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Flashcards in Mixed Infection Deck (55)
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1
Q

A multi-system infection is caused by an agent that can…

A

1) disseminate (spread) to infect multiple tissues
2) Replicate and/or persist in those tissues
3) Cause disease in multiple tissues

2
Q

What is the difference between bacteria that MUST cause multisystem infection vs. those that are opportunists

A

The opportunists are bugs that are artificially introduced into places they don’t normally go
Several Genera of opportunists - commensal flora
Normally cause problems primarily in immunocompromised patients

3
Q

Professional multisystem pathogens

A

All can cause disseminated infections in immunocompotent hosts

4
Q

Blood and tissue donors are screened for which types of multisystem pathogen?

A

Professionals

5
Q

Important mechanisms used by professionally multisystem bacteria

A
Immune evasion
- Antigenic variation
- Serum resistance
- Cloaking
Invasiveness
- cell invasion
- tissue invasion
6
Q

Antigenic Variation in Lyme disease Borrelia

A

Recombination of VIs locus (surface protein)

7
Q

Serum resistance in Borrelia

A

Complement inactivation - binding to factor H

8
Q

Cloaking in Borrelia

A

Binding of fibronectin and other plasma proteins

9
Q

Opportunists route of entry:

A

Disruptions to physical barriers constituting first line of host defenses
SYSTEMIC disruptions to host defenses maybe be due to chemotherapy, irradiation, immunosuppressive therapy

10
Q

Professional pathogens route of entry

A

Overcoming physical barriers and dissemination are essential to biology of organism

11
Q

The most prevalent multisystem bacterial infections in the US
Vector borne:
NON-vector borne:

A

Vector Borne: Anaplasmosis; Ehrlichiosis; Rocky Mountain Spotted Fever; Lyme Disease
NON-vector borne: Syphilis

12
Q

Key information for Vector-Borne Infections

A

Biological transmission: specific life stage in vector; transmission through oral or fecal routes
Vector Competence: The ability of a vector to transmit pathogen

13
Q

Transstadial transmission:

A

When a pathogen is transmitted or maintained in the different life stages of the same individual vector

14
Q

Transovarial transmission

A

WHen a pathogen is transmitted from one vector generation to the next

15
Q

Key information for Vector-Borne Infections

A

LOCATION

SEASON

16
Q

Mosquito-Borne Diseases in US

A

NONE are bacterial

17
Q

Tick Borne Diseases in Wisconsin

A

Lyme Disease
Human granulocytic anaplasmosis
New: Ehrlichia muris like species Ehrlichiosis

18
Q

Larvae Ticks are usually __ _____ and have __ legs

Nymphs and adults have ___ legs and are ______ ______

A

not infected; 6; 8; potentially infected

19
Q

Pathogens are acquired by ticks from _____ ______ during first bloodmeal as larvae

A

reservoir animals

20
Q

____ to _____ _____ is peak season for nymphs to transmit infections

A

Spring; Early Summer

21
Q

____ is secondary peak of infection from adults

A

Fall

22
Q

Why are the shapes of the incidence curves for RMSF and ehrlichiosis somewhat different from those of Lyme disease and anaplasmosis?

A

Geographic distribution of vector ticks

23
Q

What does Enzootic mean?

A

Endemic in animals (A. phagocytophilum)

24
Q

Anaplasmosis
Structure:
Locaton/Secretion:
Invasion:

A

Structure: TINY gram negative coccobacillus
Locaton/Secretion: Obligate intracellular, replicates in vacuoles, no LPS, has type IV secretion
Invasion: Invades neutrophils, inhibits apoptosis

25
Q

Enzootic cycle of E. Chaffenisis (Reservoir Host)

A

Deer

26
Q

Ehrlichiosis:
Agents:
Structure:
Invasion/Secretions:

A

E. Chaffeensis - transmitted by Amblyomma americanum
Emerging: E. muris-like
Structure: Tiny gram negative coccobacilli
Invasion/Secretions: Obligate intracellular, invade monocytes and neutrophils; replicates in vacuoles - Type IV secretion

27
Q

Anaplasmosis and Ehrlichiosis CLINICAL

A
Incubation is 1-2 weeks
Most Common Signs/Symptoms:
- Fever/Chills
- Headache
- Anoresia
- Leukopenia
- Increased liver aminotransferases
28
Q

Anaplasmosis and Ehrlichiosis Diagnosis

A

Morulate in neutrophils or monocytes, seen in blood smear
May be difficult to find in smear
PCR can be used to identify organism based on temperature
Serology at 30 days is marker of infection

29
Q

Anaplasmosis and Ehrlichiosis Therapy

A
Oral doxycycline (also for lyme disease)
If under 8 or pregnant: doxycycline 3 days past defervescence
Rifampin is alternative
30
Q

Enzootic cycle of Rickettsia Rickettsii

A
Eggs are infected
Hatch into infected larvae
Small rodents = bloodmeal
Infected nymph
Infected adult tick
Human = incidental host
31
Q

Rocky Mountain Spotted Fever Agent:

A

Rickettsia rickettsii

32
Q

Rickettsia Rickettsii
Structure:
Invasion:
Secretion:

A

Structure: Tiny gram negative coccobacilli - DOES HAVE LPS AND PEPTIDOGLYCAN
Invasion: Obligate intracellular, replicates in cytoplasm, may also invade nucleus - bacterium escapes phagosome by forming actin tail
Secretion: Type IV secretion

33
Q

Rocky Mountain Spotted Fever Rickettsiosis: CLINICAL

A

Incubation time: 1 week
Fever, malaise, sever headache, myalgia, anorexia…
Rash 3-5 days after onset of illness: starts on ankles, wrist, forehead; small red macules progress to maculopapules then to petechiae
Thrombocytopenia, pro-coagulant coagulopathy

34
Q

Rocky Mountain Spotted Fever Diagnosis

A

CDC: There is no test available at this time that can provide a conclusive result in time to make important decisions about treatment

35
Q

Rocky Mountain Spotted Fever: Therapy

A

Oral Doxycycline

Chloramphenicol if patient has allergy to tetracyclines or if patient is pregnant and disease is mild

36
Q

Lyme Disease: Epidemiology

A

Most common vector-borne infection in Northern Hemisphere

37
Q

Lyme disease Enzootic Cycle

A

Humans - Inadvertent host
Larvae/Nymph host: small rodents
Adult tick host: Deer

38
Q

Lyme Disease
Agent:
Structure:
Invasion:

A

Agent: Borrelia burgdoferi
Structure: Gram negative spirochete, extracellular, no LPS, toxins, special secretion systems
Invasion: Requires >36 hours of tick bite for transmission; antigenic variation, complement evasion

39
Q
Lyme Disease: Clinical
Early localized:
Early, disseminated:
Late:
Size of Lesion:
A

Early localized: Days - 2 weeks
Early, disseminated: Days - months
Late: Months - Years
Size of Lesion: > 5cm

40
Q

Lyme Disease:
Early Disseminated:
Late:

A

Early Disseminated: Fever, malaise, secondary EM, AV nodal block, arthralgia, facial palsy
Late: Arthritis, encephalopathy

41
Q

Lyme Disease: Diagnosis

A

Current recommendations:
- Clear EM lesion - Sufficient to start therapy
IF no clear EM lesion at presentation (> 3 weeks)
- Antibody titer (IgM vs IgG - strain to strain variability)
- ELISA, then immunoblot

42
Q

Lyme Disease Serology

A

Not necessary if there is a clinical diagnosis of EM rash without evidence of systemic infection
IgM typically becomes positive in 2-3 weeks
IgG typically becomes + in 3-6 weeks, continues expanding
Both IgM and IgG may remain positive for years after treatment

43
Q

Lyme Disease: Therapy

A

Preferred: oral doxycycline for early, or with no CNS involvement
amoxicillin for patients who are pregnant or under 8
CNS involvement - IV ceftriaxone

44
Q

Vector Borne Infections - Take home points

A

Geography and Season are Key
Symptoms may vary with individual patients
Symptoms are often non specific
Few specific virulence factors identified
Difficult to grow in culture (not useful for diagnosis)
Diagnoses rely on taking a thorough history of the patient

45
Q

Syphilis - Causative agent

A

Treponema Pallidum

46
Q

Enzootic cycle of Treponema Pallidum

A

THERE IS NONE

47
Q

Syphilis

Agents:

A

Treponema pallidum pallidum - world wide STD
Treponema palidum endemicum: regions of Africa, not STD
Lots of oral treponemes

48
Q

Syphilis clinical:

A

Primary - lesion called a “shanker” - painless - highly infectious
Secondary - Several highly infectious lesions
Tertiary (30%) (Gumma, Cardiovascular syphilis, neurosyphilis)

49
Q

Syphilis: Secondary

A

6 weeks - 6 months after primary; lasts 4-12 weeks
Difuse, non-itchy rash all over
Condyloma latum - wart-like infectious lesion

50
Q

Syphilis: Latent

A

Patient is asymptomatic

Can last years to decades

51
Q

Syphilis: Tertiary

A

Tabes dorsalis; loss of sensory and motor neuron function leading to intense pain, personality changes, dementia, ataxia, deterioration of optic nerves leading to blindness
Gummas (granuloma like lesions)
Aortic aneurism
DAMAGE IS DUE TO HOST RESPONSE

52
Q

Syphilis: Congenital

A

Transmitted from mother to child during pregnancy or birth
Some symptoms/signs in child:
- Failure to thrive, fever, no bridge to nose
- rash of mouth genitals and anus

53
Q

Syphilis: Diagnostics

A
Non-specific, screening serology:
- Rapid Plasma Reagin (RPR)
Venereal disease Research Laboratory
- Anti-cardiolipin test
Specific, confirmatory serology (fluorescent antibody absorbed test)
54
Q

Syphilis: Therapy

A

Preferred: Long Acting Penicillin for primary and secondary; IV for tertiary
Alternatives: Ceftriaxone, Erythromycin, Doxycycline

55
Q

Bacteria that cause multisystem infections TAKE HOME POINTS

A

Cause disseminated infection and disease involving multiple organ systems including CNS in intact, immunocompetent individuals
Are available to avoid the host immune response to cause relapses or persistent infection
Should be treated with antibiotics with high tissue penetrance
Diagnostics do not rely on culture