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GRAM-NEGATIVE RODSRELATED TO ANIMAL SOURCE
(ZOONOTIC ORGANISMS)
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INTRODUCTION
There are four medically important gram-negative rods thathave signicant animal reservoirs:
Brucella species,
Francisella tularensis,
Yersinia pestis, and
Pasteurella multocida
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BRUCELLA
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Disease
Brucella species cause brucellosis (undulant fever).
Important Properties
Brucellae are small gram-negative rods without a capsule.
The three major human pathogens and their animal reservoirsare Brucella melitensis (goats and sheep), Brucella abortus(cattle), and Brucella suis (pigs).
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PATOGENESIS
The organisms enter the body either by ingestion of!ontaminate" mi#$ pro"%!ts or t&ro%'& t&e s$in "ire!t!onta!t in an o!!%pationa# settin' s%!& as an aattoir*
They localize in the reti!%#oen"ot&e#ia# sstem+ name#+ t&e#mp& no"es+ #i,er+ spleen, and bone marrow. any organismsare !illed by macrophages, but some survive within these cells,where they are protected from antibody.
The host response is granulomatous, with lymphocytes andepithelioid giant cells, which can progress to form focal abscesses.
"ndoto#in is involved. $o e#oto#ins are produced.
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EPIDEMIOLOG
%mported cheese made from unpasteurized goats& mil!produced in either e#ico or the editerranean region hasbeen a source of B. melitensis infection in the 'nited (tates.
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CLINICAL .INDINGS
)fter an incubation period of * to + wee!s, nonspecicsymptoms such as fever, chills, fatigue, malaise, anore#ia, andweight loss occur. The onset can be acute or gradual. Theundulating rising-and-falling fever pattern that gives the
disease its name occurs in a minority of patients. "nlargedlymph nodes, liver, and spleen are freuently found.
/ancytopenia occurs. B. melitensis infections tend to be moresevere and prolonged, whereas those caused by B. abortus aremore self-limited.
0steomyelitis is the most freuent complication. (econdaryspread from person to person is rare.
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LA/ORATOR DIAGNOSIS
1ecovery of the organism reuires the use of enriched culturemedia and incubation in *23 40
The organisms can be presumptively identied by using a slideagglutination test with Brucella antiserum, and the species can
be identied by biochemical tests. %f organisms are not isolated, analysis of a serum sample from
the patient for a rise in antibody titer to Brucella can be used tomae a diagnosis.
!n the absence of an acute-phase serum specimen, a titer of atleast *:*52 in the convalescent-phase serum sample isdiagnostic.
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TREATMENT
The treatment of choice is tetracycline plus rifampin.
There is no signicant resistance to these drugs.
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PREVENTION
/revention of brucellosis involves pasteurization of mil!,immunization of animals, and slaughtering of infected animals.
There is no human vaccine.
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FRANCISELL A
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Disease
Francisella tularensis causes tularemia.
Important Properties
F. tularensis is a small, pleomorphic gram-negative rod. !t has a sinserologic type.
There are two biotypes, ) and B, which are distinguished primarily virulence and epidemiology.
Type ) is more virulent and found primarily in the 'nited (tates, wB is less virulent and found primarily in "urope.6
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PATOGENESIS 0EPIDEMIOLOG
F. tularensis is enzootic endemic in animals in every state
%t has been isolated from more than *22 di7erent species of 1i#"anima#s+ t&e most important of which are rabbits, deer, and avariety of rodents.
The bacteria are transmitted among these animals by vectorssuch as ti!$s+ mites+ an" #i!e+ espe!ia## the "ermacentortics that feed on the blood of #ild rabbits.
$he tic maintains the chain of transmission by passing thebacteria to its o7spring by the transovarian route.
%n this process, the bacteria are passed through ovum, larva, andnymph stages to adult tic!s capable of transmitting the infection.
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8umans are accidental 9dead-end hosts who acuire the infectionby being bitten by the vector or by having s!in contact with the an
1arely, the organism is ingested in infected meat, causing gastroin
tularemia, or is inhaled, causing pneumonia. There is no person-to-person spread.
The main type of tularemia in the 'nited (tates is tic!-borne tularerabbit reservoir.
The organism enters through the s!in, forming an ulcer at the site cases.
%t then localizes to the cells of the reticuloendothelial system, and gare formed.
4aseation necrosis and abscesses can also occur.
(ymptoms are caused primarily by endoto#in. $o e#oto#ins have bidentied.
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CLINICAL .INDINGS
/resentation can vary from sudden onset of an in;uenzali!esyndrome to prolonged onset of a low-grade fever andadenopathy.
)ppro#imately isease usually confers lifelong immunity.
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LA/ORATOR DIAGNOSIS
)ttempts to culture the organism in the laboratory are rarely undertbecause there is a high ris! to laboratory wor!ers of infection by inhand the special cysteine-containing medium reuired for growth is navailable.
The most freuently used diagnostic method is the agglutination tesacute- and convalescent-phase serum samples.
?luorescent-antibody staining of infected tissue can be used if availa
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TREATMENT
(treptomycin is the drug of choice. There is no signicant antibiotic resistance.
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PREVENTION
/revention involves avoiding both being bitten by tic!s andhandling wild animals.
There is a live, attenuated bacterial vaccine that is given onlyto persons, such as fur trappers, whose occupation bringsthem into close contact with wild animals.
This and the bacillus of 4almette-@uArin B4@ vaccine fortuberculosis are the only two live bacterial vaccines for humanuse.
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YERSINIA
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DISEASE 0 IMPORTANTPROPERTIES
Yersinia pestis is the cause of plague, also no#n as the blac death.
Important Properties
Y. pestis is a small gram-negative rod that e%hibits bipolar staining
(i.e., it resem#e s a sa2et pin+ 1it& a !entra# !#ear area)* .res iso#ate" or'anisms possess a capsule composed of a
polysaccharideprotein comple#.
The capsule can be lost with passage in the laboratoryC loss of thecapsule is accompanied by a loss of virulence. %t is one of the most
,ir%#ent a!teria $no1n an" &as a stri$in'# #o1 %>=2 i.e., * to*2 organisms are capable of causing disease.
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PATOGENESIS 0EPIDEMIOLOG
The enzootic sylvatic cycle consists of transmission among 1i#"ro"ents 3eas* In t&e Unite" States+ prairie "o's are t&emain reser,oir*
Ro"ents are relatively resistant to diseaseC most are asymptomatic.
8umans are accidental hosts, and cases of plague in this country occuras a result of being bitten by a ;ea that is part of the sylvatic cycle.
The urban cycle, consists of transmission of the bacteria among urbanrats the reservoir, with the rat 3ea as vector.
This cycle predominates during times of poor sanitation e.g.,wartime, when rats proliferate and come in contact with the ;eas inthe sylvatic cycle.
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The organisms inoculated at the time of the bite spread to the regionanodes, which become swollen and tender.
These swollen lymph nodes are the %oes t&at &a,e #e" to t&e na%oni! p#a'%e *
T&e or'anisms !an rea!& &i'& concentrations in the blood bacteredisseminate to form abscesses in many organs.
The en"oto4in-re#ate" smptoms+ in!#%"in' "isseminate" intra,coagulation and cutaneous hemorrhages, probably were the genesis of#a!$ "eat&*
The organism has several factors that contribute to its virulence:
* the envelope capsular antigen, called ?-*, which protects against p
D endoto#inC + an e#oto#inC and
E two proteins !nown as F antigen and G antigen.
The F and G antigens allow the organism to survive and grow intracelltheir mode of action is un!nown. The action of the e#oto#in is un!nown
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0ther factors that contribute to the e#traordinary pathogenicity ofare &
' group of virulence factors collectively called ops (Yersinia out proteins).
These are injected into the human cell via type %%% secretion systeminhibit phagocytosis and cyto!ine production by macrophages andneutrophils.
?or e#ample, one of the Hops proteins HopI is a protease that cleavsignal transduction pathway proteins reuired for the induction of t
necrosis factor synthesis. This inhibits the activation of our host defenses and contributes to
of the organism to replicate rapidly within the infected individual.
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CLINICAL .INDINGS
Bubonic plague, which is the most freuent form, begins with painand swelling of the lymph nodes draining the site of the ;ea biteand systemic symptoms such as :
8igh fever,
myalgias, and prostration. The a7ected nodes enlarge and become e#uisitely tender. These
buboes are an early characteristic nding.
(eptic shoc! and pneumonia are the main life-threateningsubseuent events.
/neumonic plague can arise either from inhalation of an aerosol orfrom septic emboli that reach the lungs.
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LA/ORATOR DIAGNOSIS
(mear and culture of blood or pus from the bubo is the bestdiagnostic procedure.
@reat care must be ta!en by the physician during aspiration ofthe pus and by laboratory wor!ers doing the culture not to
create an aerosol that might transmit the infection. @iemsa or Gayson stain reveals the typical safety-pin
appearance of the organism better than does @ram stain.
?luorescent-antibody staining can be used to identify theorganism in tissues. ) rise in antibody titer to the envelopeantigen can be useful retrospectively.
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TREATMENT
The treatment of choice is a combination of streptomycin anda tetracycline such as do#ycycline, although streptomycinalone can be used.
Jevo;o#acin can also be used. There is no signicant antibioticresistance.
%n view of the rapid progression of the disease, treatmentshould not wait for the results of the bacteriologic culture.
%ncision and drainage of the buboes are not usually necessary.
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PREVENTION
/revention of plague involves controlling the spread of rats inurban areas, preventing rats from entering the country by shipor airplane, and avoiding both ;ea bites and contact with deadwild rodents.
) patient with plague must be placed in strict isolationuarantine for
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PASTEURELLA
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DISEASE 0 IMPORTANTPROPERTIES
Pasteurella multocida causes #ound infections associated #ithcat and dog bites.
Important Properties
P. multocida is a short, encapsulated gram-negative rod thate%hibits bipolar staining.
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PATOGENESIS 0EPIDEMIOLOG
The organism is part of the normal ;ora in the mouths of manyanimals, particularly "omesti! !ats an" "o's+ an" istransmitte" itin'*
Ao%t 567 o2 anima# ites become infected with the organism,with sutures acting as a predisposing factor to infection.
ost bite infections are polymicrobial, with a variety of facultativeanaerobes, especially treptococcus species, and anaerobicorganisms present in addition to P. multocida.
Pathogenesis is not #ell understood, e%cept that the capsule is avirulence factor and endoto#in is present in the cell wall.
$o e#oto#ins are made.
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CLINICAL .INDINGS
) rapidly spreading cellulitis at the site of an animal bite isindicative of P. multocida infection.
$he incubation period is brief, usually less than * hours. 0steomyelitis can complicate cat bites in particular, because
cats& sharp, pointed teeth can implant the organism under theperiosteum.
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LA/ORATOR DIAGNOSIS
The diagnosis is made by nding the organism in a culture of asample from the wound site.
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TREATMENT
/enicillin @ is the treatment of choice. There is no signicant antibiotic resistance.
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PREVENTION
/eople who have been bitten by a cat should be givenampicillin to prevent P. multocida infection. 'nimal bites,especially cat bites, should not be sutured.