Rickettsial infections

GENERAL
CONSIDERATIONS
 The Rickettsiaceae are aerobic, gram negative coccobacilli that
are obligate intracellular parasites
 The patogenesis of illnes due to the Rickettsiae is vasculitis
 All of the important rickettsial infections are vectorborne except
Q fever
 Confirmation of the diagnosis is almost always serologic and
thus retrospective
 Proper treatment cannot be given unless the diagnosis is
suspected
 The arthtropodborne rickettsioses are diseases of the spring and
summer in temperate climates, while Q fever can occur at any
season
 CLASIFICATION OF
RICKETTSIAL

 The genus Rickettsials

 The new genus Orientia
 The Erlichia group
 CLASIFICATION OF
RICKETTSIALS
(based on clinical presentation)

 The spotted fever group

 The typhus group
 The scrub typhus
 Q-fever
 SPOTTED FEVER GROUP
 Rocky Mountain spotted fever
 Boutonneuse
 Queensland tick typhus
 North Asian tick typhus
 Japanese spotted fever
 Flinders Island spotted fever
 African tick-bite fever
 Fleaborne spotted fever
 Rickettsialpox
 ROCKY MOUNTAIN SPOTTED
FEVER (RMSF)

 The causative agent is Rickettsia rickettsii

 The incubation ranges from 2 to 14 days
 The major clinical signs are fever, rash, severe
headache, myalgias, nausea, vomiting and severe
abdominal pain
 COMPLICATIONS OF RMSF
 Meningismus
 Meningitis
 Renal failure
 Pulmonary involvement
 Hepatic dysfunction with development of jaundice
 Myocarditis
 Thrombocytopenia
 Splenomegaly
 DIAGNOSIS OF RMSF

 High clinical suspicion

 Skin biopsy
 Serological tests (Weil-Felix reaction, IIF,
ELISA)
 TREATMENT OF RMSF
 Early therapy is important!
 Therapy of choice is oral doxycycline, 100mg
every 12 hours (second choice is
chloramphenicol 50-75mg/kg/day)
 Duration of therapy is 7 days, continuing for 2
days after the patient has become afebrile
 OTHER SPOTTED FEVER
GROUP RICKETTSIA
Rickettsialpox
 First reported in 1946 in New York
 The reservoir is the house mouse(Mus musculus) and
the vector for transmission to humans is the mouse
mite
 Manifestations include chills, fever, headache myalgia,
backache and photophobia, papulovesicular rash,
 Compliactions are very rare
 Treatment is the same as the other Rickettsia
 TYPHUS GROUP

 Epidemic typhus (louseborne typhus)

 Murine typhus
 Scrub typhus
 EPIDEMIC OR LOUSEBORNE
TYPHUS

 Until 1971 quarantine disease

 Epidemic and relapsing disease
 The causative agent-Rickettsia prowazekii
 Vector- louse Pediculus humanis corporis
 Reservoir of infection is infected people
 Incubation ranges from 8-16 days
 Major clinical manifestations-fever, headache, chills,
severe myalgia, rash
 DIAGNOSIS AND DIFERENTIAL
DIAGNOSIS OF EPIDEMIC
TYPHUS
 Difficult, except in epidemic conditions
 Dif. Diagnosis includes: abdominal typhus, measles
and other spotted fever diseases
 Confirmation of diagnosis:
a) Weil Felix-reaction (titer >1:160)
b) 4-fold rise in titer antibodies between acute and
convalescent serum specimens
c) positive CF after 10 days
 TREATMENT AND
PREVENTION OF EPIDEMIC
TYPHUS
 Therapy is the same as the other Rickettsial
diseses (7-10 days)
 No vaccine is currently available
 The only prevention available is control of body
lice by hygiene and insecticides
 BRILL-ZINSSER DISEASE
 Recrudescent typhus
 Sporadic disease in endemic area
 No season related
 No louse related
 Onset of the disease is related to diminished
immunological surveillance in people who had
epidemic typhus
 Pathogenesis and clinical picture similar to mild
epidemic typhus
DIAGNOSIS OF BRILL-ZINSSER
DISEASE
 Analyze of antibodies titers!
 In Brill disease CF titer has peak about 10th day
of the disease, but in epidemic typhus about
16th day
 In epidemic typhus antibodies belong to IgM
class until Brill disease in IgG class
 WF reaction titers in Brill disease are low or
negative
 TREATMENT OF BRILL-
ZINSSER DISEASE

 Therapy is the same as epidemic typhus

 No vaccine is currently available for the
prevention
 The most important measure is control of body
lice by hygiene and insecticides to prevent of
epidemic typhus
 MURINE TYPHUS
 The causative agent is Rickettsia typhi
 The reservoirs are Rattus spp. and vector is the
flea Xenopsylla cheopis
 Case fatality rate is 1%to 4%
 Incubation rate is 1 to 2 weeks
 Symptoms are similar to other Rickettsial
 Treatment is the same as in other Rickettsial
diseases
 SCRUB TYPHUS
 The causative agent is Orientia Tsutsugamushi and
vector is trombiculid mite(chigger)
 Incubation rate is 6 to 18 days
 The main symptoms are fever,headache,mental
changes, lymphadenopathy myalgia and rash
 Complications:haemorrhage, pneumonia, heart, renal or
respiratory failure
 Case fatality rate is almost 30% in untreated
 Treatment of choice is Doxycycline or
Chloramphenicol
 Q FEVER
 Non-vectorborne disease
 Two clinical presentations: acute and chronic
disease
 The causative agent is Coxiella burnetti
extremely infectious organisam
 The route of infection is inhalation of
aerosolized particles from infected animal
 The incubation period is 9 to 39 days
 CLINICAL PRESENTATION OF
ACUTE Q FEVER
 The most common symptom is fever
 The other symptoms include:chills, headache
(often severe), retrobulbar pain, myalgias,
arthralgias, neck pain and stiffness, pleuritic
chest pain, cough, nausea, vomiting, diarrhea,
janudice, hepatomegaly and splenomegaly
 Rash is very rare (about 4% of patinets)
 CLINICAL PRESENTATION OF
CHRONIC Q FEVER
 Endocarditis
 Chronic hepatitis
 Infections of vascular prostheses and aneurysms
 Osteomyelitis
 Interstitial pulmonary fibrosis
 DIAGNOSIS OF Q FEVER
 Clinical suspicion
 Serological findings
CF titer >1:8 for acute and >1:200 for a
chronic Q fever
IFA titer >1:150 for acute and> 1:800 for a
chronic Q fever
 Confirmation of the diagnosis is made by a 4-fold rise
in titer between acute and covalescent serum specimens
 TREATMENT OF Q FEVER
 Acute Q fever:
Drug of first choice is tetracycline or doxycycline
for 2 weeks
Drugs of second choice: chloramphenicol,
trimethoprim-sulfametoxazol, rifampin
 Chronic Q fever: Combination of doxycyclin
with a quinolone(ciprofloxacin) or rifampin or
hydroxychloroquine for 2 years
 PREVENTION OF Q-FEVER

 Nonspecific measures-protective masks,

pasterized milk, izolation of infected cattle)
 Specific measure-vaccination of exposed people
(veterinarian, laboratory staff)
 EHRLICHIOSIS AND
ANAPLASMOSIS
 Family Anaplasmataceae:
-Ehrlichia chaffensis-causative agent of
human monocytic erlichiosis (HME)
-Ehrlichia ewingii-causative agent of
human ewingii ehrlichiosis(HEE)
-Anaplasma phagocytophilum-causative
agent of human granulocytic
anaplasmosis (HGA)
 GENERAL
CONSIDERATIONS
 Obligate intracellular gram-negative bacteria
 These agents cycle in nature between invertebrate (arthropod)
and vertebrate (mammalian)
 The tick vector for E. Chaffensis and E. Ewingii is Amblyomma
americanum and for A phagocytophilum is Ixodes species
 Reside in specific hard-body tick hosts
 All documented reports have been limited to the North America
continent
 Incidence rate varied up to 58 cases per 100000 for HGA and
414 cases per 100000 for HME
 Incubation rate is between 1-2 weeks after tick bite
 PATHOGENESIS OF
EHRLICHIOSIS
 Tick vector takes a blod meal from a mammal host
 Bacteria become injected with the tick saliva
 Bacteria adhere to specific leukocyte cell-membrane receptors
 Bacteria enter through the host cell cytoplasmic membrane by
endocytosis and infect leukocytes
 Bacteria reside within cytoplasmic endosomes where they
multiply to form infectious agregates called morulae
 Bacteria subvert the host cell allowing it to tolerate their
presence by altering intracellular signaling and the cell
regulatory gene response
 CLINICAL MANIFESTATIONS
OF EHRLICHIOSIS
 HME, HEE and HGA present as clinically
similar illnesses
 The symptoms and signs range from
asymptomatic to fatal disease
 Abrupt onset of non-specific symptoms (fever,
chills, severe headache, myalgias)
 One-third to one-half patients require
hospitalization
 Self-limited disease
 LABORATORY FINDINGS IN
EHRLICHIOSIS
 Laboratory test abnormalities observed with
HME, HEE and HGA are similar and non
specific:
-leukopenia (increased neutrophils)
-thrombocytopenia
-elevated transaminase concentrations
 DIAGNOSIS OF EHRLICHIOSIS

 Compatible exposure history

 Clinical picture
 Smear examination (finding morulae)
 Polymerase chain reaction (PCR)
 IFA
CONFIRMATION OF DIAGNOSIS

 4-fold rise in titer between acute and covalescent

serum specimens
 Blood culture
 Combinated criteria: positive titer of antibodies
confirmed by IFA technique combined with
detection of morule in peripheral blood or
positive PCR finding
THERAPY OF EHRLICHIOSIS

First choice
Doxycycline 100mg -twice daily (10-14 days)
Second choice
Rifampin 300mg-twice daily (5-7 days)