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MultiSystem Module > MultiSystem Final Lectures > Flashcards

MultiSystem Final Lectures Flashcards

0
Q

Pasteurella multocida

A 
Carried in nasopharynx of 50-90% cats
Avg incubation 15 hrs
Local cellulitis, low grade fevers
Range of infectious complications
Sensitive to B lactams, azithromycin (augmentin)
AVOID eyrthomycin, clindamycin
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1
Q

Capnocytophaga canimorsus

A 
Normal flora in dogs and cats
Severe infection in immunocompromised
Wide spectrum (fevers, myalgias rash GI complaints -> sepsis)
Bacteremia/sepsis very rare!
Resistant to TMX/SMX and aminoglycosides
Augmentin is drug of choice
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2
Q

CA-MRSA

A

Colonization in domestic animals
S intermedius > S. Aureus
Outbreaks in vet hospitals
Dermatitis, pustular disease, perineal cellulitis

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3
Q

Management of Animal Bite Wounds

A

Irrigation: sterile saline, debridement if necrotic tissue
Surgical evaluation
Leave wound open except for complex facial wounds
Elevation
Antibiotics
Gram Stain! Esp if there is abscess, cellulitis etc…
Imaging (rule out foreign body)

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4
Q

Antibiotic Prophylaxis Indications

A
  • Deep puncture wounds (esp. cat bites)
  • Mod-severe wounds with associated crush injury
  • Wounds in areas of venous/lymphatic compromise
  • Wounds on hands or close to joint/bone
  • Wounds that require surgical repair
  • Wounds in immunocompromised
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5
Q

Oral Antibiotics for Dog/Cat bites

A

•Drug of Choice:
–Amoxicillin-clavulanate 875/125mg BID
•Alternate Empiric Regimens:
–Doxycycline/TMP-SMX/Penicillin VK/Cefuroxime/Moxifloxacin
plus
–metronidazole/clindamycin
•AVOID: cephalexin, dicloxacillin, erythromycin

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6
Q

IV antibiotics for the dog/cat patient who is admitted

A

•Monotherapy with B-lactam/B-lactamase inhibitors:
–Ampicillin-sulbactam 3gm q6hrs
–Piperacillin-tazobactam 4.5gm q8hrs

•Ceftriaxone plus metronidazole

•Alternative IV regimens:
–Fluoroquinolone plus metronidazole
–Monotherapy with carbapenems:

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7
Q

What organism causes Cat Scratch Disease?

A 
•Caused by Bartonella henselae
•Bites or scratches from felines
–Kittens, strays
•Most cases in fall/winter
–Infected fleas?
•Most common in children
< 15 years old
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8
Q

Cat Scratch Disease Symptoms

A

Papule or Pustule at inoculation site
Fever
Enlarged, tender lymph nodes that develop…

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9
Q

Cat Scratch Disease Diagnosis

A

–Clinical
–Serology
–PCR or culture
•Pus, lymph node aspirates

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10
Q

Cat Scratch Disease Treatment

A

–Most cases resolve spontaneously

–Azithromycin (Z-pak) for disseminated or severe disease

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11
Q

Human Bites Pathogens

A

–Staphylococcus and Streptococcus species
–Anaerobes:
•Eikenella, Fusobacterium, Peptostreptococcus, Prevotella, Porphyromonas spp.
•Most often polymicrobial
•Viral pathogens:
–Hepatitis B/C, HIV, HSV

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12
Q

Boar/Pig Bite Organisms

A

•Polymicrobial infections
–Streptococcus and Staphylococcus spp., P. multocida, anaerobes
–Actinobacillus suis

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13
Q

Rat Bite Fever Organisms

A

Streptobacillus moniliformis

Spirillum minus

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14
Q

Seal Finger

A

Mycoplasma species
Papular lesion -> pain, swelling, joint involvement
Treatment: tetracyclines

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15
Q

What infection are you most concerned with monkey bites?

A

Herpes B Virus
Persists in sensory ganglia for lifetime
Incubation 5-21 days

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16
Q

Bacteria cultured in war wounds, from one study from a fresh wound

A

Coagulase-negative Staphylococcus - common

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17
Q

War wound organism 5 days after the initial injury

A

Acinetobacter - war wound

Soldiers started on Gram + coverage antibiotics, so after a few days patients start developing gram - rod infections

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18
Q

VHF properties

A

all enveloped RNA viruses
Survival is dependent on an animal or insect host
geographically restricted to areas where host species live
human outbreaks of VHF occur sporadically and irregularly
no cure

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19
Q

Viral Families Containing VHF agents

A

Arenaviruses
Bunyaviruses
Flaviviruses
Filoviruses

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20
Q

Key clue in history for patient that is exhibiting VHF

A

Foreign travel to endemic or epidemic area

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21
Q

VHF treatment

A

Supportive Care
Ribavirin possibly effective for:
Arenaviruses, Bunyaviridae (CCHF, Hantavirus, RVF)

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22
Q

Vaccines for VHF

A

Candid #1: Argentine hemorrhagic fever (Junin virus)

Yellow fever 17D: Yellow fever virus

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23
Q

Crimean-Congo hemorrhagic Fever (CCHF) transmission

A

Ticks

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24
Q

CCHF viral family

A

Bunyavirus

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25
Q

Arenaviruses, how do humans get infected?

A

Contact with rodent excreta - ingestion of contaminated food, direct contact with broken skin, inhalation of tiny particles soiled with rodent urine or saliva (aerosol transmission)

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26
Q

Lassa Fever

A

Hemorrhagic illness caused by arenavirus Lassa

Endemic in areas of West Africa

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27
Q

Who is affected by Lassa Fever the worst?

A

pregnant women

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28
Q

Most common complication of Lassa Fever?

A

Hearing loss

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29
Q

Lassa Fever Virus Protection

A

Rotent control

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30
Q

What differentiates small pox from chicken pox?

A

In smallpox:
vesicles are in the same stage of disease
•Denser on face, arms, hands, legs, and feet than on body
•Involvement of palms & soles

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31
Q

Organism causing Lumpy Jaw

A

Actinomycosis caused by Actinomyces

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32
Q

Infections of Prosthetic Devices Organism

A

Propionibacterium

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33
Q

Anaerobes are concentrated where in our body?

A

Oral Cavity and Large Intestine

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34
Q

Unique characteristics of anaerobes

A

crepitation - gas formers/ferment
bad odors
brownish serous fluid - digest tissues

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35
Q

Anaerobic infections above the waist are almost always related to what?

A

Dentition.

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36
Q

What anaerobic infections (above or below the waist) are sensitive to antibiotics?

A

Above

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37
Q

Free radical ozone (O3).

What is it composed of? What are they affects on lungs?

A

Nitrogen Oxides + volatile organic compounds + UV

Free radical damage of lung epithelial and Type I alveolar cells -> increases SOB in asthma or emphysema

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38
Q

People who are most likely susceptible to having complications from pollutants

A

Asthmatic Individuals

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39
Q

Name 5 outdoor air pollutants

A

Ozone, nitrogen dioxide, sulfur dioxide, acid aerosols, particulates

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40
Q

Indoor Pollution

A

Tobacco Smoke, CO, Nitrogen oxide (component of smog could also affect indoors), asbestos, radon, formaldehyde

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41
Q

Definition of Toxicology

A

science of poisons.

distribution, effects and MOA of toxic agents affecting our metabolism

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42
Q

What is the most preventable cause of death?

A

Smoking

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43
Q

60+ substances in tobacco are a/w carcinogenesis. Name a few of those constituents.

A

Tar, benzopyrene, nitrosamine, polycyclic aromatic hydrocarbons (carcinogenesis)
Nicotine, phenol (tumor promotion)
CO (impaired oxygen transport and utilization)
Formaldehyde (toxicity to cilia)

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44
Q

Complications from smoking

A 
Cancer of oral cavity, larynx, esophagus, lung, pancreas, bladder
Chronic bronchitis, emphysema
MI
Systemic atherosclerosis
Peptic Ulcer
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45
Q

Legally drunk

A

> = 80 mg/dL

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46
Q

Alcohol consumption is responsible for how many deaths annually?

A

100,000

50% are MVA, homicide or suicide

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47
Q

Metabolism of alcohol

A

Ethanol is absorbed unaltered in the stomach and Small intestine, then distributed to all tissues and fluids of the body in direct proportion to the blood level. Less than 10% is excreted unchanged in the urine, sweat, and breath. Most of the alcohol in the blood is biotransformed to acetaldehyde in the liver by three enzyme systems consisting of alcohol DH, microsomal ethanol-oxidizing system (MEOS) and catalase.

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48
Q

T/F The rate of metabolism affects the blood alcohol level

A

True.
Chronic alcoholics can tolerate up to 700 mg/dL, partially explained by accelerated ethanol metabolism caused by 5-10-fold induction of liver CYPs.

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49
Q

What is the main enzyme system involved in alcohol metabolism? Where is it located

A 
alcohol dehydrogenase (ADH)
cytosol of hepatocytes.
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50
Q

At high blood alcohol levels, besides ADH what other system comes into play for metabolism of alcohol?

A

MEOS

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51
Q

Three enzyme systems involved in alcohol metabolism.

What is the end product of these three systems?

A

Alcohol DH, MEOS, Catalase

Acetaldehyde

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52
Q

Acetaldehyde is converted to ______ by _______, which is then utilized in the mitochondrial respiratory chain

A 
acetate
acetaldehyde DH (ALDH)
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53
Q

The microsomal oxidation system involves CYPs, particularly which one?

A

CYP2E1 located in smooth ER

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54
Q

Why do alcoholics have an accumulation of fat within the liver?

A

Ethanol conversion to acetaldehyde by ADH converts NAD+ to NADH. NAD+ is needed for fatty acid oxidation in the liver.

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55
Q

Why are some Asians unable to tolerate alcohol?

A

50% of Asians have very low ALDH activity, due to substitution of lysine for glutamine at residue 487. The mutant allele has dominant-negative activity, such that even 1 copy of the allele reduces ALDH activity significantly. individuals homozygous are completely unable to oxidize acetaldehyde and cannot tolerate alcohol, experiencing nausea, flushing, tachycardia, and hyperventilation after its ingestion.

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56
Q

Chronic Alcoholism affects many different systems and contributes to significant morbidity. Name some of the systems affected and common consequences.

A

Liver: fatty change, alcoholic hepatitis, cirrhosis
GI: massive bleeding from gastritis, peptic ulcer, esophageal varices
CNS: vit B1 def, cerebral atrophy, cerebellar degeneration
CVS: dilated CHF, HTN
Endo: Acute and chronic pancreatitis
OB: fetal alcohol syndrome
Increased risk of cancer

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57
Q

Principle lesions resulting from Thiamine deficiency that is common in chronic alcoholics.

A

Peripheral neuropathies

Wernicke-Korsakoff syndrome

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58
Q

What are moderate amounts of alcohol (20-30 g daily intake) shown to increase?

A

HDL levels and inhibit platelet aggregation, protecting against coronary heart disease

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59
Q

What does fetal-alcohol syndrome consist of?

A

microcephaly, growth retardation, facial abnormalities in the newborn, reduction in mental functions as child grows older

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60
Q

What is considered to be the main agent associated with alcohol induced laryngeal and esophageal cancer

A

acetaldehyde

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61
Q

What does red wine contain that may be protective against obesity and cardiovascular disease?

A

resveratrol

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62
Q

What are four heavy metals most commonly associated with harmful effects in humans?

A

lead, mercury, arsenic, cadmium

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63
Q

Morphology of lead poisoning

A

punctuate basophilic stippling of the red cells.

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64
Q

Metabolite seen in serum that would tell you that a person has cocaine in their system.

A

Benzoylecgonine (BE)

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65
Q

Metabolites found in blood when individual is taking heroin

A

6-monoacetylmorphine (6-MAM) and morphine

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66
Q

Classification of Blunt Force Injury

A

Abrasion
Contusion
Laceration
Fractures

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67
Q

Abrasion Definition

A

Scraping and removal of the superficial surface of the skin

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68
Q

Types of abrasions

A

Road Rash
Pattern Abrasion
Impact

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69
Q

Contusion Definition

A

Area of bleeding(hemorrhage) into the skin or soft tissue as a result of rupture of blood vessels due to blunt force injury or pressure
contusion = bruise

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70
Q

Hematoma

A

focal collection of blood

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71
Q

Is aging bruises a reliable system?

A

No! Do not worry about color just identify contusion

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72
Q

Laceration Definition

A

Tearing of the skin or tissue due to stretching, crushing, shearing, or avulsing due to a blunt force.
Soft tissue bridging of blood vessels from blunt force
NOT A CUT, STAB, SHARP FORCE INJURY

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73
Q

Three types of sharp force injuries

A

Stab/puncture: depth greater than width
Incised/cut
Chop wounds

THESE ARE NOT LACERATIONS

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74
Q

Double edged knife

A

Both margins with a V-shaped margin

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75
Q

Length greater than depth?

A

Incised/cutting wounds

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76
Q

Most common cause of death in sharp force injury

A

Hemorrhage

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77
Q

Gunshot wound

A

Range of fire:

contact, intermediate, distant

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78
Q

perforation

A

entrance AND exit

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79
Q

penetration

A

Entrance but NO exit

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80
Q

Reasons for death due to malaria in U.S.

A
  1. failure to take chemoprophylaxis
  2. not promptly seeking medical care
  3. low suspicion of disease/late diagnosis
  4. improper therapy
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81
Q

What type of pathogen is malaria and what type of cells does it infect?

A

Protozoa parasite

Single cell eukaryotic pathogen affecting RBC and hepatocytes

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82
Q

In non-immune patients, falciparum malaria is a medical emergency!!

A

…

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83
Q

Risk factors for severe malaria

A

Nonimmune individuals
children less than 5 yo
pregnant women
asplenic patients

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84
Q

Species of Malaria

A

Plasmodium falciparum, P. vivax, P. ovale, P. malariae, P. knowlesi

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85
Q

Vector for Malaria

A

anophelene mosquitoes

non-human reservoir

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86
Q

What is the infected form of the parasite of malaria

A

Sporozoites

come from mosquito, travel to liver, infect hepatocytes (liver schizont)

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87
Q

Merozoites infect RBCs where they form ring-stage what?

A

trophozoites.

these mature into schizonts which rupture and release merozoites, which infect more RBCs

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88
Q

•Dormant liver stage in P. vivax and P. ovale

A

Hypnozoite

Release blood stage parasites weeks to months after primary infection

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89
Q

How long after infection does one develop symptoms?

A

Pf 8-11 days
Po 10-17 days
Pv 10-17 days
Pm 18-40 days

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90
Q

Onset of symptoms of malaria usually coincides with what?

A

the start of the erythrocytic cycle.

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91
Q

Malaria classical presentation

A 
Fever
Chills
Headache
.... remember to ask HISTORY OF TRAVEL
about 1/5 of cases, patients have abdominal pain
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92
Q

Malaria Lab Values

A

Not specific
Only about a quarter of people have anemia
more people will have a low platelet count (avg. 148K)

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93
Q

Malaria Clinical Types

A

Uncomplicated malaria

Severe Malaria

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94
Q

Uncomplicated (mild) malaria occurs with what species?

Classic paroxysms

A

ALL plasmodium species.
Classic paroxysms
sudden episodes of:
1. cold stage with shaking
2. hot stage with high temperature (>104°F)
3. sweating stage with resolution of fever

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95
Q

How does severe malaria kill people?

A

-cerebral malaria, respiratory distress, severe anemia (children of endemic countries.
Adults more often get multi-organ failure.

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96
Q

Complications of severe anemia are usually caused by which Plasmodium species?

A

These complications primarily occur with

Plasmodium falciparum, usually when parasitemia >2%.

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97
Q

Why are P. falciparum infections the most severe?

A

No limit on the degree of parasitemia. (slide)

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98
Q

What is a major cause of tissue hypoxia and lactic acidosis in Pf?

A

SEQUESTRATION!
Erythrocytes containing mature P. falcip. parasites develop “knobs” and express adhesion molecules that bind to endothelial cells of capillaries and post-capillary venules.

Additionally, there is decreased deformability of infected AND non-infected RBCs, contributing to sludging, rosetting, aggregation, and eventual blockage of blood vessels.

This causes tissue hypoxia and organ failure.

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99
Q

What is cerebral malaria?

A

•acute encephalopathy not attributable to other causes in a patient with malaria
–>obstruction of vessels is heterogenous
(some blocked, some not)

   -->the brain is swollen because of mass effect of all the
        sequestered RBCs, not because of cerebral edema  •mortality: 100% without Rx, 20% with Rx

•gross neurologic sequelae in 10% of survivors

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100
Q 
Severe malaria manifestations mechanism?
lactic acidosis?
Hypoglycemia?
Renal Failure?
Anemia?
Pulmonary Edema?
A

lactic acidosis  hypoperfusion from sequestration

hypoglycemia  ↑ demand and ↓ consumption

renal failure  filtration of hemolysis products

anemia  hemolysis, sequestration, splenic removal

pulmonary edema  unknown

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101
Q

How do you diagnose Malaria?

A
  • blood smear (thick and thin)
  • antigen testing
  • PCR
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102
Q

When could you get a false negative test with the Binax Now malaria card test?

A

Very low levels of parasitemia… Just wait 12 hrs and do the test again.

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103
Q

Schuffner’s Dots and enlarged infected cells -> which species of Plasmodium?

A

P vivax or ovale

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104
Q

P vivax vs P ovale… distinguish?

A

Mature schizont … merozoites

P vivax has more merozoites

105
Q

p. falciparum

A

Multiple ring forms trophozoites

banana shaped gametocyte

106
Q

P. malariae

A
  • band form
  • Owl eye trophozoite
  • smaller infected cells
  • yellow/brown pigment
107
Q

Malaria Prevention

A 
•Personal protection measures
•Chemotherapy
–doxycycline
–atovaquone/proguanil
–mefloquine
–Primaquine
–Chloroquine (in chloroquine-sensitive areas)
108
Q

Most important risk factor for developing malaria in the U.S.?

A

Immigrant families visiting friends and relatives most important risk factor

109
Q

Anti-malarial treatment (4 categories to consider)

A

•quinoline derivatives
(incl. quinine, chloroquine, mefloquine, and primaquine)
•artemesin compounds
•antifolates (incl. proguanil and pyrimethamine/sulfadoxine)
•other (incl. tetracycline, atovaquone/proguanil)

110
Q

Which anti-malarial drug do you need to make sure to test for G6PD deficiency?

A

Primaquine

111
Q

Atovaquone:

MOA

A
  • Inhibits parasite mitochondrial electron transport

- Effect potentiated when paired with proguanil

112
Q

What type of virus is measles?

A

Paramyxovirus:
Enveloped
SS-linear Nonsegmented
Helical

113
Q

Characteristic findings of Measles (rubeola) virus

A

Koplik spots

descending maculopapular rash

114
Q

3 C’s of measles:

A

Cough
Coryza
Conjunctivitis

115
Q

Spirochetes (General Info)

A

Spirochetes are spiral-shaped organisms that exhibit corkscrew motility,
don’t Gram stain, grow slowly in vitro or not at all

116
Q

Spirochetes include which organisms?

A

BLT. B is Big
Borrelia (big size)
Leptospira
Treponema

117
Q

Which organism causes Lyme Disease?

A

Borrelia burgdorferi

118
Q

How is Borrelia burgdorferi transmitted?

A

Tick borne- most common arthropod-borne infection in US

in Northeast and Midwest = Ixodes scapularis (also called Ixodes dammini.

119
Q

Which stage in the lifecycle of ticks is primarily responsible for transmission of the Borrelia burgdorferi infection? When are they most active?

A

nymphal stage

Late spring and early summer

120
Q

Describe the 3 stages of Lyme Disease.

A

Stage 1 localized infection: erythema chronicum migrans, flulike symptoms
Stage 2 disseminated infection: neurologic (Bell’s palsy) and cardiac manifestations (AV nodal block)
Stage 3: chronic monoarthritis and migratory polyarthritis

121
Q

Describe erythema chronicum migrans

A

Expanding “bull’s eye” red rash with central clearing.

122
Q

Which animal is important to the tick life cycle that transmits Borrelia burgdorferi?

A

deer and mice

123
Q

Treatment for Lyme Disease:

A

Usually can be treated with oral antibiotics (doxycycline)

Patients with arthritis or neurological abnormalities may require IV antibiotics treatment

124
Q

Is there a vaccine for Lyme Disease?

A

No, it was taken off of the market.
Had to be given every year, and thought that it might make arthritis worse. It was expensive.
They have talked about trying to reintroduce it.

125
Q

Relapsing Fever: which organism causes it?

A

Borrelia sp. and characterized by recurrent episode of fever separated by asymptomatic intervals.

126
Q

Leptospira interrogans

A

Question mark-shaped bacteria found in water contaminated with animal urine

127
Q

Leptospirosis

A

Flulike symptoms
Conjunctival suffusion: reddening of the conjunctiva (the front surface of the eye) caused by increased blood flow.
Jaundice
Photophobia with conjunctivitis!

128
Q

Who gets leptospirosis?

A

military
surfers
veterinarians
people in the tropics

129
Q

What is Weil’s Disease?

A

icterohemorrhagic leptospirosis

severe form with jaundice and azotemia from liver and kidney dysfunction; fever, hemorrhage, anemia

130
Q

Spirochetes are sensitive to penicillins, so why are these diseases treated with doxycycline?

A

Doxycycline can cross the CNS more readily than penicillins. The CNS manifestations are the most traumatic and want to be readily avoided… so prophylaxis in adults.
Remember you do not treat doxycycline in pregnant women and children!

131
Q

STARI

Southern Tick Associated lllness

A

similar primary illness to Lyme Diseas but NOT caused by B. burgdorferi

A rash similar to the rash of Lyme disease has been described in humans residing in southeastern and south-central states and is associated with the bite of the lone star tick, Amblyomma americanum. This Lyme disease-like rash has been named Southern tick-associated rash illness (STARI).

132
Q

Borrelia recurrentis: epidemic relapsing fever-lice

A

..

133
Q

Borrelia hermsii:

A

Endemic relapsing fever

Ticks

134
Q

Rabbit fever AKA Tularemia AKA Glandular Fever: Which organism causes this?

A

Francisella tularensis

135
Q

Francisella:
Gram Stain
Morphology

A

Gram Negative

Rod (bacillus)

136
Q

What are the Facultative intracellular organisms?

A 
Some Nasty Bugs May Live FacultativeLY
Salmonella
Neisseria
Brucella
Mycobacterium
Listeria
Francisella
Legionella
Yersinia pestis
137
Q

Transmission and source of Francisella tularensis?

A

Ticks, RABBITS, deer fly

138
Q

Tularemia Spectrum of Infections:

4 types

A

•Ulceroglandular
Follows primary infection of the skin
75-85% of cases; 5% fatality rate

• Oculoglandular
   Contaminate eye (conjunctiva) with infected material
   0-5% of cases

• Pneumonic
Transmission via aerosol or via 2° spread to the lung
30% fatality rate

• Typhoidal
Ingestion of the organism; symptoms similar to typhoid fever

139
Q

What causes Brucellosis/undulant fever?

A

Brucella spp.

140
Q

Major transmission route to humans of Brucella sp.?

A

Infected milk, milk products
Direct contact with infected animals
“Unpasteurized Dairy”
NO INSECT vector

141
Q

Chronic Brucellosis (Undulant Fever):
Incubation Period
Clinical Presentation

A

Incubation period: 2- 8 weeks

Fever, night sweats, headaches, chills, myalagia, weight loss
Organs of the RES often NOT enlarged

Complications:
hepatic lesions
arthritis
meningitis
endocarditis

DIFFICULT TO DIAGNOSE!

142
Q

Occupational Recreational Risks for Brucellosis

A

slaughterhouse workers, meat packing employees, veterinarians, lab workers, hunters

143
Q

Is there a Brucella vaccine?

A

Yes, Live-attenuated brucella vaccine given to cattle… prevents them from getting active infection or shedding into their milk.
This is why there are a lot less cases of Brucellosis in the U.S.
BUT bison, buffalo still have the infection

144
Q

What organism causes Cat scratch Disease? What is the transmission and source of this organism?

A

Bartonella henselae
Cat scratch (duh) ; cats are reservoir, humans are incidental host
vector is a flea

145
Q

Carrion’s disease: what are the two phases? What organism causes it? What is the reservoir host?

A

1st: Oroya fever (hemolytic anemia)
2nd: Verruga peruana

Bartonella bacilliformis

human reservoir; Sand fly vector

146
Q

What sorts of things should you consider for toxic history?

A

Trauma,
size matters (how many pills, mgs, co ingestions?)
medical and psych history

147
Q

Why do acutely poisoned/intoxicated patients die?

A

TRAUMA!
Intentional (suicide- usually pills, and “roofies”)
Accidental (heroin, alcohol, etc., children, elderly)
envenomations
bioterrorism

148
Q

What is a toxidrome? What are some key features?

A

Toxic physical exam:
Exclude trauma!
Key features: vital signs, pupils, skin (wet or dry), bowel sounds, mental status

149
Q

Which drug is not clinically detectable with an overdose?

A

Acetaminophen!
acetyl cysteine is the antidote which is very successful so it is unfortunate that we cannot clinically tell an acetaminophen overdose.

150
Q

Pinpoint pupils is characteristic of what drug overdose?

A

opiates

151
Q

Wet or dry skin in cocaine overdose?

A

wet

152
Q

Treatment principles for poisoning

A

Decontamination
-clothes/washing, dialysis, supportive care works
Lots of treatment that do not work well or only in very specific situations: lavage,whole bowel irrigation, Emetics, charcoal

153
Q

How do you treat compartment syndrome?

A

Fasciotomy

154
Q

Rickettsiaeceae

A 
Obligate Intracellular Bacteria
Transmitted by arthropods
Fastidious
Gram Negative coccobacilli
Visible with Giemsa stain
Require host cell for many functions (synthesis of nucleotides and amino acids)
155
Q

Classification of Rickettsiaeceae

A

Classification: Based on clinical features, epidemiologic aspects, and immunologic characteristics

156
Q

Major groups of Rickettsiaeceae

A

Typhus

Spotted Fever

157
Q

Genera of Rickettsiaeceae

A

Rickettsia

Orientia

158
Q

How does Rickettsia spread?

A

Cell-to-Cell involves actin polymerization

similar to Listeria and Shigella

159
Q

General disease features with spotted fever and typhus?

A
  • The pathogenesis of both spotted fever and typhus organisms is vasculitis caused by proliferation of the organisms in the endothelial lining of small arteries, veins, capillaries. Vascular lesions are prominent in the skin.
  • Clinical manifestations: Skin rash, fever, severe headache, malaise, prostration, and enlargement of the spleen and liver.
160
Q

Which organism is naturally occurring that is on the East Coast of the United States that causes Rocky Mountain Spotted Fever?

A

Rickettsia rickettsii

Tick-Borne -> adult dog tick bites you -> it’s big so you may remember.

161
Q

New competent (carry and transmit) vector for RMSF? Who is the primary host?

A

Brown dog tick (Rhipicephalus sanguineus)

  • Recently identified as a reservoir of R. rickettsii, causing Rocky Mountain spotted fever, in the southwestern U.S. and along the U.S-Mexico border.
  • Found throughout the U.S. and the world. Dogs are the primary host.
162
Q

Most common vector tick species to carry RMSF?

A

Dermacentor

163
Q

How do you treat RMSF?

A

Doxycycline

164
Q

Difference between measles and RMSF rash?

A

RMSF has rash on palms and soles (the only other disease that could do that is secondary syphilis)

165
Q

What does Rickettsia akara cause?

A

Cause of rickettsial pox;
mite-borne (rodent -> mite -> human)
Cosmopolitan in distribution; occurs in USA

166
Q

What does mite borne mean?

A

Rodent -> mite -> human

167
Q

What does the rash of Rickettsia akara look like?

A

Rash more like that of chicken pox (papulovesicular). Eschar at site of mite bite.

168
Q

Rickettsia prowazekii

A

prototype, cause of epidemic typhus (WWI and WWII)Body louse, not in USA; in places of war (Somalia)

169
Q

Orientia tsutsugamsushi causes what?
Vector? Reservoir?
Does it occur in the US?

A

Cause of scrub typhus
mite (chiggers, red mites)-borne; reservoir is mite (transovarial passage) or rodent population infected by mites; does not occur naturally in US but was of military importance in Vietnam.

170
Q

Rickettsia typhi causes what?

Vector?

A

Cause of endemic or murine typhus; disease occurs worldwide to include USA (about 50-100 cases/year mostly in Gulf Coast area); flea-borne; rodent vectors

171
Q

Murine typhus is also called what?

A

Fleaborne or Endemic Typhus…

Murine typhus, also called fleaborne or endemic typhus, is caused by the organism Rickettsia typhi. Another organism, R. felis, may also play a role in causing murine typhus. Most of the murine typhus cases in Texas occur in South Texas from Nueces County southward to the Rio Grande Valley..

172
Q

Ehrlichia & Anaplasma what type of cells do they survive in?

A

obligate intracellular bacteria that survive in cytoplasmic vacuoles of mammalian hematopoetic cells (in contrast to Rickettsia and Orientia that live in endothelial cells)

173
Q

Distinguishing feature of Ehrlichia Chaffeensis on HME stain?

A

morula

174
Q

Primary tick vector species for the most common type of ehrlichiosis (Ehrlichia chaffeenis)?

A 
Amblyomma americanum (Lone Star Tick)
Southeast in the US
175
Q

Anaplasma phagocytophilum.
Primarily infects what type of cell?
What species transmits it? What does this species also transmit?

A

Anaplasma phagocytophilum
primarily infects granulocytes (neutrophils and rarely eosinophils). The pathogen is often referred to as the agent of HGE. Transmitted by Ixodes scapularis -can co-transmit the agent of Lyme disease, Borrellia burgdorferi

176
Q

Ixodes scapularis, common name?

A

Deer Tick

Black legs distinguishing factor

177
Q

Coxiella burnetii
How are humans infected?
What does this cause?

A 
Coxiella burnetii (Q fever), humans infected through contact with cattle, goats, sheep (aerosol route)
ticks probably important in animal to animal transmission; atypical pneumonia; rarely endocarditis
178
Q

Best known species of chigger in Northern America?

A

Hard-biting Trombicula alfreddugesi of SE United States and humid mid-west and Mexico
After crawling into their host, they inject disgestive enzymes into skin that break down cells.
Form a hole in the skin called a stylostome, chew up tiny parts of inner skin, causing severe irritation and swelling.

179
Q

Tick-borne bacterial infections

A

Lyme disease, HGE (human granulocytic ehrlichiosis), HME, STARI, endemic relapsing fever, RMSF and sometimes tularemia and Q fever

180
Q

Mites-borne bacterial infections

A

Scrub typhus

Rickettsialpox

181
Q

Lice-borne bacterial infections

A

Trench Fever (WWI)
Epidemic typhus
epidemic relapsing fever

182
Q

Flea-borne bacterial infections

A

endemic typhus (=murine typhus)
murine typhus like
bubonic plague
cat scratch fever

183
Q

Poxviruses:
DNA or RNA?
Where does is replicate?
Common diseases?

A

BIGGEST VIRUS, DNA virus that replicates in the cytoplasm, resistant to inactivation
Diseases: Smallpox; Molluscum contagiosum
Vaccine for smallpox

184
Q

Smallpox

A

SMALLPOX
•Disfiguring disease with high mortality
•Spread by secretions from mouth & nose and by material from pocks or scabs
•Thus, transmission requires close contact with patients or their clothing or bedding

185
Q

Molluscum contagiosum.
Clinical presentation of disease?
How is it spread?

A

Molluscum contagiosum –
Wart-like, 2-5 mm papular lesions on the face, back, and buttocks, mainly in children.
Spread via towels in swimming pools and gymnasiums, by direct contact, possibly through minor skin lesions, and sexually in young adults.

Self limiting after 4 to 6 months, but second attacks are common.
If you are immunocompromised -> can go systemic.

186
Q

Orf lesion is caused by what?

A

Poxvirus of sheep or goats, cowpox and vaccinia can cause this type of lesion as well.
Does not go systemic

187
Q

Monkeypox

A

Disease can be serious but is very rare with a few hundred total cases limited to West and Central Africa.
Does go systemic, can lead to scarring.

188
Q

Rabies
Viral family? Envelope? RNA or DNA?
What clinical manifestation doe it cause?
“Key words”

A

Rhabdovirus
Raccoon main reservoir in the US
Enveloped, negative-sense ss-RNA, bullet shaped
causes an acute encephalitis in all warm-blooded hosts, including humans.

Bullet shaped, negri bodies
Uniformly fatal (untreated)
189
Q

Treatment post exposure for rabies?

A

For persons who have NEVER BEEN VACCINATED against rabies, post-exposure anti-rabies vaccination include passive antibody (HRIG) and vaccine (killed)

190
Q

Coronaviruses cause what infections?

A

common cold

SARS

191
Q

Coronavirus
Envelope?
RNA/DNA?
Capsid symmetry?

A

Enveloped
SS-linear RNA
Helical

192
Q

MERS

A

Coronavirus that looks like SARS

Saudi Arabia, London

193
Q

Influenza virus contains which two antigens on the outside?

A

Hemagglutinin (promotes viral entry)

Neuramidinase (promotes progeny virion release)

194
Q

How do humans get infected with rodent-borne viral illnesses such as CMV and Hantavirus?

A

Contact with rodent excreta - ingestion of contaminated food, direct contact with broken skin, inhalation of tiny particles soiled with rodent urine or saliva (aerosol transmission)

195
Q

Lassa Fever encephalitis is caused by what viral family?

A

Arenavirus
Enveloped SS-circular with 2 segments
Genome contains 2 strands of ambisense RNA (+ and - strands together, S and L

Rodent-borne diseases; each virus usually is associated with a particular rodent host.

The virions are enveloped, and have a grainy appearance caused by ribosomes from their host cells (name is derived from Latin “arena,” which means “sandy.“)

Their genome contains 2 strands of ‘ambisense’ RNA i.e. + and – strands together, S and L.

196
Q

Lassa Fever
Found where?
Reservoir?
How is infection spread?

A

Found predominantly in West Africa, in particular Nigeria, Sierra Leone and Liberia.
The natural reservoir is the multimammate rat (Mastomys)
Infections are through contact with infected urine and feces.
Human to human transmission can occur through infected body fluids.

Well documented nosocomial outbreaks

197
Q

Reassortment, which virus should come to mind?

A

FLU

198
Q

LCMV (Lymphocytic choriomeningitis virus)
Viral family
Clinical Presentation
How is it spread?

A

Arenavirus
Presents as aseptic meningitis or encephalitis: asympt. infection or mild febrile illness.
Biphasic febrile illness: initial phase (week) fever, malaise, anorexia, muscle aches, headache. few days of remission then…
second phase: meningitis, or encephalitis

Spread by common house mouse, mus musculus

199
Q

Hantavirus:
Viral family?
How is it transmitted?

A

Bunyavirus
Enveloped, SS- circular, 3 negative segments (L, M, S)
>Unlike other bunyaviridae, its transmission is by inhalation of infected rodent excrement or by direct contact through skin (not an insect)

200
Q

Hantavirus pulmonary syndrome (HPS)

Clinical presentation

A

Bunyavirus!
damage to the capillaries occurs predominantly in the lungs rather than the kidney (compared to HFRS)

majority of HPS cases caused by the Sin Nombre virus
“Four Corners” area of New Mexico

201
Q

Common Features of Hantavirus

A

Headaches, back/abdominal pain, fever, chills, nausea, blurred vision
Then… HFRS vs HPS
Think of patient history! (Southwest US)

202
Q

Hemorrhagic Fever with Renal Syndrome (HFRS)

A

Hantavirus
Fever headache hemorrhage and acute renal failure
Systemic

203
Q

Arbovirus means what?

A

transmitted by arthropods (mosquitos or ticks)

The vector is insect, reservoir is usually an animal (zoonosis) and humans are dead-end host

204
Q

NEED to know arboviruses! (all in first aid)

A

West Nile virus, St. Louis Encephalitis, Yellow Fever, Dengue- Flavivirus
EEE, WEE - Togavirus
California serogroup (most common cause mosquito borne encephalitis) , La Crosse (peds in midwest) - Bunyavirus

205
Q

What are some distinguishing features of reoviruses?

A

NOT enveloped

DOUBLE STRANDED RNA virus

206
Q

How many segments do bunyaviridae have?

A

3 segments

207
Q

How do you diagnose arbovirus infection?

A

Serology- acute titer and convalescent weeks later

Direct Detection Tests - assays for detection of antigen or nucleic acids (PCR)

208
Q

Yellow Fever
Viral family
Where is it?

A

Flavivirus

Now mainly in West Africa and South America

209
Q

Yellow Fever, how many forms?

A

Occurs in two major forms (urban and jungle)

Jungle YF is the natural reservoir of the disease in a cycle involving non-human primates and forest mosquitoes. Humans may become incidentally infected upon venturing into jungle.

Urban YF is transmitted between humans by the Aedes aegypti mosquito.

210
Q

Symptoms of Yellow Fever

A

Symptoms: Classically yellow fever presents with chills, fever, and headache, generalized myalgias and GI complaints (N+V).
GI haemorrhage leads to “black vomit” and liver involvement causes jaundice (hence, “Yellow fever). 50% of patients with frank YF will die.

211
Q

How is diagnosis made for Yellow Fever?
Is there an antiviral treatment?
Is there a vaccine?

A

Diagnosis: Usually made by serology.

There is no specific antiviral treatment

An effective live attenuated vaccine (17D) is available and is used for persons living in or travelling to endemic areas.

212
Q

Dengue
Viral Family?
Where is it found?

A

Flavivirus, 4 serotypes.
Biggest arbovirus problem in the world today! Over 2 million cases per year.
Found in SE Asia, Afica, and Caribbean and S America

213
Q

Is there a vaccine for Dengue?

A

NO, there are 4 serotypes of Dengue. If you are infected with 1 serotype youll feel crappy, 2nd infection youll feel even worse… etc. If you vaccinate your population, you need a vaccination that has all 4 serotypes in the vaccine. If only 1 or 2 work in the vaccine, if the patient gets the other strains, you are priming them for a severe infection the first time they are exposed.

214
Q

Symptoms of Dengue?

A

Classically, high fever, lymphadenopathy, myalgia, bone and joint pains, headache, and a maculopapular rash.
Severe cases may present with hemorraghic fever and shock with a mortality of 5-10% (Dengue HF or Dengue shock syndrome). Seen most often in patients previously infected with a different serotype, suggesting a immunopathogenic mechanism

215
Q

Flaviviruses

A 
HCV
Yellow Fever
Dengue
St. Louis Encephalitis
West Nile Virus
216
Q

Toga (alpha) viruses transmitted by what?

A

insects, mosquito borne

217
Q

Togaviruses?

A

Rubella
Eastern equine encephalitis
Western equine encephalitis

218
Q

Most important cause of pediatric arbovirus encephalitis in US?

A

La Crosse Virus
Bunyavirus
Localized in Midwest states

219
Q

Colorado tick fever Virus
Viral family?
Tranmission?
Disease?

A

Reovirus
Wood tick transmission high in the colorado mountains!
Disease: generally mild or subclinical. Symptoms of acute disease resembles those of dengue. Incubation period 3 to 6 days, then fever, chills, headache, myalgia, athralgia, photophobia, lethargy.

220
Q

First line of treatment for Q fever?

A

Doxycycline, adults and children with severe illness. If patient does not respond, they may not have Q fever.

221
Q

What organism causes Q fever?

A

Coxiella Burnetti

222
Q

Leptospirosis caued by what organism?

A

Leptospira interrogans

223
Q

Question mark-shaped bacteria found in water contaminated with animal urine

A

Leptospira interrogans

224
Q

What are the symptoms of Leptospirosis

A

Flulike symptoms, jaundice, photophobia with conjunctivitis.

225
Q

Most prevalent infection among surfers and in the tropics

A

Leptospira interrogans

226
Q

What is Weil’s Disease?

A

Icterohemorrhagic leptospirosis

Severe form of jaundice and azotemia from liver and kidney dysfunction; fever hemorrhage and anemia

227
Q

How do you have to examine Leptospira organisms?

A

Best visualized by dark-field microscope

228
Q

RABBIT. What disease?

A

Tularemia

229
Q

What organism causes Tularemia?

A

zoonotic infection caused by Francisella tularensis, fastidious gram negative bacteria

230
Q

Tularemia: what is the most common presentation?

A

Ulceroglandular
Most common form of tularemia, occurs following a tick or deer fly bite or after handling of an infected animal.
Skin ulcer: at the site where the organism entered the body. Ulcer accompanied by swelling of regional lymph glands, usually in the axillae or groin.

231
Q

Tularemia Treatment

A

Streptomycin

232
Q

Conjugate vaccines are good for what age group?

A

children
T independent antigens, like polysaccharides, are not recognized by children less than 2.

When polysaccharide is conjugated to protein, all ages recognize it and respond with T cell help, and then IgG and memory cells can come too. Allow young children to make anti-polysaccharide responses.

233
Q

DTaP vaccine

A

Tetanus, diptheria, acellular pertussis

234
Q

Whooping cough organism

A

Bordetella pertussis.
Gram negative, short coccobacilli, pleomorphic, encapsulated when virulent.

Acute infectious disease of tracheobronchial tree with characteristic clinical picture

235
Q

Bordetella Pertussis growth requirements

A

Bordet-Gengou agar

or, preferred, Regan Lowe (RL) charcoal medium supplemented with horse blood

236
Q

Two toxins associated with Bordetella pertussis

A

Pertussis toxin -> ADP is on -> increased cAMP -> increased fluid -> increased secretions. Also systemic effect.

Adenylate cyclase toxin resembling anthran edema toxin effect -> inc. cAMP increased fluid secretion in URT

237
Q

Adhesive factors of the Bordetella pertussis

A

Filamentous hemagglutinin and pertactin are the adhesive factors.

238
Q

Does Bordetella pertussis get in the blood stream?

A

No!

239
Q

What is the organism that causes Diphtheria

A

Corynebacterium diphtheriae

240
Q

“chinese letters” with bacteria

A

Corynebacterium diphtheriae

241
Q

Corynebacterium diphtheriae toxin

A

Potent exotoxin inhibits protein synthesis via ADP ribosylation of EF-2. Exotoxin encoded by Beta-prophage

242
Q

Diphtheria clinical symptoms

A

Pseudomembranous pharyngitis (grayish-white membrane) with lymphadenopathy

243
Q

Corynebacterium diphtheriae ABCDEFG

A 
ADP ribosylation
Beta-prophage
Corynebacterium
Diphtheria
Elongation Factor-2
Granules
244
Q

Macularpapular rashes

A

Measles
Rubella
Parvovirus P19

245
Q

Vesicular/papular

A

Varicella
Smallpox
Coxsackievirus Group A members (HFMD)

246
Q

Any RNA virus that is negative sense has to go to positive sense RNA… how does it do this?

A

RNA-dependent RNA polymerase

247
Q

Paramyxoviruses

A

Parainfluenza - croup
RSV - bronchiolitis in babies
Rubeola (Measles) Mumps

248
Q

What is the MOST important cause of lower respiratory tract disease in young children

A

RSV
Will infect virtually all infants by age 2
Symptoms resemble common cold

249
Q

Common cold virus

A

Rhinovirus

250
Q

Mumps virus POM

A

Parotitis
Orchitis
Meningitis

Flu like symptoms.

251
Q

Does infection or vaccine cause life long immunity?

A

Yes!

Infection confers lifelong immunity because there is one serotype worldwide and infection is systemic.

252
Q

Two systemic paramyxoviruses

A

Measles

Mumps

253
Q

Rubeola common name

A

Measles

254
Q

With measles virus, patients with reduced cell-mediated immunity (CMI) do not develop a rash. What will they develop instead?

A

Measles giant cell pneumonia

255
Q

MMR vaccine

A

Measles Mumps Rubella

Live attenuated virus

256
Q

What viral family does Rubella belong to?

A

Togavirus

257
Q

German Measles

A

Rubella

258
Q

Clinically apparent rubella

A

Clinically apparent rubella: any combination of symptoms that include maculopapular rash (Rubelliform) lymphadenopathy, low-grade fever, conjunctivitis, sore throat, and arthralgia.

259
Q

The Rubella vaccine is primarily a benefit to whom?

A

The benefit of the unborn to inhibit a congenital infection (toRches)
An infection in the young will almost always just lead to a rash and thats it

260
Q

Parvovirus B19 nickname

A

Slap cheek syndrome!

261
Q

Human Disease associated with B19

A

Erythema infectiosum (EI, 5th disease)
Apastic crisis in people with chronic hemolytic anemia (sickle cell anemia)
Hydrops fatalis (anemia & congestive heart failure)
Polyarthritis

MultiSystem Module (6 decks)

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