell and monocyte infiltrates, and tissue damage caused by activated macrophages.

*This is the response detected in the PPD skin test for individuals with past or present mycobacterial infections.

Front 68

Delayed Type Hypersensitivity (DTH)

Back 68

In an individual previously exposed to an antigen, skin challenge with that antigen elicits a DTH reaction. Histopathologic examination of the reaction shows perivascular mononuclear cell infiltrates in the dermis.




At higher magnification, the infiltrate is seen to consist of activated lymphocytes and macrophages surrounding small blood vessels in which the endothelial cells are activated.

Front 69

Summary of Host Defense

Back 69

1. The innate immune system includes physical barriers such as skin, epithelial layers, mucus, etc. which are in place to prevent pathogen colonization
2. Once a pathogen has gotten past these barriers, inflammation mediated by innate immune cells and their secreted factors kicks in and attempts to eradicate pathogen and activate adaptive response.
3. Adaptive immunity is activated to provide memory response for next encounter with pathogen

Front 70

The following diseases are to be reported by PHIDDO (web-based Public Health Investigation and Disease Detection of Oklahoma) or telephone immediately upon suspicion, diagnosis, or positive test:

Back 70

Anthrax, Hepatitis B duringpregnancy (HBsAg+), Rabies, Smallpox, Measles (Rubeola), Botulism, Meningococcal invasive disease, Tularemia, Diphtheria, Outbreas of apparent Infectious Disease, Typhoid, Viral Hemorrhagic Fever, Plague, HIB , HEp A, Poliomyelitis, HIV, etc...

Front 71

State of Oklahoma requires medical providers and laboratories to report communicable diseases, goals?

Back 71

- Protect & improve public health
- Prevent disease spread
- Eliminate some diseases entirely

Front 72

Spirochetal disease

Back 72

Lyme borreliosis or Lyme disease

Front 73

Rickettsial disease

Back 73

Rocky Mountain spotted fever

Front 74

Zoonotic infections

Back 74

Spirochetal disease
Lyme borreliosis or Lyme disease
Rickettsial disease
Rocky Mountain spotted fever
Plague

Front 75

Reservoirs

Back 75

host in which a microorganism lives & multiplies
Host does not develops the disease
i.e., white-footed mouse, rats, squirrels

Front 76

Vectors

Back 76

usually an arthropod that carries the zoonotic agent from one host to another
i.e., ticks, fleas, mosquitoes

Front 77

Zoonotic Infections: Emerging Infections

Back 77

Increased outdoor activities with increasing contact with animals and disease-spreading vectors
Deforestation
Increasing populations of deer in close proximity to urban areas
Spread of housing to more rural areas
Travel

Front 78

What are spirochetes?

Back 78

Gram-negative
Motile
Cork screw-like bacteria

Front 79

Example spirochete organisms and associated diseases...

Back 79

Treponema pallidum - syphilis
Leptospira interrogans - fever, meningitis, hepatitis
Borrelia recurrentis - relapsing fever
Borrelia hermsii - relapsing fever
Borrelia burgdorferi - lyme disease

Front 80

Lyme Disease

Back 80

Caused by spirochete, Borrelia burgdorferi

Front 81

Where are lyme daises cases concentrated?

Back 81

Cases concentrated in 2 areas:
NE: Mass. to Maryland
Midwest: Wisconsin
West: Northern Calif & Oregon

Front 82

Incidence ages for lyme disease?

Back 82

Incidence by age: 2 peaks:
5-9y (children) & 50-54y (middle-aged adults)

Front 83

How is lyme disease transmitted?

Back 83

Transmitted by nymph Ixodes tick from deer to white-footed mouse to humans
-Tick must attach for 48-72 hours to transmit the spirochete

Front 84

Where does lyme disease begin?

Back 84

Infection begins in the skin (erythema migrans)
Then disseminates throughout the body
Induces immune responses; organisms survive for yrs in joint fluid, CNS, skin of untreated humans

Front 85

What are the 3 stages of lyme disease?

Back 85

Early localized infection/ primary Lyme disease
Early disseminated disease/ secondary Lyme disease
Late disease/ tertiary Lyme disease

Front 86

What is the hallmark of primary lyme disease?

Back 86

Hallmark: erythema migrans
Macular expanding erythemous lesion with central clearing
Begins one month after tick bite
Mean diameter: 15cm
Painless, can cause burning or itching

Front 87

What illness is associated with secondary lyme disease? What other system involvement is there?

Back 87

Dissemination assoc with small annular lesions & flu-like illness
malaise, fatigue, myalgias, intermittent arthraligas
CNS involvment:
Waxing & waning headache, meningitis, Bell’s palsy, peripheral neuritis
Cardiovascular involvement:
AV nodal block (conduction defects)

Front 88

When does the systemic lyme disease develop? What systems are associated?

Back 88

Tertiary Lyme Disease

Systemic disease develops months-years after primary disease
Musculoskeletal complaints are most common
Prolonged arthritis/arthragias
Joint effusions
Neurologic manifestations:
Chronic encephalopathy assoc with mood,cognitive & sleep disorder
Chronic skin infection: acrodermatitis chronica atrophicans
Fibromyalgia or chronic fatigue-like syndrome

Front 89

How do you diagnose Lyme disease?

Back 89

Made by combining history of possible tick exposure, clinical manifestations & serology
ELISA assay detects IgG & IgM antibodies
Western blot analysis is recommended to confirm (+) ELISA tests

Front 90

Lyme disease treatment?

Back 90

Doxycline 100mg PO BID x10d
Patients with other manifestions: Doxycline 100mg PO BID x30d
Alternative: amoxicillin 500mg PO q8h
Rheumatology & neurology consult

Front 91

What abc can you not give to pregnant women because baby teeth will be gray?

Back 91

doxyclycine or any tertracycline

Front 92

Lyme disease prevention?

Back 92

Avoidance of ticks & areas associated with ticks
Inspection
Animals
Fur/skin inspection & tick removal
Repellants
Skin - DEET; Clothing - Permethrin
Vaccination – no longer available

Front 93

What is Rickettsia?

Back 93

Gram negative bacterium
Non-motile
Non-spore forming
Pleomorphic
Obligate intracellular parasites
Cause of typhus and RMSF
One of the closest living relatives to the mitochondrial precursor bacteria

Front 94

What causes RMSF? How?

Back 94

Tick-borne disease caused by Rickettsia rickettsii
Tick vectors: Dermacentor variabilis (dog tick) & Dermatcentor andersoni (wood tick)
-Most common in SE and South central US

Front 95

What is the hallmark of rocky mountain spotted fever?

Back 95

Hallmark: petechial rash beginning on palms & feet

Front 96

Pathogenesis of RMSF?

Back 96

Ticks becomes infected by:
Feeding on blood of infected animals
Fertilization (male to female ticks)
Transovarial (female tick to eggs)
Transmitted from dog or wood tick to humans during feeding (not the Lone Star spotted tick)
Tick must attach for 6-10 hours to transmit the bacterium
bacterium spreads through body via blood & lymphatic system
Incubation period ranges from 5-10 d

Front 97

Vasculitis with tropism for endothelial cells

Back 97

Increased vascular permeability
Causes hemorrhage in skin, GI tract, lungs (pneumonia). heart (myocarditis), pancreas, liver, kidney, skeletal muscle

Front 98

RMSF CP?

Back 98

Difficult to dx in early stages
Patients visit medical provider during 1st week following an incubation period of 5-10 day
Initial s/sxs: fever, N/V, severe headache, malaise, myalgias
Rash appears 2-5d after onset of fever
Flat, pink, non-itchy spots on wrists & ankles, then spread to trunk
-Later s/sxs: rash, abdominal pain, joint pain, diarrhea

Front 99

What is the characteristic symptom of RMSF? And when is it observed?

Back 99

The characteristic red, spotted (petechial) rash of RMSF not seen until 6th day after onset of symptoms

Front 100

Sx of RMSF in severe cases?

Back 100

Aseptic meningitis, conjunctivitis, fundoscopic hemorrhages, acute respiratory distress syndrome

Front 101

RMSF: Host RFs

Back 101

RMSF is a very severe illness & patients often require hospitalization
Risk factors assoc with severe or fatal RMSF:
Advanced age
chronic alcohol abuse
G6PD deficiency (sex-linked genetic condition)

Front 102

RMSF Dx?

Back 102

Made by combining history of possible tick exposure and clinical manifestations
Lab findings: nonspecific
WBC – usually normal
Thrombocytopenia
Serology – indirect immunofluorescent antibody, latex agglutination, ELISA
Skin biopsy – rapid histologic staining using direct immunofluoresent microscope
Sensitive 73%, specific 100%

Front 103

RMSF Tx?

Back 103

Early initiation of antibiotic therapy reduces mortality rate from 20% to 5%
Pt requires O2 or intubation, fluids to prevent dehydration, monitor urine output
Report to public health department
Infectious disease & dermatology consult
Doxycycline 200mg PO BID x3d loading dose, then 100mg PO BID x4d
Alternative: chloramphenicol 125mg IV QID x7d

Front 104

RMSF Cx?

Back 104

DIC
Pulmonary edema
Acute tubular necrosis (ATN)
Shock with myocarditis
Skin necrosis & gangrene
Others: seizures, encephalopathy, peripheral neuropathy, bladder and bowel incontinence, cerebral/vestibular dysfunction

Front 105

What are the 6 stages in the lift cycle of (non-retroviral RNA) viruses?

Back 105

1- Attachment
2- Penetration
3- Uncoating
4- Replication
5- Assembly
6- Release

Front 106

What virus is is a bullet-shaped, enveloped, negative-sense, enveloped, RNA virus?

Back 106

The rabies virus

Front 107

The word rabies is derived from what latin verb?

Back 107

"to rage"

Front 108

Most common animal vectors of rabies?

Back 108

-bats, raccoon, skunks, wolves, and foxes
-Domestic animal immunization = widely practiced in U.S.
-Can be transmitted via any infected carrier

Front 109

Is rabies serious?

Back 109

Life-threatening viral infection of the CNS
Fatal without early & aggressive post-prophylaxis

Front 110

CP of rabies?

Back 110

-Hx of bite
-Pt notes numbness, tingling in bite area
-Nonspecific Sx: HA, Fever, nausea, vomiting
-Various degrees of limb and facial weakness
-Onset of Encephalitis
-Hydrophobic Period

Front 111

Describe the onset of encephalitis in rabies?

Back 111

combativeness, agitation, hallucinations,
muscle spasms, seizure

Front 112

dysphagic drooling, confusion, double vision,
decreased lucidity, involuntary muscle contractions are characteristic of what stage in rabies?

Back 112

Hydrophobic Period

Front 113

When does death occur in rabies?

Back 113

respiratory paralysis

Front 114

When is the incubation period of rabies?

Back 114

-10-365 days
Average: 20-90 days
-No symptoms
-Site of bite, muscle cells

Front 115

When is the prodrome stage of rabies?

Back 115

-2-10 days
-S/S: Nonspecific symptoms, malaise, headache, fever, nausea, vomiting, upper respiratory distress, subtle mental changes (insomnia), pain, itching, tingling at site of bite
-Virus replication in the CNS

Front 116

When and what happens in the acute neurologic stage of rabies?

Back 116

-2-7 days
-Furious or dumb presentation
Furious: Hyperactivity, excitement, disorientation, hallucination, bizarre behavior, hydrophobia, convulsions, aggressive
Dumb (paralytic phase): Lethargy, paralysis, (respiratory)
-Virus replication in brain and transported to other sites (salivary glands and other organs)

Front 117

When and what happens in the coma stage of rabies?

Back 117

-0-14 days
-Patient in coma; respiratory paralysis, cardiac arrest, drop in blood pressure, secondary infections
-Virus replication in brain and transported to other organs

Front 118

What happens once rabies symptoms are present?

Back 118

Once symptomatic rabies is evident,
patients rarely survive

Aggressive intensive care is required but
offers little chance for recovery

Front 119

Rabies Dx?

Back 119

Clinical Dx: Based on history of rabid animal bite
ELISA:
Increase in antibody levels maybe too late to be diagnostic
Definite diagnosis:
postmortem finding of Negri bodies in the brain tissue of presumed rabid animal
Isolation of virus from infected tissue
Rabies virus DNA by PCR

Front 120

Rabies Tx?

Back 120

Post-prophylaxis:
Thorough wound cleaning & debridement
Human anti-rabies immune globulin & human diploid cell vaccine
Pre-prophylaxis for persons at high risk :
(veterinarians, laboratory personnel, cave explorers, human service workers)
Human diploid vaccine at day #1, 3, 7, 14, 28

Front 121

What virus is large, enveloped,
double-stranded DNA?

Back 121

Herpes

Front 122

Primary Zoster infection?

Back 122

Varicella (chicken pox)
Infants & children
Life-long immunity; reside in sensory ganglia in dormant condition

Front 123

Secondary Zoster infection?

Back 123

Herpes zoster (shingles)
Reactivation of dormant virus
Higher incidence in immunodeficient patients

Front 124

How is varicella-zoster spread?

Back 124

Highly contagious
Spread via respiratory droplets & direct contact with infectious lesions
2-3 weeks incubation period

Front 125

Varicella-zoster CP?

Back 125

Often a history of prior exposure to chicken pox or shingles
Chicken pox develops in persons with no prior history of varicella
Minor constitutional symptoms (fever, malaise) followed by eruption of clusters of red macules on trunk & face – rapidly evolve into tiny vesicles on erythematous base
Vesicles become pustular, pruritic, then encrust & scab over

Front 126

Herpes-Zoster (Shingles)?

Back 126

Not as contagious as primary infection, Varicella
Capable of being transmitted to susceptible persons (unvaccinated), causing primary chicken pox

Front 127

Herpes Zoster CP?

Back 127

Pain or pruritis occur prior to rash in the eventual eruption site
Continue during active rash
May recur for variable period after rash disappears (post-herpetic neuralgia)
Rash presents as eruption of clusters of vesicles on erythematous base, found unilaterally along a single dermatome, often on the trunk or face
Ophthalmic zoster = serious corneal damage & visual impairment

Front 128

Varicella-Zoster Dx?

Back 128

Clinical Dx: presentation of rash & history-taking
Microscopy: Tzanck Test: look for multinucleated giant cells with inclusions
Diagnosis support by detection of VZV antigens in skin lesion (increasing sensitivity/specificity)

Front 129

Herpes Zoster DDx?

Back 129

Rashes similar to chicken pox (vesicles presentation):
Impetigo, scabies, coxsackievirus infection, rickettsial pox
Rashes similar to shingles (dermatome presentation):
Contact dermatitis, herpes simplex, linear impetigo lesions

Front 130

Varicella Zoster Tx?

Back 130

Drug of choice: Acyclovir
Herpes zoster: 800mg by mouth 5x daily x7-10d
Chickenpox: 20mg/kg by mouth 4x daily x5d
Supportive treatment for pain/pruritis, good general hygiene to prevent secondary bacterial infection

Front 131

Varicella Zoster Prevention?

Back 131

Children should not return to school until lesions are healed & scabbed over
Lesions are infective until begin to encrust & scab
Vaccination with live attenuated varicella virus
Varicella:
2 doses (12-15mo, 4-6 yrs) - Varivax
Herpes-Zoster:
Adults >60 years
One dose (Zostavax)

Front 132

Varicella Zoster Cx?

Back 132

Secondary bacterial infection
Treatment with topical or systemic antibiotics

Front 133

Epstein-Barr infections?

Back 133

Cause of infectious mononucleosis (“mono”, “kissing disease”)
Heterophile antibody test (+) aka monospot
Transmitted by infected human salvia
Classic manifestation: atypical lymphocytes
in peripheral blood smear
Also connected with development of
several lymphoproliferative diseases
Burkitt’s lymphoma, B-cell leukemia,
Hodgkin’s disease, & nasopharyngeal carcinoma

Front 134

Epstein-Barr CP?

Back 134

Typically seen in young adults
Prodrome: malaise, fatigue, persistent headache
Fever, sore throat, tender lymphadenopathy, splenomegaly
Some cases: rash or jaundice with hepatic involvement

Front 135

Epstein-Bar Dx?

Back 135

CBC: leukocytosis with predominately lymphocytosis & atypical lymphocytes
Liver enzymes: elevated
Positive heterophile antibodies (Monospot test)
Positive test for antibodies to EBV-specific antigen
Dx of Lymphoma: cytohistology of biopsied lymph node tissue

Front 136

Epstein Bar Tx?

Back 136

Self-limiting
Therapy is mainly supportive
Patients in acute stage of infectious mononucleosis:
Avoid contact sports & heavy lifting
Treatment of Lymphoma: depending on stage of disease
radiation therapy, chemotherapy, stem-cell transplantation

Front 137

CMV infection?

Back 137

Acquired congenitally & perinatally, & via sexual transmission
Becomes latent after primary infection & may reactivate years later
Asymptomatic in immunocompetent persons
CMV retinitis = cause of blindness in immunocompromised pts

Front 138

How does CMV present in infants?

Back 138

Infants born with symptomatic CMV:
Premature & retarded intrauterine growth
Petechiae, jaundice, microcephaly, hepatosplenomegaly

Front 139

CMV in immunocompetent adults?

Back 139

Mild mononucleosis-like syndrome

Front 140

Immunocompromised adults with CMV CP?

Back 140

CMV retinitis
CMV pneumonitis: fever, cough, dyspnea, night sweats
GI CMV: ulceration, bleeding, N/V, abdominal pain, bloody stools
CMV meningoencephalitis

Front 141

What disease are "Owl Eye Cells" in the cytohistology diagnostic for?

Back 141

CMV; Serology
Cytohistology: look for
CMV nuclear inclusions “Owl eye cells”

Front 142

CMV Tx?

Back 142

Drug of choice: Ganciclovir 5mg/kg IV bid
x 2-3week, then maintenance 6mg/kg daily
Prevention: CMV Immunoglobulin

Front 143

Toxoplasma gondii

Back 143

Toxoplasmosis

Front 144

Prevalence of toxoplasmosis?

Back 144

22.5% of U.S. population 12yr and up is infected
up to 95% of other populations throughout world
rampant in hot/humid/low altitude climates

Front 145

Modes of toxoplasmosis transmission?

Back 145

Foodborne – tissue cysts in undercooked/raw meat
unwashed vegetables

Zoonotic – cats
(ingestion of sporulated oocytes from feces)


Congenital - mother to unborn child

Front 146

Toxoplasmosis clinical manifestation in normal adults?

Back 146

Normal (Healthy) Individuals
Asymptomatic (80-90%)
Mild Flu like symptoms for few weeks
Fever & self-limiting lymphadenopathy (mono-like)

However, parasite remains in tissue – latent
Tissue cysts can get reactivated with immunosuppression

Front 147

Toxoplasmosis CP in immunocompromised?

Back 147

Immunocompromised Patients

In advanced AIDS, 12-month incidence of Toxoplasmosis was 33% among toxoplasma-seropositive patients who were not on prophylaxis or ART
Occurs primarily in patients with CD4 counts of <200 cells/µL

Focal encephalitis with headache/confusion or motor weakness and fever
Focal neurologic abnormalities may progress to seizures/
altered mental status/coma
Dissemination may occur (rare) with chorioretinitis/pneumonia/
other organ involvement

Front 148

Toxoplasmosis CP in pregnant women?

Back 148

Pregnant Women
If new infection for pregnant women there can be severe consequences for unborn baby: miscarriage/stillborn/chorioretinitis/
microcephaly/jaundice
Risk to fetus: gestational age when maternal infection occurs
1st trimester: 15% transmission: severe consequences
3rd trimester: 60% transmission: milder consequences

Infants infected at birth sometimes show no symptoms until later in life:
mental retardation, seizures, visual defects, spasticity

Front 149

Dx toxoplasmosis?

Back 149

Diagnosis:
Compatible clinical syndrome + serological testing

Lumbar puncture to rule out cryptococcal or syphilis infection

PCR can detect toxo in amniotic fluid
Imaging
CT Scan/MRI of brain – look for multiple ring enhancing lesions
PET Scan – differentiate between toxoplasmosis and primary CNS lymphom

Front 150

Tx of toxoplasmosis?

Back 150

Treatment only recommended immunocompromised/pregnant patients.


Treatment for Acute:
Pyrimethamine – anti-malarial medication
Sulfadiazine – antibiotic


Spiramycin – antibiotic given to pregnant women to prevent infection of child

Front 151

Prevention of toxoplasmosis?

Back 151

Avoid eating raw meat, unpasteurized milk, uncooked eggs; wash hands after handling raw meat

Wash vegetables

Little or no gardening; wash hands after handling soil

Avoid contact with kitty litter

Patients with CD4 count <200: prophylaxis
Pyrimethamine-Sulfadiazine
Trimethoprim-Sulfamethoxazole

Front 152

Malaria; agent, prevalance, source, invasiveness?

Back 152

Etiological Agent: Plasmodium vivax, P. ovale, P. falciparum, P. knowlesi and
P. malariae

Prevalence: endemic to the tropics and subtropics

Source: Anopheles mosquito

Invasiveness: Blood , liver,
P. falciparum can cause cerebral malaria

Front 153

Malaria Transmission?

Back 153

1. Mosquito ingests parasite
2. Sporozoites mature
3. Transfer to human
4. Incubation – 8-60 days


1. Sporozoites invade 2. hepatocytes
2. Mature as tissue schizonts
3. Schizonts rupture
4. Invasion of RBCs (modified parasite)
5. Multiplication/Rupture RBCS (hide from immune system)
Timeframe - 48hrs
6. Cycle: Invade, multiply, rupture

Front 154

CP of malaria?

Back 154

Cyclical 3-Stage Attacks:

Cold Stage: shaking chills
Hot Stage: fever
Sweating Stage: diaphoresis

Patients fatigued between attacks
Release of cytokines and tissue necrosis factors =
headache, fatigue, dizziness, GI complaints,
muscle/joint pain, backache, dry cough

Front 155

More sever CP of Malaria?

Back 155

P. Falciparum infection = more severe

Cerebral malaria
Hyperpyrexia
Hemolytic anemia
Non-cardiogenic pulmonary edema
Acute tubular necrosis
Adrenal insufficiency
Cardiac dysrhythmia

Front 156

Dx of Malaria?

Back 156

Travel History, Symptoms, Blood Smear

Blood films stained with Giemsa or Wright - examined at 8hr intervals for 3 days during and between attacks. Percentage of infected RBCs – 5-20%

During attacks leukocytosis or leucopenia may develop

Severe infections: hepatic changes, hemolytic jaundice,
thrombocytopenia, anemia, reticulocytosis

Antibodies appear 8-10 days later – too late for diagnosis, persist for 10yrs

Front 157

Factors to consider when treating malaria?

Back 157

1 – the infecting Plasmodium species (will be more severe)

2 – clinical status of the patient (complicated or uncomplicated; is it life-threatening or not)

3 – geographic location where infection acquired = drug resistance

Front 158

Tx for severe malaria?

Back 158

Severe Illness:
Quinine or quinidine + doxycycline or clindamycin or tetracycline
or chloroquine + doxycycline or clindamycin or tetracycline

Front 159

Alternative drug Tx for malaria?

Back 159

If chloroquine resistance suspected –
Malarone, mefloquine, hydroxychloroquine,
Atovaquone/doxyclyine or other combos

Front 160

Prognosis for malaria?

Back 160

Good if treated except for P. falciparum infections =
14-17% mortality with treatment

Front 161

Malaria Prevention?

Back 161

1- Reduce Risks of Exposure
Clothing, repellant, spraying, barriers (nets)

2- Vaccine (RTS,S) – 50% effective – phase 3 clinical trials in Africa

Front 162

Malaria prevention for travelers?

Back 162

Chemoprophylaxis: recommended for travelers
Chloroquine – both for prophylaxis and treatment
Well tolerated, safe in pregnancy
Can cause transient side effects (GI, headache, dizziness, hives, malaise) –
Take with meals and give in divided doses 2x/week rather than daily

Front 163

Roundworm types?

Back 163

Enterobiasis (Pinworms)
Hookworm
Ascariasis
Trichinosis

Front 164

Tapeworm types?

Back 164

Cysticerosis

Front 165

“Itchy Buns Sucky Thumbs Syndrome”

Back 165

Pinworms (Enterobiasis)

Front 166

What is the etiological agent for pinworms and what is its host?

Back 166

Enterobius vermicularis – humans only host

Front 167

What is the prevalence of pinworms?

Back 167

worldwide distribution, children most often infected

Front 168

How is pinworms spread?

Back 168

eggs transmitted on food, hands, drink, fomites –
contaminated bedding, clothing

Front 169

CP of pinworm

Back 169

Many patients are asymptomatic

Perianal pruritus (crawling sensation worse at night)
Insomnia, weight loss, bed wetting, irritability

Migration can cause vulvovaginitis, diverticulitis, appendicitis, cystitis and granulomatous reactions

Front 170

What can be detected by eggs can be captured on a piece of cellophane tapeover the perianal skin
3 tries over 3 consecutive nights is 90% successful

Back 170

Pinworm

Front 171

Tx of pinworm?

Back 171

Treatment: albendazole or pyrantel
Single dose and then repeated 2-4 weeks later

Note: All members of household should be treated concurrently

Front 172

Prevention of pinworm?

Back 172

Hand washing after defecation and before meals must be stressed.
Linens should be washed thoroughly
Discourage children from sucking their fingers!

Front 173

Intestinal roundworm agent?

Back 173

Hookworm (Ancylostoma duodenale  & Necator americanus)

Front 174

Roundowrm prevalence?

Back 174

Uncommon in U.S (Sporadic in southeast);
endemic in moist tropics/subtropics
25% worldwide population infected

Front 175

Source of round worm?

Back 175

soil contaminated with human feces – humans only host (“Night soil” )

Front 176

What is the invasiveness of the roundworm (hookworm)?

Back 176

: skin, bloodstream, heart, lungs, small intestine

Front 177

Hookworm pathophysiology in body?

Back 177

Larvae penetrate the skin, carried
by the blood to the pulmonary capillaries,
where they destroy alveoli and are carried
by cilia to the mouth. Once swallowed,
larvae attach to the small bowel mucosa
and suck blood. Mature female worms
lay eggs, which are then eliminated
from body.


Light infection = 1000eggs/g feces
Moderate infection = 2000-8000 eggs/g feces

Front 178

What it ground itch? WHat is it a sign of?

Back 178

at site of penetration,
erythematous dermatitis and/or vesicular rash

Hookworm

Front 179

What is the Pulmonary stage, and what is it a CP of?

Back 179

coughing, wheezing, blood tinged sputum, low grade fever

Hookworm

Front 180

What is in the Intestinal Stage and what is it a CP of?

Back 180

Light Infection: may be asymptomatic with adequate iron intake
Heavy Infection: anorexia, diarrhea, pain, ulcer like epigastric symptoms
Severe Infection: anemia, protein loss, and malabsorption

Front 181

Dx of hookworm?

Back 181

eggs in feces, stool positive for occult blood
Hypochromic microcytic anemia (small pale RBC) and eosinophilia may be found

Front 182

Tx of hookworm?

Back 182

Pyrantel or albendazole (preferred) (1x per day for 2-3 days)

Front 183

Supportive Tx of hookworm?

Back 183

high protein diet, vitamins, and ferrous sulfate

Front 184

Hookworm prognosis?

Back 184

Cure rate of 95%
Egg reduction rate of 99%

Front 185

Prevention of hookworm?

Back 185

Community control is challenging in developing countries
Sanitation programs
Avoid bare feet, Improved footwear

Front 186

What is the agent of "giant intestinal roundworm?

Back 186

Ascaris lumbricoides – “giant intestinal roundworm”

Front 187

Prevalence of ascariasis?

Back 187

worldwide – tropical/subtropical – inadequate sanitation, uncommon in the U.S

Front 188

Source of contamination for ascariasis?

Back 188

: contact with contaminated feces – contaminated vegetables, direct hand to mouth

Front 189

Invasiveness of ascariasis?

Back 189

small intestine – bloodstream - lungs

Front 190

“Erratic ascariasis”

Back 190

adult worms can migrate to vital organs where they don’t normally go – liver, brain, lungs. Can occur because of fever, anesthesia and some medications.

Front 191

larval stage of ascariasis?

Back 191

cough, fever and pneumonia-like symptoms.

Front 192

adult stage of ascariasis?

Back 192

symptoms are related to the amount of worm load.
can be asympotmatic – few worms.
heavy infections can produce a bolus - can
block the intestine or cause a twisting of the bowel.

Front 193

Dx of ascariasis?

Back 193

Complete blood count - eosinophilia
Stool exam

Front 194

Tx for ascariasis? Preffered Tx for pregnant women?

Back 194

Albendazole - - 3 day course


Pyrantel is the preferred medication for pregnant patients

Front 195

Prognosis of ascariasis?

Back 195

Most people recover with or without treament
Complications arise from worm migration

Front 196

Agent of trichinosis?

Back 196

Trichinella Spiralis

Front 197

Prevalence of trichinosis?

Back 197

Trichinosis is a common infection worldwide, but is seldom seen in the United States because of strict rules regarding the feeding of domestic animals and meat-processing inspections.

Front 198

Source of trichinosis?

Back 198

humans are incidental hosts, caused by eating larvae cysts
primarily from pork (where pigs eat uncooked garbage)

Front 199

Invasiveness of trichinosis?

Back 199

intestines, bloodstream, lungs, brain
muscle tissues- including the heart and diaphragm

Front 200

MC CP of trichinosis?

Back 200

“Most infections with Trichinella are asymptomatic…”

Front 201

CP heavy infection trichinosis?

Back 201

diarrhea, abdominal pain, vomiting during intestinal phase
follow by fever, periorbital edema, subconjunctival hemorrhages & chemosis
muscle pain, swelling & weakness are common

Front 202

Death and trichinosis?

Back 202

myocarditis, encephalitis, pneumonia

Front 203

Dx of trichinosis?

Back 203

Complete Blood Count: leukocytosis with marked eosinophilia
Elevated Creatine Kinase (CPK)
Elisa: antibodies to trichinella







Muscle Biopsy: definitive diagnosis look for coiled trichinella larvae

Front 204

Tx for trichinosis?

Back 204

Albendazole
Effective for treating intestinal worms
Goal: prevent systemic invasion
Ineffective against muscle larvae

Front 205

Tx for tissue invasion in trichinosis?

Back 205

Bed rest, analgesics, antipyretics
Prednisone for severe myocarditis

Front 206

Prevention of trichinosis?

Back 206

cook meat >160F until browned (no pink flesh)
Freezing: 5F x20d or -10F x10d or -20F x6d

Front 207

Agent of Cysticerosis?

Back 207

Taenia solium

Front 208

Disease caused by Taenia solium?

Back 208

Taeniasis – eggs hatch, larvae released into stomach and
become worms
Cysticercosis – larvae can penetrate and eventually encyst in
various tissues

Front 209

Prevalence of cysticerosis?

Back 209

common in developing countries, rare in the U.S.

Front 210

Source of taenia solium?

Back 210

eggs from contaminated food – pork, fruits, vegetables

Front 211

Invasiveness of cysticerosis?

Back 211

muscles, brain, heart, eye, spine

Front 212

CP of cysticerosis?

Back 212

Adult intestinal worms rarely cause symptoms
Symptoms develop after many years when larvae die, causing increased inflammation

Front 213

CP of neurocysticerosis?

Back 213

Seizures, chronic headache,
hydrocephalus, & meningitis

Front 214

Dx of cysticerosis?

Back 214

CT-head or MRI-brain:
preferred diagnostic study look for cerebral edema, ring enhancing lesions

Cerebral Spinal Fluid:
lymphocytes, eosinophilia, low glucose level & high protein level

ELISA: antibodies against Taenia

Front 215

Tx and prevention of cysticerosis?

Back 215

Dilantin (phenytoin): to control seizures

Prednisone: to reduce edema & inflammation

Albendazole: 400mg per day x15d (controversial)
Kills living cysts
Death of larvae may cause inflammation & edema = may exacerbate symptoms

Prevention: proper cooking of meat & avoidance of fecal-oral transmission routes

Front 216

When to not use albendazole in cysticerosis?

Back 216

MRI 2 or fewer cysts don’t use albendazole. Surgery may be an option.

Front 217

Parasites differential Dx?

Back 217

Diarrhea:
If it lasts for more than a week this may warrant checking for parasites

Eosinophilia: adults >500/ul of blood (0-5% normal)
Parasitic infections are one of the main causes of eosinophilia.
(Also causes eosinophilia…Asthma, atopic derm. )

Fecal Exam: Ova and Parasite Test (O&P)


History: The right questions may be your best tool for diagnosis!
Travel? Food/Water Sources? Pets?

Diarrhea:
If it lasts for more than a week this may warrant checking for parasites

Eosinophilia: adults >500/ul of blood (0-5% normal)
Parasitic infections are one of the main causes of eosinophilia.
(Also causes eosinophilia…Asthma, atopic derm. )

Fecal Exam: Ova and Parasite Test (O&P)

History: The right questions may be your best tool for diagnosis!
Travel? Food/Water Sources? Pets?

Front 218

26 yr old female – 8 weeks pregnant

Asymptomatic, however routine blood work reveals history of recent infection
IgG (249 IU/ml) (normal = 0-6 IU/ml)
IgM (160 IU/ml) (normal = 0-10 IU/ml)

What questions would you ask this patient?

Back 218

Cats?


Dx: Toxoplasmosis
-PCR of amniotic fluid was positive for the parasite
Tx: Spiramycin – 1g – 3 times a day for remainder of pregnancy
Healthy baby girl

Front 219

A 54 year old man who resided in Franklin County, TN.

Symptoms: 3-week history of diaphoresis, fever, weakness, tachycardia, diarrhea, an 8-pound weight loss, and dry cough. Laboratory testing indicated an elevated white blood cell (WBC) count with 33% eosinophils, hyponatremia, elevated lactate dehydrogenase and elevated creatine kinase.

What questions would you ask this patient?

Back 219

Pt reported reported eating 2 pounds of bear meat
Dx; Trichinosis
-Remaining bear meat looked at
Tx: Albendazole

Front 220

A 36 year old woman living in southern California.

Symptoms: seizures, fever, headache, confusion, black outs

MRI result:

Back 220

Dx: Neurocystercosis
F/U ELISA= positive for T. Solium
Tx: Albendazole 800mg twice 3-7 days and anti-epileptics

Front 221

Etiology of Diptheria?

Back 221

gram+ bacillus, Corynebacterium diphtheria
Diphtheria toxin causes progressive deterioration of myelin sheaths in central & peripheral nervous systems

Front 222

Epi of Diphtheria?

Back 222

1920’s: 200 cases per 100,000 population
1980-1996: 45 cases in total/US population
Former Soviet Union: increase in incidence: >150,000 cases beginning in 1990

Front 223

What causes respiratory diphtheria?

Back 223

Caused by toxin-producing strains of C.diphtheriae
Incubation 2-5 days after infection

Front 224

What causes cutaneous diphtheria?

Back 224

Caused by toxigenic or nontoxigenic strains
Causes chronic nonhealing sores or shallow ulcers with dirty gray membranes
Less severe than respiratory

Front 225

Transmission of diphtheria?

Back 225

Direct person-person physical & respiratory contact

Front 226

Is resp dipt droplet or airborne?

Back 226

droplet

Front 227

-Neck swelling in severe disease “bull neck”
-Sore throat, low grade fever, adherent gray membrane on tonsils, pharynx, or nose

Back 227

Diphtheria

Front 228

Cx of Diphtheria?

Back 228

Myocarditis, polyneuritis, airway obstruction

Front 229

Dx of diphtheria?

Back 229

Culture, special media

Front 230

Tx of diphtheria?

Back 230

Severe cases – antitoxin
Erythromycin: 40 mg/ kg/ day x14 days

Front 231

Diphtheria vaccination?

Back 231

DTaP = diptheria/tetanus toxoids/acellular pertussis
5 doses of DTaP vaccine – 2mo, 4 mo, 6mo, 15-18mo, 4-6yrs
Adult- booster shot every 10yrs
Adverse reactions
- Injection site erythema, induration (swelling)
- Fever & systemic symptoms uncommon

Front 232

Tx of tetanus?

Back 232

Tetanus immunoglobulin IV or IM
Metronidazole IV x10days
Muscle relaxers - Diazepam

Front 233

Tetanus vaccination?

Back 233

5 doses of DTaP vaccine – 2mo, 4 mo, 6mo, 15-18mo, 4-6yrs
Adult- booster shot every 10yrs

Front 234

Eti of pertussis?

Back 234

Bordetella pertussis
Gram negative coccobacillus bacterium

Front 235

Pathogensis of pertussis?

Back 235

Bordetella pertussis transmitted via respiratory droplets (base through the air as opposed to in the air)
Organism adheres to ciliated epithelium of nasopharynx, bacterial proliferation into lower respiratory airways
Highly contagious, 90% of susceptible household contacts develop disease following contact
Incubation 7-10 days

Front 236

CP Pertussis? (3 Stages)

Back 236

3 stages
Catarrhal: rhinorrhea, occasional cough 1-2 weeks
Paroxysmal: on/off forceful continuous cough followed by whoop; 1-6 weeks duration
Convalescent: gradual resolution, weeks to months

Front 237

Dx of pertussis?

Back 237

Clinical diagnosis: consider in all children presenting w cough >14days
Bacterial culture
PCR testing

Front 238

Clinical criteria for pertussis Dx?

Back 238

A cough illness lasting at least 2 weeks with one of the following: paroxysms of coughing, inspiratory "whoop," or posttussive vomiting, without other apparent cause (as reported by a health professional).
This clinical case definition is appropriate for endemic or sporadic cases. In outbreak settings, a case may be defined as a cough illness lasting at least 2 weeks (as reported by a health professional).

Front 239

Laboratory Dx for Pertussis?

Back 239

Isolation of Bordetella pertussis from clinical specimen
Positive polymerase chain reaction (PCR) for B. pertussis

Front 240

Pertussis Tx?

Back 240

Supportive care: hospitalization, avoid cough triggers, fluid & nutritional management
Antimicrobial therapy: may shorten duration & decrease transmission
Erythromycin, or clarithromycin or azithromycin

Front 241

Pertussis vaccination?

Back 241

5 doses of DTaP vaccine – 2mo, 4 mo, 6mo, 15-18mo, 4-6yrs
Adult- booster shot every 10yrs

Front 242

HiB Eti?

Back 242

Haemophilus influenzae serotype b
Aerobic gram – bacteria, polysaccharide capsule

Front 243

Epi of HiB?

Back 243

Due to routine use of the Hib conjugate vaccine since 1990, the incidence of Hib disease in infants and young children has decreased by 99% to fewer than 1 case per 100,000 children under 5 years of age. In the United States, Hib disease occurs primarily in underimmunized children and among infants too young to have completed the primary immunization series. In developing countries, where routine vaccination with Hib vaccine is not widely available, Hib remains a major cause of lower respiratory tract infections in infants and children.

Front 244

Pathogenesis of HiB?

Back 244

Transmission: direct contact with respiratory droplets
Invasion of nasopharynx, may invade bloodstream with subsequent seeding of other organs

Front 245

HiB Prevalance?

Back 245

Accounted for ~50-65% of meningitis cases in prevaccine era
Hearing impairment or neurologic sequelae in 15-30% of meningitis cases
Case fatality rate: 2-5% despite effective antimicrobial therapy

Front 246

Invasive disease caused by Haemophilus influenzae type b can affect many organ systems. The most common types of invasive disease are:

Back 246

Meningitis
Epiglottitis
Pneumonia
Septic arthritis
Occult febrile bacteremia
Osteomyelitis
Cellulitis

Front 247

Tx of HiB?

Back 247

Antibiotics, such as cefotaxime, ceftriaxone, or ampicillin with chloramphenicol, are generally used to treat serious infections. Rifampin is used in some circumstances as preventive treatment for persons who have been exposed to Hib disease.

Front 248

HiB vaccination?

Back 248

4 doses (2mo, 4mo, 6mo, 12-15mo*)
Children over 5 usually do not need.
Older adults/children = sickle cell, HIV/AIDS, removal of spleen, BM transplant or chemotherapy patients

Front 249

Eti of poliomyelitis?

Back 249

Enterovirus, 3 Poliovirus serotypes: 1,2,3

Front 250

Epi of poliomyelitis?

Back 250

1952: 57,628 cases in US
1979: last reported cases of naturally-occurring polio in US
Found among Amish community that refused vaccination
1991: last case of poliovirus in the Western Hemisphere in Peru

Front 251

Polio path?

Back 251

Polio Virus enters through mouth & replicates w/in GI tract
Enters blood & spread to CNS
Destroys motor neuron cells

Front 252

CP of Polio?

Back 252

Asymptomatic in up to 95% of pts infected w polio
4-6% will have flu-like symptoms w complete resolution
<1% result in permanent paralysis of limbs
Fever, headache and muscle stiffness in infection stage
Tightness in neck, back, and hamstring muscles
Severe damage to motor neurons
Permanent weakness or paralysis

Front 253

Polio vaccination?

Back 253

Inactivated polio vaccine
Used in US since 2000
>90% immune after 2 doses
>99% immune after 3 doses
4 doses (2mo, 4mo, 6-18mo, 4-6 years)

Front 254

Eti of measles?

Back 254

Paramyxovirus
Rapidly inactivated by heat & light

Front 255

Epi of measles?

Back 255

2010 global figures
299,201 reported cases
164,000 estimated deaths (2008)      
85% estimated MCV coverage      
65% of countries reached >=90% MCV coverage

Front 256

What disease is Transmitted via respiratory droplets
Contagious 4 days before to 4 days after rash onset
Incubation period 10-12 days ?

Back 256

Measles

Front 257

What disease has a CP of Prodrome
Increasing fever (can be high)
Cough, coryza, conjunctivitis
Koplick spots?

Back 257

Measles

Front 258

What is the measles rash like

Back 258

Developed 2-4 days after prodrome
Maculopapular, erythematous rash
Starts on scalp line & descends
Lesions may become confluent
Persists 5-6 days

Front 259

Cx of measles?

Back 259

20% of cases develop Complications:
Pneumonia
Otitis media
Diarrhea
Subacute sclerosing pan-encephalitis

Front 260

Measles vaccination

Back 260

Combination measles, mumps, rubella (MMR)
2 doses (12-15mo, 4 -6years)
Ninety-five percent of those who receive the MMR or monovalent measles vaccine at 12 months of age or older are immune after the first dose. After the second dose, 99.7% of those immunized are protected. Immunity is lifelong.

Front 261

Eti of mumps?

Back 261

Paramyxovirus
Incubation period: 14-24 days

Front 262

Epi of mumps?

Back 262

1941: 250 cases/ 100,000 people
1968: 76 cases/ 100,000 (start of vaccine)
1985: 1.1 cases/ 100,000
2006 outbreak: 6584 cases
2009 outbreak: 1,5 21 cases

Front 263

Pathogenesis of mumps?

Back 263

Transmitted by droplets of saliva or mucus from an infected person, usually when the person coughs, sneezes, or talks
Contagious 1-7 days before onset of parotid swelling to 9 days after onset
Specific painful enlargement of salivary glands

Front 264

CP of mumps?

Back 264

Fever, headache, fatigue, inflammation of salivary glands

Front 265

Meningitis, orchitis, spontaneous abortion, deafness
are complications of what disease?

Back 265

mumps

Front 266

Mumps Dx?

Back 266

Serology: IgM antibody w/in 5 days of illness onset
Swab from parotid duct or other affected salivary gland (PCR done from swabs)
If IgM is negative: second specimen should be obtained 2-3 weeks after onset of illness
Negative tests should not be used to rule-out mumps

Front 267

Tx mumps?

Back 267

Symptomatic
Acetaminophen (Tylenol) or ibuprofen for pain
Cold or hot compresses
Avoid fruit juice, acidic foods

Front 268

Vaccination for mumps?

Back 268

MMR
2 doses (12-15mo, 4-6 years)

Front 269

Also called “3-day measles” and “German Measles”

Back 269

Rubella

Front 270

Eti of Rubella?

Back 270

Togavirus, RNA virus
Rapidly inactivated by chemical agents, UV light, low pH & heat

Front 271

Epi of rubella?

Back 271

1964-1965: 12.5 million cases in US
11,000 miscarriages, 12,000 infants born with congenital rubella syndrome
2004 the CDC announced that both the congenital and acquired forms of rubella had been eliminated from the U.S.

Front 272

Path of rubella?

Back 272

Transmitted via direct contact w nasopharyneal secretions & crosses placental barrier
Contagious 7 days before & 5-7 days after rash onset

Front 273

CP of rubella?

Back 273

Prodrome of low grade fever
Lymphadenopathy in second week
Maculopapular rash 14-17 days after exposure

Front 274

Rubella Cx?

Back 274

Congenital Rubella Syndrome
Deafness
Cataracts
Heart defects
Microcephaly
Mental retardation
Arthralgia
Adults: up to 70%
Children: rare
Miscarriage

Front 275

Rubella vaccination?

Back 275

MMR
2 doses (12-15mo, 4-6years)
All unvaccinated women of child-bearing age

Front 276

Eti of pneuomococcal?

Back 276

Streptococcus pneumoniae
Gram positive bacteria
Polysaccharide capsule : important virulence factor

Front 277

Epi of pneumococcal?

Back 277

Leading cause of bacterial meningitis <5years of age
>700 cases of meningitis/year
13,000 cases of bacteremia
5 million cases of otitis media

Front 278

Path of pneumococcal?

Back 278

Transmitted via respiratory secretions via human carriers

Front 279

Clinical syndromes of pneumococcal?

Back 279

Pneumonia
Bacteremia
Meningitis
Otitis media

Front 280

CP of pneumococcal?

Back 280

Abrupt onset
Fever with shaking chills
Pleuritic chest pain, Productive cough
Dyspnea, tachypnea, hypoxia

Front 281

Pneumococcal pneumonia?

Back 281

~175,000 hospitalizations/year in the US
Up to 36% of adult community-acquired pneumonia & 50% of hospital-acquired pneumonia
Common bacterial complication of influenza & measles
Case-fatality rate: 5-7% higher in elderly

Front 282

Pneumococcal bacteremia

Back 282

>50,000 cases/year in the US
Rates higher among elderly & very young infants
Case-fatality rate: 20%; up to 60% among the elderly

Front 283

Pneumococcal meningitis

Back 283

~3,000-6,000 cases/year in the US
Case-fatality rate: 30%; up to 80% in the elderly
Neurologic sequelae common among survivors
Increased risk in pts with cochlear implants

Front 284

Pneumococcal Disease in Children

Back 284

Most common clinical presentation: Bacteremia w/o known site of infection
Streptococcal pneumoniae = leading cause of bacterial meningitis among children <5 years of age
Highest rate of meningitis among children <1 year of age
Common cause of acute otitis media

Front 285

2 diff types of pneumococcal vaccines?

Back 285

pneumococcal conjugate vaccine (PCV13)
pneumococcal polysaccharide vaccine (PPSV)

Front 286

Pneumococcal Conjugate Vaccine (PCV13)

Back 286

Highly immunogenic in infants & young children, including those with high-risk medical conditions
97% effective against invasive disease caused by vaccine serotypes
73% effective against pneumonia
7% reduction in all episodes of acute otitis media

Front 287

Pneumococcal Conjugate Vaccine (PCV13)Recommendations

Back 287

All children <24 months of age
Unvaccinated children 24-59 months with a high-risk medical condition
4 doses (2mo, 4mo, 6 mo 12-15mo)
1st dose as early as 6 weeks
Minimum interval of 4 weeks between 1st 3 doses
At least 8 weeks between dose 3 & dose 4

Front 288

Pneumococcal Polysaccharide Vaccine (PPSV)

Back 288

Purified pneumococcal polysaccharide (23 types)
Not effective in children < 2years old
60-70% effective against invasive disease
Less effective in preventing pneumococcal pneumonia

Front 289

Pneumococcal Polysaccharide Vaccine
(PPSV) Recommendations

Back 289

Adults >65 years of age
Children >2 years of age with:
Chronic illness
Anatomic or functional asplenia
Immunocompromised
Environments or settings with increased risk

Front 290

Eti Neisseria meningitidis

Back 290

Neisseria meningitidis
Aerobic gram – bacteria
At least 13 serogroups based on characteristics of the polysaccharide capsule

Front 291

Path of meningitis?

Back 291

Organism colonizes nasopharynx
May invade bloodstream & cause infection at distant sites
Antecedent upper respiratory tract infection may be contributing factor

Front 292

Transmission of meningitis?

Back 292

Transmission: The bacteria are transmitted from person to person through droplets of respiratory or throat secretions.
It is believed that 10% to 20% of the world population carries Neisseria meningitidis at any given time. – World Health Organization estimate

Front 293

CP of meningitis?

Back 293

Incubation period: 3-4 days (ranges 2-10 days)
Abrupt onset of fever, meningeal symptoms, hypotension, & rash

Front 294

Meningococcal Meningitis:

Back 294

Most common pathologic presentation
Result of hematogenous dissemination
Clinical presentation
Fever
Headache
Stiff neck
Case-fatality rate: 9-12%

Front 295

Meningococcemia

Back 295

Bloodstream infection
May occur with or without meningitis
Clinical presentation
Fever
Petechial/purpuric rash
Hypotension
Multiorgan failure
Case-fatality rate: up to 40% with meningococcemia

Front 296

Dx of meningitis

Back 296

Gram stain
Bacterial culture
Serology: antigen detection in CSF

Front 297

Tx of meningitis

Back 297

Initial broad-coverage antibiotic therapy until confirmation by appropriate cultures
Penicillin alone recommended after confirmation of N.meningitidis

Front 298

Meningococcal Vaccination

Back 298

Meningococcal Conjugate Vaccine – MCV4
All children at 11-18 years of age
All college freshmen living in a dormitory
Other persons 2 through 55 years of age at increased risk of invasive meningococcal disease
2 doses (at least 8 wks apart)– 2-10yrs of age – persistent complement component deficiency and anatomic or functional asplenia
2 doses - HIV
1 dose - 2-10yrs of age who travel to countries with high endemic or epidemic disease

Front 299

Types of HPV?

Back 299

More than 100 types:
More than 60 cutaneous types
Can lead to skin warts
40 mucosal types
high risk types (particularly 16 and 18)
cervical cell abnormalities
certain anogenital cancers
Low risk types (particularly 6 and 11)
cervical cell abnormalities- usually resolve spontaneously and do not lead to cancer
genital warts
respiratory papillomatosis

Front 300

HPV4 vaccine is approved for

Back 300

females 9 through 26 years of age for the prevention of cervical cancers, precancers and genital warts
males 9 through 26 years of age for the prevention of genital warts

Front 301

HPV2 vaccine is approved for

Back 301

females 10 through 25 years of age for the prevention of cervical cancers and precancers
not approved for males or for the prevention of genital warts

Front 302

HPV4 (Gardasil)

Back 302

contains types 16 and 18 (high risk) and types 6 and 11 (low risk)

Front 303

HPV2 (Cervarix)

Back 303

contains types 16 and 18 (high risk)
Both vaccines are supplied as a liquid in a single dose vial or syringe
Neither vaccine contains an antibiotic or a preservative

Front 304

The significance of the white blood cell count ?

Back 304

cells that are part of the body’s defense system against infections and cancer and also play a role in allergies and inflammation.

Front 305

The 3 types of blood cells found on a CBC?

Back 305

i. WBC – part of body’s defense system against infections and cancer and also play a role in allergies and inflammation
ii. RBC – transport oxygen throughout the blood
iii. Platelets – cell fragments that are vital for normal blood clotting

Front 306

c. What is meant by a differential

Back 306

includes WBCs, Bands, Neut/segs, Eos, Baso, Lymph, Mono

Front 307

1. Causes of Monocytosis:

Back 307

a. TB
b. Syphilis
c. Malaria
d. Rickettsia
e. Malignancy

Front 308

i. Leukocytosis

Back 308

refers to an increase in the total number of WBCs due to any cause. Traditionally classified according to the component of white cells that contribute to an increase in the total WBCs.

Front 309

i. Neutrophilia

Back 309

1. Although neutrophilia is not normally associated with viral it can be in the early stages of infection.
2. Causes of Neutrophilia:
a. Infection (usually bacterial)
b. Inflammation
c. Malignancy
d. Exercise/Stress

Front 310

ii. Causes of lymphocytosis

Back 310

1. Viral infection
2. Malignancy

Front 311

iii. Causes of Eosinophilia

Back 311

1. Connective Tissue Diseases
2. Helminthic Infections – MC WW (parasites)
3. Idiopathic
4. Neoplasia
5. Allergies – USA MC cause (Drug rxns, atopic asthma) Parasitic infections rare
6. Neither associated with mortality really

Front 312

iv. Bandemia

Back 312

aka “left shift” of the WBC count. Refers to an excess of band cells (immature white blood cells) released by the bone marrow into the blood. It is a marker for infection of inflammation.

Front 313

neutropenia

Back 313

i. Decreased WBC count.
ii. Neutropenia can be associated with bacterial or viral infection. Infants, pre term in particular have small storage pools of neutrophils in the bone marrow. Therefore, neutropenia develops in chronic or severe conditions because supply does not meet demand.

Front 314

a. Why resistant bacteria are increasing in numbers worldwide

Back 314

i. Abx are too often prescribed to meet a pt expectation not need
ii. A single abx can not meet all infectious needs
iii. Bacteria, fungi and viruses highly adaptable
iv. Therapy is dynamic and microbiology should be understood
v. The “shotgun” approach must end

Front 315

b. How to decrease the selection of highly resistant organisms

Back 315

i. No more shot gun
ii. Use the minimum number and least broad
iii. Doctors should switch to a narrower spectrum after 3 days after cultures
iv. Don’t use multiple drugs

Front 316

c. The strategies that underlie optimal antibiotic usage

Back 316

i. Assess probability of bacterial infection
ii. Be familiar with pathogens responsible for infection at anatomic sites
iii. Be familiar with bacterial flora in local hospital and community
iv. Take into account previous antibiotic therapy
v. Take into account host factors (age etc)
vi. Use minimum number and narrowest spectrum
vii. Switch to narrower spectrum based on culture
viii. Take into account acquisition cost and the costs of toxicity
ix. Obey the 3-day rule

Front 317

d. What is the “shotgun approach” to infectious diseases

Back 317

i. Broadspectum antibiotic, multiple Abx, basically throw everything you got at it at once.

Front 318

e. How colonization differs from infection and why the distinction is important

Back 318

i. Colonization is just when there is a bacterial population present in the host, but it does not necessarily mean they are invading the host. The happens especially after Tx rounds with Abx. Too often physicians try to eradicate new bacteria that have colonized with more powerful abx.
ii. Evidence supporting the onset of a new infection include a new fever or a change in fever. A rise in the peripheral WBC with an increase in Gram stain demonstrating an increased number of PMNs in association with predominance of bacteria that are morphologically consistent with the culture results. In the absence of these findings, colonization is more likely.

Front 319

The definition of fever

Back 319

elevation of core body temperature above the daily range for an individual is characteristic of infections but is also found in non-infectious autoimmune or autoinflammatory diseases. Greater than or equal to 38C or 100.4F.

Front 320

Where is temperature regulated

Back 320

hypothalamus

Front 321

The diurnal variation of temperature

Back 321

sleep, metabolic processes throughout the day, hormones. Lower in the morning, higher in the evening.

Front 322

Why does fever occur

Back 322

elevated core temperature from fever increases the demand for oxygen and can aggravate preexisting cardiac or pulmonary insufficiency.

Front 323

Reasons to treat fever –

Back 323

antipyretics reduces systemic symptoms of HA, myalgia and arthralgias. Should only be reduced in pt with ischemic heart disease, pulmonary disease, elderly, childrens with Hx of febril seizures.

Front 324

Reasons to not treat fever

Back 324

when fever is actually hyperthermia. Low-rish fever debated because it does not slow resolution of common infection but is not harmful. Is protective.

Front 325

The definition of pyrogen

Back 325

any substance that causes a fever. Can be exogenous (microbe, i.e. lipopolysaccharide endotoxin produced by all Gram-negative bacteria)

Front 326

Treatment options for fever, risks of aspirin

Back 326

Aspirin and NSAIDs may causes unwanted side effects on platelets and GI. Acetaminophen preferred. Aspirin/acetaminophen combo most effective. Aspirin should not be usedin kids less than 18 bc risk of Reyes.

Front 327

Definition of FUO

Back 327

i. Fever>38.3C on several occasions
ii. Fever lasting > 3 wks
iii. No Dx despite 3 days of inpatient workup or 3 outpatient visits

Front 328

Most common etiologies FUO

Back 328

i. Infection
ii. Noninfectious CT disease
iii. Malignancy

Front 329

Diagnostic approach?

Back 329

i. History and physical
ii. Establishing lab
iii. Further lab and imaging

Front 330

Rate of no diagnosis?

Back 330

30-50% no Dx

Front 331

Nosocomial Infection Definition

Back 331

Hospital acquired infections. Arising 48 hours after admission.

Front 332

Pathophysiology of nosocomial infection

Back 332

Inhalation of droplets in the air or spread by direct hand contact from hospital staff or visitors. May be endogenous or exogenous.
i. Endogenous – include body sites normally inhabited by microorganisms. i.e. nasopharynx, GI GU.
ii. Exogenous – includes sources that are not part of the body. i.e. visitors, staff, equipment.

Front 333

Epidemiology of nosocomial?

Back 333

i. Occurs in 5% of all hospitalizations in the U.S.
ii. 1.7 million occurred in 2002, resulting in 99,000 deaths

Front 334

Rfs for nosocomial infections?

Back 334

severity of illness, underlying immunocompromised state and/or the length of in-pt stay.

Front 335

CP nosocomial infection?

Back 335

i. Febrile pt not admitted with febrile illness
ii. Systemic S/S: fever, tachycardia, tachypnea, skin rash, general malaise
iii. Source of infection may be associated with instrumentations of procedures

Front 336

Common types of nosocomial in adults and children

Back 336

i. Adults – UTI MC in adults
ii. Children – Bacteremia, sepsis, pneumonia, UTI MC Children

Front 337

Contaminants versus pathogens causing infection

Back 337

In lab studies, eg a urine culture obtained through a newly placed foley catheter is less likely to be contaminated by microbial colonization.

Front 338

Common organisms of nosocomial?

Back 338

i. C. difficile
ii. MRSA
iii. Vancomycin Resistant Enteroccocci

Front 339

Components of standard precautions

Back 339

i. Hand hygiene, gloves, safe sharp disposal, proper disposal of soiled linens

Front 340

Significance of fingernails for infection control

Back 340

much of the residents microflora of hands is found in the periungal and subungal areas

Front 341

Types of isolation precautions

Back 341

contact(gloves, gown), droplet (facemask), airborne (negative air pressure, respirator)

Front 342

Importance of hospital surveillance for infection control

Back 342

allows infection control practitioners to identify and understand important pathogens and to detect outbreaks.

Front 343

Big 3, little 6?

Back 343

1- Infection
2- Neoplasm
3- Autoimmune disease

1- Granulomatous disease
2- Regional Enteritis
3- Familial MEditerranean fever
4- Drug Fever
5- Pulmonary Emboli
6- Factitious Fever

Front 344

Causes of the TB resurgence in US between 1985 and 1992

Back 344

1. Inadequate funding for TB control and other PH efforts
2. HIV epidemic
3. Increased migration from countries where TB common
4. Spread of TB in certain settings (jails, homeless shelters)
5. The spread of muiltidrug resistant TB

Front 345

Probability that TB transmission will occur depends on

Back 345

1. How infectious or contagious is the TB Pt
2. In what kind of environment did the exposure occur
3. How long did the exposure last
4. How virulent is the tubercle bacilli

Front 346

Pathophysiology of TB

Back 346

1. Larger droplets become lodged in the upper respiratory tract )nose and throat) where infection is unlikely to occur
2. Smaller droplet nuclei reach small airsacs of the lung (alveoli) where infection may begin
3. In alveoli, some tubercle bacilli are killed but others multiply and enter the bloodstream and spread throughout the body
4. These areas include upper lungs, kidneys, brain and bone
5. W/in 2-8wks immune system kicks in to prevent further spread, person usually has latent TB infection.

Front 347

What does latent TB infection mean?

Back 347

mean that tubercle bacilli are in the body, but the body’s immune system is keeping the bacilli under control and inactive by macrophages the surround the bacilli. Positive Mantoux TB test. NOT infectious. Normal chest xray.

Front 348

What does TB disease mean?

Back 348

develops when immune system cannot keep tubercle bacilli under control and bacilli begin to multiply rapidly. Risk higher for some than others.

Front 349

Recognize high-risk groups of people for exposure to or development of LTBI or TB disease

Back 349

i. HIV, chest X rays suggestive of TB, substance abuse, resent TB infection, corticosteroid or immunosuppresives, organ transplant, silicosis, DM, severe kidney disease, certain types of cancer, certain intestinal conditions, low body weight

Front 350

Describe how to give and interpret a Mantoux tuberculin skin test

Back 350

i. Contain antigens
ii. Liquid tuberculin between layers of skin on forearm (intradermally)
iii. Read between 48 and 72 hours
iv. Most people with TB infection will habe a positive reaction to tuberculin
v. Measure the induration NOT the erythema
vi. 5 or more mm positive for high risk group
vii. 10 mm or more for broader high risk groups
viii. 15 mm or more for people with no known risk factors
ix. People who have a positive TST will have a positive reaction everytime bc it tests immune response to TB not presence of bacilli
x. TST should not be performed on a person who has a documented hx of either a positive TST result or Tx for TB disease

Front 351

f. Describe the components of a medical evaluation for diagnosing TB disease

Back 351

i. Medical Hx
ii. PE
iii. Test for TB infection
iv. Chest x-ray
v. Bacteriologic Examinations

Front 352

g. Describe the recommended treatment for LTBI

Back 352

i. Isoniazid daily for 9 mo

Front 353

h. Understand the DOT treatment adherence strategy

Back 353

i. Directly observed Therapy – people especially high risk for TB. A healthcare worker or another designated person watches the pt swallow each dose of the prescribed drugs.

Front 354

Necrotizing fasciitis

Back 354

flesh eating bacteria, infection of deeper tissue such as subcutaneous fat and fascia. Infection spreads along and muscle is spared and superficial skin is initially uninfected due to lack of vasculature

Front 355

Types of necrotizing fasciitis

Back 355

Type 1: Mixes microbial is type one and includes mix of anaerobic and aerobic . RF include immunosuppressed or decreased vascular supply (DM). MC legs or perineum

Type 2 – GAS, healthy individuals with recent surgary, injury, childbirth, IV drug use, rarely thru throat infection

Front 356

Clinical presentation of necrotizing fasciitis?

Back 356

fever, toxicity, tissue involvement, pain with unsupported clinical findings, crepitus, rash or something under the skin

Front 357

Dx methods of necrotizing fasciitis

Back 357

i. Labs are usually not specific or helpful
1. CBC differential
2. Blood Cultures
3. Serum Creatine Kinase
4. Radiographic Imaging
ii. Definitive Dx
1. Surgical exploration – only definitive should not be delayed

Front 358

Tx methods of necrotizing fasciitis

Back 358

i. 1st early and aggressive surgical exploration and debridement
ii. Empiric broad-spectrum Abx therapy (sue of abx w/o debridement has mortality rate of 100%)
iii. Hemodynamic support in the ICU-IV fluids and vasodilators

Front 359

Prognosis of necrotizing fasciitis

Back 359

a. mortality rate is great even with optimal therapy 10%-40% sites of difficult debridement that lead to increase risk of morbidiy:
i. Abdomen, head, neck, thorax

Front 360

Epidemiology in the U.S. for chlamydia and gonorrhea

Back 360

i. Chlamydia: 3 million estimated cases in the US each year, rates highest amoung adolescents and young adults, racial and ethnic minorities more affected.
ii. Gonorrhea: Underestimated by 50%. More in minorities, and young people and southern region. ~718,000 cases in 2000.

Front 361

Pathogenesis of chlamydia and gonorrhea

Back 361

i. Chlamydia: C. trachomatis is highly transmissible, >50%. Genital sexual contact or vertical transmission. 7-21 incubation period. Reinfection common.
ii. Gonorrhea: Male to female rate 50-70%, female to male 20% per episode, rectal not quantified, pharyngeal from fellatio, perinatal during vaginal delivery.

Front 362

Clinical manifestations of chlamydia in men and women

Back 362

a. Men: MC Urethra as a non-gonoccocal urethritis , S/S dysuria, urethral discharge which is either mucopurulent, mucoid or clear, but most men are asymptomatic. MC local infection in epididymitis; fever, unilateral scrotal pain, swelling, tenderness, evidence of urethritis on Gram stain and epididymal tenderness or mass on exam. Most ofthese due to chlaymydia.
b. Women: Majority no S/S. Cervicitis, Urethritis, PID Perihepatitis (Fits-Hugh-Curtis Syndrome)
c. Men & Women: Conjunctivits, Proctitis, Lymphogranuloma venerum

Front 363

CLinical manifestations of gonorrhea in men and women

Back 363

a. Men: Epididymitis
b. Women: cervicitis, urethritis, accessory gland infections, PID, Perihepatitis (Fits-Hugh-Curtis Syndrome)
c. Men and Women: urogenital, pharyngeal, rectal infections, conjunctivitis. Can facilitate HIV transmission. Disseminated gonococcal infection (DGI) can include skin lesions, arthralgia, tenosynovitis, arthritis, hepatitis, myocarditis, endocarditis, meningitis.

Front 364

CLinical presentation of chlamydia in children and infants

Back 364

a. Conjunctivitis, chlamydial pneumonia, urogenital infections in pre-adolescent males and females

Front 365

Clinical presentation of gonorrhea in children and infants

Back 365

conjunctiva, pharynx, respiratory tract, anal canal, conjunctivitis preventable by ocular prophylaxis. Vulvovaginitis in prepubescent girls.

Front 366

Diagnostic methods of chlamydia and gonorrhea

Back 366

1. Chlamydia: culture and non-culture. New non culture on urine, Nucleic Acid Amplification test (NAAT)
2. Gonorrhea: Culture advantages – low cost, suitable for a variety of specimens sites, antimicrobial susceptibility testing can be performed. DNA tests not recommended in pharynx.

Front 367

Epi of syphilis

Back 367

37,000 people in the US a year

Front 368

path of syphillis

Back 368

sexual and vertical. Contagious in primary and secondary stage when lesion or rash present. Treponema pallidum, remains chronic w/o tx and progress in stages, incubation 10-90 days or avg of 3 wks, stages include; primary, secondary, early latent, tertiary and late latent.

Front 369

c. Clinical manifestations and sequelae of syphilis –

Back 369

i. Primary: chancre
ii. Secondary: rash, macular, popular or squamous rash. Lymphadenopahty, Malaise, mucous patches, flat patches on oral cavity, pharynx, larynx and genital.s. Condylomata latea, moist, heapers wart-like papules in folds very contagious. Alopecia.
iii. Latent: host suprresion, no S/S only serological testing
iv. Neurosyphyllis: invasion of CNS, can be at any stage, asymptomatic or meningitis, seizures, paresis, tabes dorsalis. Ocular involvement.
v. Tertiary: w/o tx 1-20 yrs. Rare bc abx. GUmmatous lesions cardiovascular syphilis.
vi. Congenital: untreated in pregnant women can lead to stillborn, neonatal death, deafness, neurologic impairment and bone deformities. Primary and secondary most transmissible during any trimester.

Front 370

Dx of syphillis

Back 370

i. Hx, PE, serologic,
ii. Serologic on secondary highest.
iii. Secondary usually first recognized clinical s/s bc primary lesions in anus or vagina may not be recognized.
iv. Nontreponemal: Venereal Disease Research Laboratory and Rapid Plasma Reagin. Test measure IgM and IgG antibody and are not specific for T. pallidum. Cheaper and faster. Titers correlate with disease activity.
v. Treponemal Tests: FTA-ABS (fluorescent treponemal antibody absorbed) and EIA (Enzyme Immunoassay). These measure antibodies directed against T. Pallidum. Don’t correlate with disease activity.
vi. Difficult to Dx latent must have: doc seroconversion, s/s of primary, soncdary, doc sex partner to have primary, secondary or early latent or the only poss exposure occurred within preceding 12 mo.
vii. CNS disease: CSF abnormalities noted in some stages

Front 371

Tx of syphillis

Back 371

Pen G

Front 372

Describe the acute HIV infection

Back 372

i. Acute Infection
1. Occurs 1-4 weeks after transmission and is accompanied by a burst of viral replication with a decline in CD4 cell count.
2. Most pts manifest a symptomatic mono like syndrome
3. Acute is confirmed by demonstrating a high HIV RNA with either a negative HIV antibody test or a reactive ELISA with a negative or interdeterminate Western blot
4. Most not dx in this stage

Front 373

Asymptomatic HIV infection

Back 373

1. Lasts a variable amount of time (~8-10yrs) accompanied by gradual decline in CD4 counts and relatively stable HIV RNA level

Front 374

iii. Early Symptomatic HIV Infection

Back 374

1. Thrush, vaginal candidiasis, herpes zoster, oral hairy leukoplakia, diarrhea, constitutional symptoms (low grade fevers, weight loss)

Front 375

iv. AIDS

Back 375

1. CD4 count <200/mm^3 or one of several AIDS-related opportunistic infections
2. i.e. Pneumocystis jirovecii pneumonia (PCP), cryptococcal meningitis, recurrent bacterial pneumonia, candida esophagitis, CNS toxoplasmosis, TB, non-hodgkins lymphoma

Front 376

v. Advanced HIV Disease

Back 376

1. CD4 count <50/mm^3
2. Most AIDS related death occurs at this point
3. Common late-stage opportunistic infections are caused by CMV retinitis or disseminated Mycobacterium avium complex (MAC)

Front 377

c. Major diagnostic methods HIV

Back 377

i. Acute is confirmed by demonstrating a high HIV RNA with either a negative HIV antibody test or a reactive ELISA with a negative or interdeterminate Western blot. Most not dx in this stage.
ii. Seroconversion – Development of a positive HIV antibody test usually occurs wihitn 6-8 weeks of acute infection and invariably by 6 mo
iii. HIV Antibody Testing – (ELISA, Western blot) and quantitative HIV RNA (HIV viral load) assays are used to Dx HIV infection. Most pt produce antibody to HIV within 6-8 wks of exposure; nearly 100% will have detectable antibody by 6 mo

Front 378

d. Assessment of HIV patients

Back 378

i. Clinical Evaluation
1. Dermatologic,
2. Oropharyngeal,
3. constitutional symptoms,
4. others
5. Baseline Labs
6. CD4 Count