Zoonotic Infectections Flashcards

(74 cards)

1
Q

Rickettsia, Ehrilichia, Coxiella:
• what are their common structural characterisitcs?
• What is unique about the location of Rickettsial infections?

A

Rickettsia and related bugs

General Characteristics: These are very short gram negative rods (weak staining) that are obligate intracellular parasites.

There are three general phyla: Rickettsia, Ehrilichia, Coxiella.

Rickettsia only infect the ENDOTHELIAL LINING of VESSELS (vasculitis) causing the edema and hemorrhages the lead to the presentation of rash

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2
Q

Given the unique method of infection for rickettsia, what would you expect to be unique about the way the rash presents?

A

Rickettsia:
• Produce a VASCULITIS by infectin the vascular endothelium leading to paplable purpura

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3
Q

Coxiella, Ehrilichia, Rickettsia
• Endotoxin?
• Exotoxin?
• Tx?

A

LPS (endotoxin) this is how they cause petechial rashes. (differentiate this from the papbable rash caused by RMSF)

They do not produce exotoxins or cytolytic enzymes. These are generally treated with tetracyclines (doxycycline).

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4
Q

Rocky Mountain Spotted Fever
• Pathogen
• Structure
• Transmission
• Reservoir

A

RMSF – Rickettsia rickettsii

Structure
very short gram negative rods (weak staining)

Transmission
Ticks, especially DOG TICKS => VECTOR
Dogs and Rats => Reservoir

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5
Q

Rocky Mountain Spotted Fever
• Pathogen and Structure
• Location of Replication

A

RMSF – Rickettsia rickettsii

Structure
very short gram negative rods (weak staining)

Replication Cycle
Obligate Intracellular Parasite – ENDOTHELIAL CELLS

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6
Q

Rocky Moutain Spotted Fever
• Disease Presentation

A

RMSF – Rickettsia rickettsii

Structure
very short gram negative rods (weak staining)

Disease Presentation

  • Acute onset of flu-like symptoms, with **myalgias ESPECIALLY IN THE CALVES
  • 2-6 days latertheRASHWILL DEVELOP on theWRISTS and spreads to PALMS, SOLES, and then Trunk. Presence of LPS means this disease can develop intoshock-like symptoms:** DIC, HypoTN, Altered mental state.
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7
Q

RMSF
• what is unique about the cells it infects?

A

RMSF – Rickettsia rickettsii

Structure
very short gram negative rods (weak staining)

Pathogenic Mechanism
These infect the ENDOTHELIAL LINING of VESSELS (vasculitis) causing the edema and hemorrhages

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8
Q

RMSF
• where do you typically get it?

A

RMSF – Rickettsia rickettsii

Structure
very short gram negative rods (weak staining)

Epidemiology
Most common in Georgria, North Carolina, and Virginia, most commonly occurring in children in the spring and summer months. 95% of rickettsial disease.

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9
Q

RMSF
• Treatment
• Mortality

A

RMSF – Rickettsia rickettsii

Structure
very short gram negative rods (weak staining)

Treatment
Doxycycline

Mortality

25% fatal if left untreated

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10
Q

RMSF
• Key findings
• Diagnosis

A

RMSF – Rickettsia rickettsii

Structure
very short gram negative rods (weak staining)

Key findings/Diagnosis

Key Findings: Calf pain + Spreading rash that starts on wrists and involves palms then Trunk

DX: Weil-Felix Test – ab. cx rxn with proteus species proteins or Immunostain (IFA)

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11
Q

Epidemic Typhus
• Causative agent
• Vector
• Reservoir

A

EPIDEMIC TYPHUS – Rickettsia prowazeki

Structure

Short gram negative rod (weak staining)

Transmission

Human to Human by Lice feces

Flying Squirrels might be a reservoir

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12
Q

Epidemic Typus
• Where does replication occur?
• Structure

A

EPIDEMIC TYPHUS – Rickettsia prowazeki

Structure

Short gram negative rod (weak staining)

Replication Cycle

Obligate Intracellular Parasite – ENDOTHELIAL CELLS

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13
Q

Epidemic Typhus
• Disease Presentation
• What kills them
• Bug

A

EPIDEMIC TYPHUS – Rickettsia prowazeki

Structure

Short gram negative rod (weak staining)

Disease Presentation

Onset occurs 1 to 3 weeks after exposure to a louse people develop flu-like symptoms. 5-9 days later you get a rash that spreads from trunk to extremities (opposite of RMSF and no rash EVER develops on palms or soles). Myocarditis and CNS involvement may come into play later. People usually die of vascular collapse and pneumonia.

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14
Q

Epidemic Typhus
• What cells does it infect
• Epidemiology
• Tx

A

EPIDEMIC TYPHUS – Rickettsia prowazeki

Structure

Short gram negative rod (weak staining)

Pathogenic Mechanism
These infect the ENDOTHELIAL LINING of VESSELS (vasculitis) causing the edema and hemorrhages

Epidemiology
Virtually absent in the US; mostly Asia, Africa, Mexico (mountains), Central/South America

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15
Q

Epidemic Typhus
• Is it fatal

A

EPIDEMIC TYPHUS – Rickettsia prowazeki

Structure

Short gram negative rod (weak staining)

Mortality
10-60% die if not treated

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16
Q

Epidemic Typus
• Key points
• Diagnosis
• Bug

A

EPIDEMIC TYPHUS – Rickettsia prowazeki

Structure

Short gram negative rod (weak staining)

Key findings/Diagnosis

Key finding: 1-3 weeks from exposure to flu, rash on trunk to extremities 1 wk later, NO PALMS

Dx: IFA to see the bugs or ELISA with 4x increase in anti-R. prowazekii titer

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17
Q

Murine Typhus
• Bug/Structure
• Transmission

A

MURINE TYPHUS – Rickettsia typhi

Structure

Small gram negative rod (weak stain)

Transmission

Rat Flea => Vector

Opossums and Rats are the => Reservoir

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18
Q

Murine Typhus
• where does it replicate

A

Replication Cycle

Obligate Intracellular Parasite – ENDOTHELIAL CELLS

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19
Q

Murine Typhus
• Disease Presentation
• Bug

A

MURINE TYPHUS – Rickettsia typhi

Structure

Small gram negative rod (weak stain)

Disease Presentation
Similar symptoms to epidemic typhus (R. prowazekii) with 1-3 wk incubation period followed by flu-like symptoms and a rash a week later that starts on the trunk and spreads to the extremities never involving the palms or soles. The difference btwn this and R. prowazekii is much milder presentation and rash is only present 50% of the time.

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20
Q

Murine Typus
• What cells does it infect
• where is it found
• Bug

A

MURINE TYPHUS – Rickettsia typhi

Structure

Small gram negative rod (weak stain)

Pathogenic Mechanism

These infect the ENDOTHELIAL LINING of VESSELS (vasculitis) causing the edema and hemorrhages

Epidemiology

NOT IN US

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21
Q

Murine Typhus
• Tx
• Mortality
• Dx

A

MURINE TYPHUS – Rickettsia typhi

Structure

Small gram negative rod (weak stain)

Pathogenic Mechanism

These infect the ENDOTHELIAL LINING of VESSELS (vasculitis) causing the edema and hemorrhages

Epidemiology

NOT IN US

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22
Q

Ehrlichiosis
• Bug
• Vector
• Where does it replicate

A

HUMAN MONOCYTIC EHRLICHIOSIS – Ehrlichia chaffeesis

Structure
Gram negative rod

Transmission
Lone Star Star Deer Tick

Replication Cycle

Intracellular – MONOCYTES

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23
Q

Ehrlichiosis
• Bug
• How does it present

A

HUMAN MONOCYTIC EHRLICHIOSIS – Ehrlichia chaffeesis

Structure
Gram negative rod

Disease Presentation

Flu-like symptoms + N/V/D + Cough + CONJUNCTIVAL INJECTION ± Rash (30% adults, 60% kids)

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24
Q

Ehrliciosis
• Where does it replicate
• Where are you most likely to get it?

A

HUMAN MONOCYTIC EHRLICHIOSIS – Ehrlichia chaffeesis

Structure
Gram negative rod

Pathogenic Mechanism

Infects by replicating inside of MONOCYTES

Epidemiology

Southeast U.S. (including TX, AK, IOWA)

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25
Ehrliciosis • Treatment • mortality
**_HUMAN MONOCYTIC EHRLICHIOSIS – Ehrlichia chaffeesis_** _Structure_ Gram negative rod _Treatment_ Doxycycline _Mortality_ 1.8%
26
Ehriliciosis • Key points • Diagnosis
**_HUMAN MONOCYTIC EHRLICHIOSIS – Ehrlichia chaffeesis_** _Structure_ Gram negative rod _Key findings/Diagnosis_ Key: **Conjunctivitis + morulae in monocytes + southeast U.S.** DX: **Blood Smear + Serology** (NOT Weil-Felix)
27
Rocky Moutain Spotless Fever • Bug • Vector • Replication location
**_ROCKY MOUNTAIN SPOTLESS FEVER – Anaplasma phagocytophilia_** _Structure_ Small gram-negative Rod (weak stain) _Transmission_ **Ixodes Blacklegged Ticks** _Replication Cycle_ Intracelluar Replication inside of *GRANULOCYTES*
28
Rocky Mountain Spotless Fever • Bug • Disease Presentation
**_ROCKY MOUNTAIN SPOTLESS FEVER – Anaplasma phagocytophilia_** _Structure_ Small gram-negative Rod (weak stain) _Disease Presentation_ **Flu-like symptoms ± (shocky symptoms) Dyspnea, Hemorrhage, Renal Failure, CNS problems** **\*\*Note the absence of rash**
29
Rocky Moutain Spotless Fever • where are you most likely to get it? • Tx
**_ROCKY MOUNTAIN SPOTLESS FEVER – Anaplasma phagocytophilia_** _Structure_ Small gram-negative Rod (weak stain) _Epidemiology_ **East especially SOUTHEast + California** _Treatment_ Doxycycline
30
Rocky Moutain Spotless Fever • Diagosis
**_ROCKY MOUNTAIN SPOTLESS FEVER – Anaplasma phagocytophilia_** _Structure_ Small gram-negative Rod (weak stain) _Key findings/Diagnosis_ Dx: **MORULAE IN NEUTROPHILS = Pathognomonic**
31
Q Fever • Bug • Stucture • where does it live
**_Q-FEVER – Coxiella burnetii_** _Structure_ **Gram-negative bacillus** that is an **obligate intraceullular parasite** living in **MACROPHAGES**
32
Q Fever • Vector • Other methods of Transmission
**_Q-FEVER – Coxiella burnetii_** _Structure_ **Gram-negative bacillus** _Transmission_ Usually happens when humans handle **contaminated viscera (during birth) or drink raw milk. TICKS** also carry this pathogen.**Aerosolized SPORES** are also very infective. **EASILY transmitted** (very low infectious dose
33
Q fever • Bug • Where does it replicate • Disease Presentation
**_Q-FEVER – Coxiella burnetii_** _Structure_ **Gram-negative bacillus** _Replication Cycle_ Obligate Intracellular – *MACROPHAGES* _Disease Presentation_ **30-50% of cases are asymptomatic**, others experience **2-4 weeks of ATYPICAL pneumonia with HIGH FEVER.** Sometimes the liver and heart are involved which can lead to **endocarditis or granulomatous hepatitis.**
34
Q fever • Where are you most likely to get this? • Tx
**_Q-FEVER – Coxiella burnetii_** _Structure_ **Gram-negative bacillus** _Epidemiology_ Affect **GOATS** mainly, but also infects cattle, and sheep. Seen in almost **every country**. _Treatment_ **Doxycycline** can be used but **resolve spontaneously**
35
Q fever • Mortality • Dx • Key findings
**_Q-FEVER – Coxiella burnetii_** _Structure_ **Gram-negative bacillus** _Mortality_ **Very low, below 2% , but 100% if left untreated** _Key findings/Diagnosis_ Granulomatous liver dz, or endocarditis, Unique Spore Transmission **Dx: SEROLOGICAL** - look for **increasing titers** to Coxiella b
36
Name the spirochete responsible for the following diseases: • Lyme disease • Relapsing Fever • Leptospirosis
Lyme Disease = Borrelia burgdoferi Relapsing Fever = Borrelia hersi/recurrentis Leptospirosis = Leptospira Interrogans
37
Lyme Disease • Bug • Structure • Vector • How long does transmission take?
**_LYME DISEASE – Borrelia burgdoferi_** _Structure_ **Small** Spirochete only visible with Darkfield microscopy, Giemsa, or Silver Stain _Transmission_ Small Nymphal Stage Ticks (24-48 hrs of feeding required) East Coast and Midwest = **Ixodes scapularis** West Coast = **Ixodes pacificus** Small mammals =\> **White Footed Mouse**
38
Lyme Disease • Bug • Most likely time to contract • Disease progression/presentation
**_LYME DISEASE – Borrelia burgdoferi_** _Structure_ **Small** Spirochete only visible with Darkfield microscopy, Giemsa, or Silver Stain _Disease Presentation_ Infection typically happens during the Summer Months _Pathogenic Mechanism_ No exotoxin or enzymes but Bites skin (*bulls eye rash*) = days =\> gets into blood (*arthralgia*) = weeks/months **=\> Heart, Joints (*arthritis*) , and CNS most affected (BILATEAL BELLS PALSY)**. **ANTIGENIC VARIATION** in outter surface proteins leads to PERSISTANT INFECTION.
39
Lyme Disease • bug • Epidemiology • Tx
**_LYME DISEASE – Borrelia burgdoferi_** _Structure_ **Small** Spirochete only visible with Darkfield microscopy, Giemsa, or Silver Stain _Epidemiology_ **Summer in NY, CT, PA, NJ;** but may be present worldwide _Treatment_ Early – Doxycycline, tetracycline, amoxicillin Chronic – IV cephalosporins or Penicllin G
40
Lyme Disease • Diagnosis • Bug
**_LYME DISEASE – Borrelia burgdoferi_** _Structure_ **Small** Spirochete only visible with Darkfield microscopy, Giemsa, or Silver Stain _Key findings/Diagnosi_ Dx: Cultures are Typically NEGATIVE so do.. **• ELISA (sensitive not specific, IgM, IgG) =\>** **WESTERN BLOT confirmation • PCR**
41
Relapsing Fever • Bug • Structure • Transmission
**_RELAPSING FEVER – Borrelia hernsii/recurrentis_** _Structure_ **Spirochete – ONLY ONE VISIBLE ON Light Micro** _Transmission_ **B. hernsii – Ioxdes tick B. recurrentis – Body Louse** **Rodents and Small animals =\> Reservoirs**
42
Relapsing Fever • Disease Presentation • Pathogenic mechanism
**_RELAPSING FEVER – Borrelia hernsii/recurrentis_** _Structure_ **Spirochete – ONLY ONE VISIBLE ON Light Micro** _Disease Presentation_ No associated skin rash (like with B. burgoderfori). **Fever for a week** then **recurs 2 weeks later**. This may occur up to **10 times.** _Pathogenic Mechanism_ **ANTIGENIC VARIATION** in Outer Surface Proteins is key to characteristic recurrent infections (no other virulence factors).
43
Relapsing Fever • Where are you most likely to get this? • Tx • Bug
**_RELAPSING FEVER – Borrelia hernsii/recurrentis_** _Structure_ **Spirochete – ONLY ONE VISIBLE ON Light Micro** _Epidemiology_ Western U.S. predominantly, but is endemic almost everywhere _Treatment_ Doxycycline or Tetracycline _Mortality_
44
Relapsing Fever • Bug • Diangosis
**_RELAPSING FEVER – Borrelia hernsii/recurrentis_** _Structure_ **Spirochete – ONLY ONE VISIBLE ON Light Micro** _Key findings/Diagnosis_ Dx: **Blood Smear with Spirochetes in Plasma**; Serology typically useless \*\*\*This is important b/c its the only spirochete you can see on LM\*\*\*
45
Leptosirosis • Bug • Structure • Vector, Reservoir
**_LEPTOSPIROSIS – Leptospira interrogans_** _Structure_ *Tightly Coiled* Spirochetes, not visible on Light Microscopy _Transmission_ **Mucosal or Cutaneous =\> No vector, Contaminated H2O** **Dogs =\> U.S. Reservoir** (other mammals may also carry)
46
Leptospirosis • bug • Disease Presentation
**_LEPTOSPIROSIS – Leptospira interrogans_** _Structure_ *Tightly Coiled* Spirochetes, not visible on Light Microscopy _Disease Presentation (BIPHASIC)_ Patients come in with **flu-like symptoms and CONJUCTIVAL SUFFUSION** (eye redness and swelling with no exudate). The **infection clears** up **the comes back and is severe***: ASEPTIC MENIGITIS, LIVER DAMAGE, IMPAIRED KIDNEY FUNCTION (UREMIA; Weil’s Disease) and/or LUNG HEMMORHAGE*.
47
Leptospirosis • Bug • Mechanism of Biphasic illness • Epidemiology
**_LEPTOSPIROSIS – Leptospira interrogans_** _Structure_ *Tightly Coiled* Spirochetes, not visible on Light Microscopy _Pathogenic Mechanism_ Bacteria spread from **skin to liver, kidney, lungs, and CNS. ANTIGENIC VARIATION** _Epidemiology_ **Urban poor, SWIMMERS, MINERS, AND FARMERS are at the highest risk**
48
Leptospirosis • Tx • Dx
**_LEPTOSPIROSIS – Leptospira interrogans_** _Structure_ *Tightly Coiled* Spirochetes, not visible on Light Microscopy _Treatment_ Penicillin G Prevention possible for animals: Vaccine _Key findings/Diagnosis_ Dx: **History, Clinical Signs, IgM titers, \*\*\*Culture is rarely possible**
49
What is a common theme in the disease presentation of spirochete? • Cause?
Antigenic variation causes multi-phasic illness
50
Cat Scratch Disease • Bug/Stucture • Transmision
**_Bartonella heneslae (Cat Scratch Disease)_** _Structure_ Small pleomorphic Rod (proteobacterium) _Transmission_ Cat Scratch/Bite (**NOT urine or feces – no risk)** No person-person transmission
51
Cat Scratch Disease • Disease Presentation • Complications • Tx
**_Bartonella heneslae (Cat Scratch Disease)_** _Structure_ Small pleomorphic Rod (proteobacterium) _Disease Presentation_ Self-limiting in immunocompetent people. **Fever and papule at site of lesion with LAD on the side of the scratch.** Long course. **Endocarditis and Encephalitis** may develop rarely. **AIDS patients may get organ involvement.** _Treatment_ Typically no Tx. Needed, Doxycycline, Erythromycin, and Azithromycin is used for serous infection.
52
Cat Scratch Disease • Dx • bug
**_Bartonella heneslae (Cat Scratch Disease)_** _Structure_ Small pleomorphic Rod (proteobacterium) _Key findings/Diagnosis_ Key finding: Does not grow on routine agar Dx: **Serology, Warthin-Starry Silver Stain**
53
Anthrax • Bug • Structure -\> be specific • Transmission
**_ANTHRAX – Bacillus anthracis_** _Structure:_ Large **gram-positive spore forming rod** with **sqaure ends**, frequently found in chains. **antiphagocytic capsule** is composed of **_d-glutamate_****.** _Transmission:_ Typically happens via **cutaneous** transmission with **animal products** but can also be transmitted from person to person via **aerosolized particles.** If ingested can cause **GI** illness too.
54
Anthrax • Where does it live in humans? • Where does it live outside of humans?
**_ANTHRAX – Bacillus anthracis_** _Structure:_ Large **gram-positive spore forming rod** with **sqaure ends**, frequently found in chains. **antiphagocytic capsule** is composed of **_d-glutamate_****.** _Replication Cycle:_ Exists in carriers as a **Facultative Intracellular** organism. **Spore forming** so may exist in **animal feces.**
55
Antrax • Presentation
**_ANTHRAX – Bacillus anthracis_** _Structure:_ Large **gram-positive spore forming rod** with **sqaure ends**, frequently found in chains. **antiphagocytic capsule** is composed of **_d-glutamate_****.** _Disease Presentation:_ **Most commonly** this is a **cutaneous infection**, but the **PULMONARY** infection is **most deadly.** **GI infections** are also extremely deadly. **Pneumonic Disease** typically sets in between **4-6** days (**spores** can sit in macs for up to **6wks**). Typically there is a **short prodromal period** (non-productive cough, sore throat, mild fever, myagia) **followed by severe illness** (tachycardia, hypoxia, sweating, chills, etc).
56
Anthrax • how is it so prolific inside of people?
**_ANTHRAX – Bacillus anthracis_** _Structure:_ Large **gram-positive spore forming rod** with **sqaure ends**, frequently found in chains. **antiphagocytic capsule** is composed of **_d-glutamate_****.** _Pathogenic Mechanism:_ **capsule prevents direct recognition by phagocytes** (PAMPS are covered and can't be see by pattern recognition receptors), it also produces **several toxins.** **NOTE:** both capsule and toxin genes are coded for an **separate plasmids.**
57
Anthrax • what kills you • bug
**_ANTHRAX – Bacillus anthracis_** _Structure:_ Large **gram-positive spore forming rod** with **sqaure ends**, frequently found in chains. **antiphagocytic capsule** is composed of **_d-glutamate_****.** **Death** is caused by **blockage of pneumonic vessels** (leading to edema and death) or by **cytokine storm** causing **septic shock and death**
58
Anthrax • Who typically gets it? • Tx (explain)
**_ANTHRAX – Bacillus anthracis_** _Structure:_ Large **gram-positive spore forming rod** with **sqaure ends**, frequently found in chains. **antiphagocytic capsule** is composed of **_d-glutamate_****.** _Epidemiology_ **Cattle and Sheep** carry this toxin **(consider wool and other animal products** made from these) _Treatment_ * *Prophylaxis - Ciprofloxacin 60 days** * *Severe Dz: Cipro + Penicillins, Vancomycin, or Rifampicin**
59
Anthrax • Mortality • Key findings
**_ANTHRAX – Bacillus anthracis_** _Structure:_ Large **gram-positive spore forming rod** with **sqaure ends**, frequently found in chains. **antiphagocytic capsule** is composed of **_d-glutamate_****.** _Mortality_ 50%-70% mortality in pulmonary form even with proper tx. _Key Findings/Diagnosis_ * *CXR: Mediastinal Widening or pleural effusion** * *Dx: Culture or Test blood for Abs. or Toxins**
60
Meliodosis • Bug • Structure • Transmission
**_MELIOIDOSIS - Burkhoderia pseudomallei_** _Structure_ Small **ENCAPSULATED** **motile gram-negative rod** that is a**facultative intracellular bacterium** _Transmission_ Occurs via **Aerosolized bacteria after RAIN STORM (MOST COMMON ROUTE) =\> VERY TRANSMISSIBLE**. Direct contact can also lead to **cutaneous** infections. **Person-to-person transmission is possible with BODY FLUIDs.**
61
Meliodosis •Bug • disease presentation
**_MELIOIDOSIS - Burkhoderia pseudomallei_** _Structure_ Small **ENCAPSULATED** **motile gram-negative rod** that is a**facultative intracellular bacterium** _Disease Presentation =\> **Whitmore's disease**_ Disease may present as **acute, subacute, or chronic.** Due to latency diseas symtoms of HIGH fever, muscle soreness, chest pain, cough (productive or non-prod.) **may present in 2-3 days or in years. Sepsis is very possible.**
62
Meliodosis • Bug • How does it proliferate
**_MELIOIDOSIS - Burkhoderia pseudomallei_** _Structure_ Small **ENCAPSULATED** **motile gram-negative rod** that is a**facultative intracellular bacterium** _Pathogenic Mechanism_ Avoiding phagocytosis via its **anti-phagocytic capsule**, Burkholderia moves into **macrophages (hence granuloma formation)** and replicates. Once replicated it can spread via **1. lysing the host and releasing progeny 2. propelling itself via ACTIN network** into adjacent cells to avoid detection. It is also able to lay **latent for many years Vietanamese time-bomb.**
63
Meliodosis • bug • Epidemiology
**_MELIOIDOSIS - Burkhoderia pseudomallei_** _Structure_ Small **ENCAPSULATED** **motile gram-negative rod** that is a**facultative intracellular bacterium** ``` _Epidemiology_ Southeast Asia (Thialand and N. Australia) found in rice, soil, and muddy H2O (**can live in H2O for a LONG time** - by inhabiting amoebas). Many farm animals can also harbor this infection. ```
64
Meliodosis • tx • mortality
**_MELIOIDOSIS - Burkhoderia pseudomallei_** _Structure_ Small **ENCAPSULATED** **motile gram-negative rod** that is a**facultative intracellular bacterium** _Treatment_ **Ceftazidime for at least 8 weeks, or 6 months if immunocompromised** (intrinsically **resistant Gentamicin and Colistin)** _Mortality_ **20-50% of cases result in sepsis or death**
65
Meliodosis • Key findings • Dx
**_MELIOIDOSIS - Burkhoderia pseudomallei_** _Structure_ Small **ENCAPSULATED** **motile gram-negative rod** that is a**facultative intracellular bacterium** _Key findings/Diagnosis_ CXR shows **UPPER lobe consolidation or Abscess with GRNAULOMAS** and may resemble MTB. **Dx: 2 steps - Isolate and culture AND look at antibodies in convelscent serum**
66
Tularemia • Bug • Vector/transmission
**_TULAREMIA – Fracicella tularensis_** _Structure_ **small pleomorphic Gram-negative rod, obligate intracellular** (w/ significant extracellular portion of life cycle), 2 type exist _Transmission_ **Ticks** are the most common vector of transmission and also mice and lice. Lives in **amoebas and survives a long time in H2O,** but can also be transmitted via **blood blood or ingestion. _VERY VERY Transmissible in aerosol. THINK DEAD RABBITS_**
67
Tularemia • Bug • How does it go undetected • Where does it infect/presentation
**_TULAREMIA – Fracicella tularensis_** _Structure_ **small pleomorphic Gram-negative rod, obligate intracellular** (w/ significant extracellular portion of life cycle), 2 type exist _Pathogenic Mechanism_ **_LPS that cannot be recognized by TLR-4_**. It can **infect skin (lymph), GI, or eye and disseminate to the lungs** or it can go directly their depending on the mode of transmission.
68
Tularemia • Bug • Where are you most likely to get it • Tx
**_TULAREMIA – Fracicella tularensis_** _Structure_ **small pleomorphic Gram-negative rod, obligate intracellular** (w/ significant extracellular portion of life cycle), 2 type exist _Epidemiology_ 2 types - **_type A - A_**_merican strain_ - **more virulent**, type B - Europe - less virulent. Most cases are in **Arkansas, Missouri, and Massachusetts.** _Treatment_ * *Streptomycin (resistance not an issue)** * *Live VACCINE is available to military personnel**
69
Tularemia • Bug • Mortality • Key findings
**_TULAREMIA – Fracicella tularensis_** _Structure_ **small pleomorphic Gram-negative rod, obligate intracellular** (w/ significant extracellular portion of life cycle), 2 type exist _Mortality_ **1-3% mortality rate** without treatment, **survivors have lifelong immunity** _Key findings/Diagnosis_ CXR: Spotted infiltrates or Lobular, pleural exudation possible **Severe Conjunctivitis, BUBO-LIKE LYMPHADENOPATHY** (in surrounding regions) **Dx: Serology**
70
Plague • Bug/Structure • Reservoir/Vector
**_PLAGUE – Yersina pestis_** _Structure_ **small encapsulated gram-negative rod** (lost upon passage in vitro) that lives **intracellularly** (in macs) and exibits **bipolar staining to resemble a SAFETY PIN** _Transmission_ **INSANELY transmissible (1-10 bugs). RATS AND PRAIRIE DOGS carry and FLEAS bite them and then bite people to transmit. AEROSOLIZED particles are also transmissible (most virulent).**
71
Plauge • Bug • Presentation
**_PLAGUE – Yersina pestis_** _Structure_ **small encapsulated gram-negative rod** (lost upon passage in vitro) that lives **intracellularly** (in macs) and exibits **bipolar staining to resemble a SAFETY PIN** _Disease Presentation_ **Lymph nodes** where the Flea bit get **very swollen** and people get**SEVERE flu-like symptoms**, and collapse is commonly seen.**Nodes continue to enlarge and Septic Shock and pneumonia (via septic emboli) are they typical killers.**
72
Plague • Bug • What factors does it have that make it so virulent?
**_PLAGUE – Yersina pestis_** _Structure_ **small encapsulated gram-negative rod** (lost upon passage in vitro) that lives **intracellularly** (in macs) and exibits **bipolar staining to resemble a SAFETY PIN** _Pathogenic Mechanism_ **Fleas bite and the infection spreads to lymph nodes** causing buboes to form (bubonic plague). Typically the infection becomes **bacteremic due to protection from the** **1****polysaccharide protein capsule**and hematogenous spread to many organs occurs. 2**LPS (ENDOTOXIN may aid in this spread.****3****V and W proteins also allow this guy to live and grow in macrophages.****4****Yersinia outer proteins (Yops) are injected (type III secretion) into host cells to inhibit phagocytosis and cytokine production.** 5Also produces **exotoxin which cause DIC an hemorrhage.** Disease may affect the lungs regardless of how it was introduced.
73
Plague • Epidemiology •tx
**_PLAGUE – Yersina pestis_** _Structure_ **small encapsulated gram-negative rod** (lost upon passage in vitro) that lives **intracellularly** (in macs) and exibits **bipolar staining to resemble a SAFETY PIN** _Epidemiology_ **99.9% of cases occur in Southeast Asia** - found in rodents everywhere _Treatment_ * *TREAT IMMEDIATELY with Streptomycin or Tetracycline** * *Vaccines are available for military for bubonic form only**
74
Plague • Bug • Key findings and diagnosis
**_PLAGUE – Yersina pestis_** _Structure_ **small encapsulated gram-negative rod** (lost upon passage in vitro) that lives **intracellularly** (in macs) and exibits **bipolar staining to resemble a SAFETY PIN** _Mortality_ **50% (bubonic), 100% (pneumonic) without tx.** _Key findings/Diagnosis_ BULBULAR Lymphadenopathy, Dx: **Giemsa or Wayson stains** will show safety pin appearance, **Serology** can also be used. `