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54 Cards in this Set

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Borrelia spp.

General Information

Fig 20.8
-gram (-) spirochete

-major pathogens:
1.) B. burgdorferi (Lyme dis, minor antigenic shifts)
2.) B. recurrentis (relapsing fever, major antigenic shifts)

-antigenically related to Treponema pallidum (syphilis)
B. burgdorferi (Lyme disease)

Pathogenesis and clinical manifestations
-occurs in stages (like syphilis)
-minor antigenic shift
1. Early infection: Stage 1
2. Early infection: Stage 2
3. Late infection: Stage 3
B. burgdorferi (Lyme disease)

Early infection: Stage 1

fig 20.7
-erythema migrans ("bulls eye" only in a minority of larger lesions)
~10% bulls eye
~30% central erythema
~50% humogenous

-perhaps fever, minor constitutional symptoms or regional lymphadenopathy
B. burgdorferi (Lyme disease)

Early infection: Stage 2
-disseminated infection

-sever fatigue, secondary annular lesions and joint and muscle pain

-less common symptoms include rash, meningitis, CN palsy including Bell's, conjunctivitis, mild hepatitis, and resp distress
B. burgdorferi (Lyme disease)

Late infection: Stage 3
-persistent infection

-longer episodes of arthritis and crhonic arthritis

-skin lesions that appear bluish-red and swollen, and perhaps chronic encephalomyelitis or keratitis
****CDC Clinical case definition of Lyme Disease
-erythema migrans (> or = 5 cm in diameter) and at least one late manifestation (musculoskeletal, nervous system, or cardiovascular involvement) and lab confirmation of infection
B. recurrentis (relapsing fever)

Pathogenesis and clinical manifestations
aka tick fever and recurrent fever
-major antigenic shifts

-generalized infection with an abrupt onset

-symptoms include chills, fever, severe headache, muscular and joint pains, and enlargment and tenderness of spleen and liver

epidemis borreliosis and endemic borreliosis -->both relapses due to cyclic antigenic variations
Epidermis borreliosis
-louse-bourne

-usually a single relapse

-it is the most severe form of relapsing fever
Endemic borreliosis
-tick borne

-usually several relapses

-less severe than louse-borne
B. burgdorferi (Lyme disease)

Epidemiology
-the CDC estimates that Lyme disease is currently the most common insect vector-borne infection, 27,444 cases in U.S. in 2007

-major foci of infections are the Northeast, upper Midwest, and Pacific West
B. burgdorferi (Lyme disease)

Epidemiology

Fig 20.9 and 20.10
-life cycle involves ticks (Ixodes scapularis) and mice (during larval and nymph stages of the ticks)
-preferred hosts for adult ticks are white tailed deer

-more than 90% believed to be transmitted by nymph stage ticks
-the ticks parasitize a number of mammals and birds, but illness is not know to develop in these hosts

-lyme may occur in some domestic animals (dogs, horses, cows)
Epidemic borreliosis

Epidemiology
-transmitted by a human louse

-picks up the bacterium when feedin on a bactermic pt

-transmission to a susceptible individual occurs when the louse is injured by a host

-cases in the U.S. are imported
Endemic borreliosis

Epidemiology
geographic location depends on the distribution of tick vectors and animal reservoirs

-infection occurs during the tick feeding process

-endemic in the western and southwestern U.S.
Lyme Disease

Diagnosis
-microscopic examination of blood or tissues is not recommended

-CDC lab crit for diagnosis is at least one of the following:
-isolation of B. burgdorferi
-demonstration of diagnostic levels of IgM or IgG (ELISA) Abs to spirochetes, sig increase in Ab titer btwn acute and convalescent serum samples
***PCR (starred in class)
-western blot is used to confirm positive ELISA
Lyme disease

Diagnosis *special notes*
***PCR (starred in class)

-IgM Abs appear 2-4 wks after onset of erythema migrans and peak after 6-8 wks of illness
IgGs appear later and peaks after 4-6 months of illness
Relapsing fever

Diagnosis
-clinical signs are not diagnostic

-demonstration of bacteria in blood

-there are no accurate serologic tests (***due to antigenic shifts)
Lyme disease and relapsing fever

Treatment
-Antibiotics
Prevention and control of Lyme disease
-avoid the vector
-in endemic areas use appropriate clothing (light colored) long sleeved
-tick repellents
-examination of the skin after walking in suspected tick environments

***vaccine withdrawn from market in 2002 bc of reported side effects, but there is one for dogs
Nonhemorrhagic fever diseases (Bacterial agents)

-See Chapt 20.8
1. Brucella spp
2. Coxiella burnetii
3. Baronella spp
4. Ehrlichia spp and Anaplasma spp
5. Rickettsia spp
6. Anthrax
Brucella spp.

General information
1. Brucellosis aka undulant fever, Bang's disease (cattle) or Malta fever

2. wide range of hosts (B. abortus -->cattle and B. suis --> pigs)

3. potential bio agent for bioterorism

4. morphology -->small, gram (-) coccobacilli
Brucella spp.

Pathogenesis and clinical manifestations
-bactera can survive and multiply in PMNs and macros, local lymphadeno may precede bacteremia, lesions consist of small granulomas

-incub peroid is days-months (avg 3 wks)
-onset is abrupt or insidious with fatigue the most common complaint

-others diurnal fever (undulant), anorexia, muscle aches, headaches, and backaches
Brucella spp.

Pathogenesis and clinical manifestations
**relapses are a hallmark, chronic brucellosis usually weakness, fatigue, vague pains, and pression can last 1-20 yrs
Brucella spp.

Epidemiology
zoonotic disease; it is related to animal infections; major reservoirs of human brucellosis in the US are infected cattle and hogs

ingestion, contact, and inhalation are the major means of transmission; in the U.S. consumption of unpastuerized milk and dairy products is the major source of infections
Brucella spp.

Epidemiology and incidence
worldwide ~.5 mill cases/yr, low in U.S. (137 in 2007), CA and TX highest

-effective vaccination programs for domestic animals has greatly reduced most human cases in developed countries

-occupational hazard (vets, dairy farmers, and lab personnel)
Brucella spp.

Diagnosis
-classified among "fevers of unknown origin" bc of nonspecific symptoms

-isolation from blood, bone mar, or liver; its intracellular position may be repsonsible for neg blood culture

-serologic tests can indicate active disease (w/ rising titer)
Brucella spp.

Control
1. if brucellosis is suspected, notify the lab, high risk for lab personnel

2. and effective vaccine for animals is available, elimination of the animal reservoir prevents human disease
Coxiella burnetii

General information
-obligate intracellular bacterium; the etiologic agent of Q fever; pot bio agent for bioterrorism

-small gram (-) pleomorph
Coxiella burnetii

Clinical manifestations
-incubation period can be months/yrs and the presentation is often insidious w/ a range of symptoms

-subclinical to flu-like, to atypical pneumonia with prolonged fever and perhaps hepatitis

-subacute endocarditis is the most common presentation, **often occurs on prosthetic or previously damaged heart valve
Coxiella burnetii

Epidemiology
-in US outbreaks are associated with livestock or their products or lab infect

-transmission is thought to be arthropod-vertebrate-arthropod cycle

-major reserviors are cattle, sheep, goats
Coxiella burnetii

Epidemiology and Incidence
-principle mode of human infection is inhalation of dust particles and aerosols contaminated with organisms from birth tissue or excreta of infected animals

-in US 171 cases were reported in 07 (TX an Cali)

-individuals with highest risk are farm workers, meat cutters, vets, lab techs, consumers of raw milk

****Endospore like forms
Coxiella burnetii

Diagnosis
-serology-->
IFA;
PCR (blood, heart valve);
tissue culture
Bartonella spp

General Information
- gram (-) bacilli

-members of the genus occur in a variety of animal reservoirs

-insect vectors have been implicated in some diseases
B. Bacciliformis
-cause Oroya fever

-endemic to Peru, Ecuador, and Colombia

-due to a sandfly vector
B. quintana*
-cause of trench fever, subacute endocarditis, and bacillary angiomatosis
B. henselae*
-also the cause of bacillary angiomatosis

-cause of subacute endocarditis

-cat scratch disease (CSD):
Bacillary angiomatosis
avascular proliferative disease seen primarily in immunocomp pts
-eg AIDS pts

-transmitted by a body louse (homeless people)

Differences:
1. B. henselae: primarily involving the skin and lymph nodes
2. B. quintana:subcutaneous tissues and bone
Cat scratch disease (CSD):

fig 20.14
exposure to cats, scratches bites, and contact with cat fleas

-usually occurs in children

-signs: fever, lymphadenopathy and ostolytic lesions

-treat with antibiotics
Ehrlichia spp and Anaplasma spp

General information
E. chaffensis--> agent for human moncytic ehrlichiosis (HME)

Anaplasma phagocytophilum--> is the agent for human granulocytic anaplasmosis (HGA)

-both are gram (-)

-obligate intracellular bacteria
Ehrlichia spp and Anaplasma spp

Clinical manifestations
-E. chaffensis is the agent for HME, the disease resembles RMSF

-about 12 days after tick bite, high fever, headache, mailaise, and myalgia develop

-leukopenia and thrombocytopenia also occur
-rsh develops in 30-40% of pts
(more commonly in children than adults, death usually occurs in old and immunocomprimised)
Ehrlichia spp and Anaplasma spp

Epidemiology
-E. chaffensis geo distribution: mid-Atlantic, southeastern, and south central areas of U.S.

-major insect vector is the Lone Star tick (Ambyomma americanum)

-white tailed deer and dogs are major reservoirs for bacterium

-2007 ~ 1650 US cases of ehrlichiosis/anaplasmosis were reported
Ehrlichia spp and Anaplasma spp

Diagnosis
-culture is not performed

-microscopy is attempted, but not highly sensitive

-IFA

-DNA amplification/probe test
Ehrlichia spp and Anaplasma spp

Treatment and control
-suspected cases treated with antibiotic prior to lab confirmation

-control is identical to other insect vector borne diseases
Rickettsia spp

General information
1. morphology: very small, gram (-) coccobacilli

2. Physiology: obligate intracellular parasites

3. notable species:
-R. rickettsii --> RMSF
-R. akari--> rickettsialpox
-R. prowazekii --> epidemic typhus
-R. typhi ---> murine typhus

*all assoc. with arthropod vectors
Rickettsia spp

Pathogenesis
-able to induce phagocytosis, enter endo cells, escape from a phagosome and replicate within the cytoplasm or nucleus of host cells

-replicate until the host cell bursts, releases org which infect other cells

-clin widespread vasculitis leads to the classic triad of rickettsial diseases: fever, headache, rash
Rickettsia rickettsii

Patho and clinical manifestations
-the etiologic agent of RMSF

-incub period 3-12 days, onset is sudden sever headache, fever, malaise and myalgia

-2-4 days after, rash on palms and soles, later it becomes generalized and may be hemorrhagic

-other symptoms include GI complaints, conjunctivitis and stiff neck
Rickettsia rickettsii

Patho and clinical manifestations--> Complications

Fig 20.16
-include resp failure, encephalitis, and renal failure

-infection results in widespread enothelial damage, with occlusion of small vessels, microhem, electrolyte changes and perhaps necrosis, shock and death
Rickettsia rickettsii

Epidemiology: Transmission
-wood tick (Dermacentor anderoni) is common vector in the Rocky Mt states
-dog tick (D. variabilis) and A. americanum are common in southeastern/central states

-ticks act as both reservoirs and vectors, acq bact from infected animal host or by transovarial infect
Rickettsia rickettsii

Epidemiology: RMSF

Fig 20.15
-most sever and common rickettsiosis that occurs in the US (2221 in 2007)

-distrib throughout the continental US

-highest incidence in NC, OK, TN, VA, GA, LA, and AK

-mostly in children and younger adults during warmer months
Rickettsia rickettsii

Diagnosis
-isolation is not recommended

-microscopy using DFA of skin lesion biopsy allows confirmation within hrs

-confirmation by detecting Abs by the end of 2nd week with MIF

-Weil-Felix test for cross reacting Abs to Proteus (no longer rec)

-PCR
Rickettsia rickettsii


Treatment and Control
-Antibiotic treatment should begin immediately based upon clinical signs and history of recent tick attachemnt

-no commercial vaccine is available

-avoidance (like Lyme dis) recomm
Anthrax
-see notes on bacterial diseases affecting the skin p. 11

-etiologic agent is Bacillus anthracis

-gram (+) endospore forming rod
Anthrax

Signs and symptoms
-skin (cutaneous anthrax)
-Lungs (pulm anthrax)
-GI tract (ingest of contaminated foods)
-CN system (anthrax meningitis)
Anthrax

Pathogenesis and Virulence Factors
eg. lethal factor
Anthrax

Transmission and epidemiology
-animal reservoir

-endospore former

-bioterrorism