Zoonotic Infectections Flashcards
Rickettsia, Ehrilichia, Coxiella:
• what are their common structural characterisitcs?
• What is unique about the location of Rickettsial infections?
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
Given the unique method of infection for rickettsia, what would you expect to be unique about the way the rash presents?
Rickettsia:
• Produce a VASCULITIS by infectin the vascular endothelium leading to paplable purpura
Coxiella, Ehrilichia, Rickettsia
• Endotoxin?
• Exotoxin?
• Tx?
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).
Rocky Mountain Spotted Fever
• Pathogen
• Structure
• Transmission
• Reservoir
RMSF – Rickettsia rickettsii
Structure
very short gram negative rods (weak staining)
Transmission
Ticks, especially DOG TICKS => VECTOR
Dogs and Rats => Reservoir
Rocky Mountain Spotted Fever
• Pathogen and Structure
• Location of Replication
RMSF – Rickettsia rickettsii
Structure
very short gram negative rods (weak staining)
Replication Cycle
Obligate Intracellular Parasite – ENDOTHELIAL CELLS
Rocky Moutain Spotted Fever
• Disease Presentation
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.
RMSF
• what is unique about the cells it infects?
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
RMSF
• where do you typically get it?
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.
RMSF
• Treatment
• Mortality
RMSF – Rickettsia rickettsii
Structure
very short gram negative rods (weak staining)
Treatment
Doxycycline
Mortality
25% fatal if left untreated
RMSF
• Key findings
• Diagnosis
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)
Epidemic Typhus
• Causative agent
• Vector
• Reservoir
EPIDEMIC TYPHUS – Rickettsia prowazeki
Structure
Short gram negative rod (weak staining)
Transmission
Human to Human by Lice feces
Flying Squirrels might be a reservoir
Epidemic Typus
• Where does replication occur?
• Structure
EPIDEMIC TYPHUS – Rickettsia prowazeki
Structure
Short gram negative rod (weak staining)
Replication Cycle
Obligate Intracellular Parasite – ENDOTHELIAL CELLS
Epidemic Typhus
• Disease Presentation
• What kills them
• Bug
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.
Epidemic Typhus
• What cells does it infect
• Epidemiology
• Tx
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
Epidemic Typhus
• Is it fatal
EPIDEMIC TYPHUS – Rickettsia prowazeki
Structure
Short gram negative rod (weak staining)
Mortality
10-60% die if not treated
Epidemic Typus
• Key points
• Diagnosis
• Bug
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
Murine Typhus
• Bug/Structure
• Transmission
MURINE TYPHUS – Rickettsia typhi
Structure
Small gram negative rod (weak stain)
Transmission
Rat Flea => Vector
Opossums and Rats are the => Reservoir
Murine Typhus
• where does it replicate
Replication Cycle
Obligate Intracellular Parasite – ENDOTHELIAL CELLS
Murine Typhus
• Disease Presentation
• Bug
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.
Murine Typus
• What cells does it infect
• where is it found
• Bug
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
Murine Typhus
• Tx
• Mortality
• Dx
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
Ehrlichiosis
• Bug
• Vector
• Where does it replicate
HUMAN MONOCYTIC EHRLICHIOSIS – Ehrlichia chaffeesis
Structure
Gram negative rod
Transmission
Lone Star Star Deer Tick
Replication Cycle
Intracellular – MONOCYTES
Ehrlichiosis
• Bug
• How does it present
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)
Ehrliciosis
• Where does it replicate
• Where are you most likely to get it?
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)
Ehrliciosis
• Treatment
• mortality
HUMAN MONOCYTIC EHRLICHIOSIS – Ehrlichia chaffeesis
Structure
Gram negative rod
Treatment
Doxycycline
Mortality
1.8%
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)
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
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
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
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
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
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
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.
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
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
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
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
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.
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
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
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
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).
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
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***
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)
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.
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
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
What is a common theme in the disease presentation of spirochete?
• Cause?
Antigenic variation causes multi-phasic illness
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
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.
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
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.
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.
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).
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.
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
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**
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**
Meliodosis
• Bug
• Structure
• Transmission
MELIOIDOSIS - Burkhoderia pseudomallei
Structure
Small ENCAPSULATED motile gram-negative rod that is afacultative 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.
Meliodosis
•Bug
• disease presentation
MELIOIDOSIS - Burkhoderia pseudomallei
Structure
Small ENCAPSULATED motile gram-negative rod that is afacultative 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.
Meliodosis
• Bug
• How does it proliferate
MELIOIDOSIS - Burkhoderia pseudomallei
Structure
Small ENCAPSULATED motile gram-negative rod that is afacultative 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.
Meliodosis
• bug
• Epidemiology
MELIOIDOSIS - Burkhoderia pseudomallei
Structure
Small ENCAPSULATED motile gram-negative rod that is afacultative 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.
Meliodosis
• tx
• mortality
MELIOIDOSIS - Burkhoderia pseudomallei
Structure
Small ENCAPSULATED motile gram-negative rod that is afacultative 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
Meliodosis
• Key findings
• Dx
MELIOIDOSIS - Burkhoderia pseudomallei
Structure
Small ENCAPSULATED motile gram-negative rod that is afacultative 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
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
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.
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 - American 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**
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
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).
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 getSEVERE flu-like symptoms, and collapse is commonly seen.Nodes continue to enlarge and Septic Shock and pneumonia (via septic emboli) are they typical killers.
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 1polysaccharide protein capsuleand hematogenous spread to many organs occurs. 2LPS (ENDOTOXIN may aid in this spread.3V and W proteins also allow this guy to live and grow in macrophages.4Yersinia 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.
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**
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.
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