3=Typhoid Fever, typhus,Relapsin Fever.ppt

Typhoid fever, relapsing fever and typhus

1. Typhoid fever
BY: Berhane G/her (MD,ped.y3R)
Lecture slides for C1 medical students
of Adigrat university
2015
1

2. Objectives of the lecture
At the end of the lecture, you are expected to:
1.Describe the etiology of typhoid fever
2.Clarify pathogenesis of typhoid fever
3.List down the different clinical picture
4.Describe diagnostic modalities
5.Outline management and prevention of
typhoid fever
2

3. Outline of Presentation
1.Introduction
2.Etiology
3.Epidemiology
4.Pathogenesis
5.Clinical features
6.Diagnosis
7.Treatment
8.Prognosis
9.Prevention
10.References
3

4. 1.Introduction
•Typhoid fever is characterized by severe systemic
illness with fever and abdominal pain.
•The organism classically responsible for the enteric
fever syndrome is S. enterica serotype Typhi
(formerly S. typhi)
•Endemic in many developing countries
4

5. 2.Etiology
--Caused by Salmonella enterica serovar Typhi (S. Typhi), a gram-negative
bacterium
–A very similar but often less severe disease is caused by S. Paratyphi A
and rarely by S. Paratyphi B (Schotmulleri) and S. Paratyphi C
(Hirschfeldii)
–The ratio of disease caused by S. Typhi to that caused by S. Paratyphi is
about 10 to 1
–The inactivation of single genes, as well as the acquisition or loss of
single genes or large islands of DNA contributed to host adaptation and
restriction of S. Typhi
–One of the most specific genes is for the polysaccharide capsule Vi
(present in about 90% of all freshly isolated S. Typhi and has a protective
effect against the bactericidal action of the serum of infected patients)
5

6. 3.Epidemiology
–Incidence in the developing countries : 100–1,000
cases per 100,000 population.
–There may also be differences in the age
distribution and population at risk (highest in
children <5 yr of age)
–S. typhi is found only in humans and is spread
person to person
6

7. Cont…
Transmission
–Direct or indirect contact with an infected person (sick
or chronic carrier) is a prerequisite for infection.
–Major modes of transmission
•Ingestion of foods or water contaminated with S.
Typhi from human feces is the most common mode
of transmission
•water-borne outbreaks due to poor sanitation or
contamination can occur in developing countries.
7

8. 4.Pathogenesis
•Disease occurs by ingestion of the organism, from fecal
contamination of street foods and water reservoirs
•Infecting dose of about 10
5
–10
9
organisms with an incubation
period ranging from 4 to 14 days, depending on the inoculating
dose of viable bacteria.
•After ingestion, organisms invade the body through the gut
mucosa in the terminal ileum, through specialized antigen-
sampling cells, known as M cells
• S. Typhi crosses the intestinal mucosal barrier after attachment
to the microvilli by an intricate mechanism involving membrane
ruffling, actin rearrangement, and internalization in an
intracellular vacuole.
8

9. Cont…
•After passing through the intestinal mucosa, organisms enter the
mesenteric lymphoid system, and then pass into the bloodstream
via the lymphatics primary bacteremia (usually
symptomless, and blood cultures are frequently negative)
•Bacteria are disseminated throughout the body and colonize the
organs of the reticuloendothelial system (liver, spleen, gall
bladder , bone marrow), where they may replicate within
macrophages.
•After replication, S. Typhi organisms are shed back into the blood,
causing a secondary bacteremia, which coincides with the onset
of clinical symptoms and marks the end of the incubation period.
9

10. 10

11. Cont…
•By avoiding the triggering of an early inflammatory response in
the gut, S. Typhi could instead colonize deeper tissues and
organ systems.
• Infection with S. Typhi produces an inflammatory response in
the deeper mucosal layers and underlying lymphoid tissue with
hyperplasia of Peyer patches, and subsequent necrosis and
sloughing of overlying epithelium with ulceration.
•The ulcers can bleed but usually heal without scarring or
stricture formation.
•The inflammatory lesion may occasionally penetrate the
muscularis and serosa of the intestine and produce perforation
11

12. Cont…
•The mesenteric lymph nodes, liver, and spleen are hyperemic
and generally reveal areas of focal necrosis as well.
•A mononuclear response may be seen in the bone marrow in
association with areas of focal necrosis.
•The morphologic changes of S. Typhi infection are less
prominent in infants compared with older children and
adults.
•In particular, in contrast to adults with typhoid, despite
bacterial multiplication in the gall bladder wall, inflammation
is both focal and mild
12

13. Cont…
•Determinants of infection and disease
–Inoculum dose
–Host factors
–Virulence factors
Host factors
–genetic susceptibility to typhoid fever
–Patients who are infected with HIV are at significantly
increased risk for clinical infection with S. Typhi and S.
Paratyphi.
– patients with Helicobacter pylori infection also have an
increased risk for acquiring typhoid fever.
13

14. Cont…
•Virulence factors
–virulence genes, including the SPI-2 TTSS, may be necessary for the
virulence properties and ability to cause systemic infection.
–The surface Vi (virulence) polysaccharide capsular antigen found in S.
Typhi interferes with phagocytosis by preventing the binding of C3 to
the surface of the bacterium.
–The ability of organisms to survive within macrophages after
phagocytosis is an important virulence trait encoded by the phoP
regulon
–The occasional occurrence of diarrhea may be explained by the
presence of a toxin related to cholera toxin and E. coli heat-labile
enterotoxin.
–The clinical syndrome of fever and systemic symptoms is produced by a
release of pro-inflammatory cytokines (IL-6, IL-1β, and TNF-α) from the
infected cells.
14

15. 5.Clinical features
–The incubation period of typhoid fever is usually
7–14 days but is also dependent on the infecting
dose (range 3–30 days).
–The clinical presentation varies from a mild illness
with low-grade fever, malaise, and slight dry
cough to a severe clinical picture with abdominal
discomfort and multiple complications
15

16. Cont…
–Factors that influence the severity and overall clinical
outcome of the infection:
• the duration of illness before the initiation of
appropriate therapy,
•choice of antimicrobial treatment, age,
• previous exposure or vaccination history,
•virulence of the bacterial strain, quantity of inoculum
ingested, and
• several host factors affecting immune status
16

17. Cont…
–The presentation of typhoid fever may also differ
according to age:
•Diarrhea, toxicity, and complications such as disseminated
intravascular complications are more common in infancy, with
higher case fatality rates (presentation of typhoid may be more
dramatic in children <5 yr of age)
• Clinical features and complications of typhoid fever seen in
adults, such as relative bradycardia, neurologic manifestations,
and gastrointestinal bleeding, are rare in children
17

18. Cont….
Common features of typhoid fever
– high-grade fever
–generalized myalgia,
–abdominal pain,
–hepatosplenomegaly,
–abdominal pain, and
–anorexia
18

19. Cont….
–In children, diarrhea may be present in the earlier stages
of the illness and followed by constipation.
–In the absence of localizing signs, the early stage of the
disease may be difficult to differentiate from other
endemic diseases such as malaria.
–The fever may rise gradually, but the classic stepladder
rise of fever is relatively rare.
–The temperature rises in a steplike manner for 2 to 7 days
to an average of approximately 40 degree C and
characteristically remains at this level for 3 to 4 weeks in
the absence of specific antimicrobial therapy.
19

20. Cont..
–In about 25% of cases, a macular or maculopapular
rash (rose spots) may be visible around the 7th–10th
day of the illness, and lesions may appear in crops of
10–15 on the lower chest and abdomen and last 2–3
days (difficult to see in dark-skinned children).
–Patients managed as outpatients will present with
fever (99%) but have less emesis, diarrhea,
hepatomegaly, splenomegaly, and myalgias than
hospitalized patients.
20

21. •Classic presentation of typhoid fever in
untreated individuals:
•First week of illness — rising ("stepwise") fever and
bacteremia
•Second week — abdominal pain and rash (rose
spots, which are faint salmon colored macules on
the trunk and abdomen)
•Third week — hepatosplenomegaly, intestinal
bleeding and perforation, related to ileocecal
lymphatic hyperplasia of the Peyer's patches, may
occur with secondary bacteremia and peritonitis
21

22. Cont…
–The presentation of typhoid fever may be tempered by
coexisting morbidities and early administration of
antibiotics.
–the presentation of typhoid may also be atypical inplaces
where malaria is endemic and schistosomiasis is common.
–If no complications occur, the symptoms and physical
findings gradually resolve within 2–4 wk.
–The illness may be associated with malnutrition.
22

23. Cont…
COMPLICATIONS.
–Intestinal hemorrhage (<1%)
–Intestinal perforation (0.5–1%) is infrequent among
children.
–Intestinal perforation may be preceded by
•a marked increase in abdominal pain (usually in the
right lower quadrant)
•tenderness
• vomiting
•features of peritonitis
23

24. Cont…
Intestinal perforation and peritonitis may be
accompanied by
•a sudden rise in pulse rate
• hypotension
•marked abdominal tenderness and guarding
•subsequent abdominal rigidity
•A rising white blood cell count with a left shift
and free air on abdominal radiographs may be
seen
24

25. 25

26. Cont…
Chronic carriage
– Individuals who excrete S. Typhi for ≥3 mo after infection
are regarded as chronic carriers ( < 2% for all infected
children)
–The propensity to become a carrier follows the
epidemiology of gall bladder disease, increasing with age
and antibiotic resistance of the prevalent strains
–Rates of chronic carriage are lower in children than adults,
but the risk increases with age.
26

27. 6.Diagnosis
–In developing world the mainstay of diagnosis of typhoid
remains clinical
–The mainstay of the diagnosis is a positive culture from the
blood or another anatomic site
–Results of blood cultures are positive in 40–60% of the
patients seen early in the course of the disease
–stool and urine cultures become positive after the 1st wk.
–The sensitivity of blood cultures in diagnosing typhoid
fever is affected by prior antibiotic prescribing
–Bone marrow cultures may increase likelihood of
confirmation of typhoid (sensitivity will be 80 – 95%)
27

28. Cont…
•Other laboratory investigations are nonspecific
–blood leukocyte counts are
•Frequently low in relation to the fever and toxicity, but
there is a wide range in counts
• In younger children leukocytosis is a common
association and may reach 20,000–25,000/mm
3
.
–Thrombocytopenia may be a marker of severe illness and
accompany DIC.
–While liver function test results may be deranged,
significant hepatic dysfunction is rare
28

29. Cont…
–The classic Widal test measures antibodies against O and H
antigens of S. Typhi but lacks sensitivity and specificity in
endemic areas
•Rising titre of widal test is helpful
–Because many false-positive and false-negative results occur,
diagnosis of typhoid fever by Widal test alone is prone to
error
– S. Typhi–specific monoclonal antigens detection
–A nested PCR
–An ELISA for antibodies to the capsular polysaccharide Vi
antigen is useful for detection of carriers but not for the
diagnosis of acute illness
29

30. Cont…
The differential diagnosis includes
acute gastroenteritis
Malaria
sepsis with other bacterial pathogens
 viral infections such as Dengue fever, acute hepatitis, and
infectious mononucleosis
infections caused by intracellular microorganisms, such as
tuberculosis
brucellosis
tularemia
leptospirosis
rickettsial diseases
30

31. 7.Treatment
An early diagnosis of typhoid fever and institution of appropriate treatment is
essential.
–Outpatient management
The vast majority of children with typhoid can be managed at home
–with oral antibiotics and
–close medical follow-up for complications or failure to
respond to therapy.
–Inpatient management
Patients with
–persistent vomiting
– severe diarrhea
–abdominal distension
31

32. Cont…
General principles of management of typhoid
–Adequate rest, hydration, and correct fluid-electrolyte imbalances
–Antipyretic therapy (paracetamol) when T
o
> 39
00
c
–A soft, easily digestible diet should be continued unless the patient has
abdominal distention or ileus
– Antibiotic therapy is critical to minimize complications
•It has been suggested that traditional therapy with either
chloramphenicol or amoxicillin is associated with relapse rates of 5–
15% and 4–8%, respectively
•The quinolones and 3rd generation cephalosporins are associated
with higher cure rates
• First line: chloramphenicol (25 mg/kg every 6 hours) PO for 14 days
•Alternative : amoxicillin, cotrimoxazole, ceftriaxone.
32

33. Cont…
33

34. 8.Prognosis
–Depends on the rapidity of diagnosis and institution of appropriate
antibiotic therapy.
–Other factors include:
•the age of the patient
•general state of health and nutrition
• causative Salmonella serotype
•appearance of complications
–Infants and children with underlying malnutrition and those infected with
multidrug-resistant isolates are at higher risk for adverse outcomes.
–Despite appropriate therapy, 2–4% of infected children may relapse after
initial clinical response to treatment.
–Children with schistosomiasis can develop a chronic urinary carrier state
34

35. 9.Prevention
–Chlorination of water, proper sewage disposal, and appropriate food-
handling practices (hand hyegine)
–In endemic situations, avoiding consumption of street foods,
especially ice cream and cut fruit
– screening food handlers and high-risk groups for S. Typhi carriage
–Two vaccines are currently available for potential use in children:
•An oral, live-attenuated preparation of the Ty21a strain of S. Typhi
has been shown to have good efficacy (67–82%) for up to 5 years.
–Significant adverse effects are rare.
•The Vi capsular polysaccharide can be used in people ≥2 yr of age.
– It is given as a single intramuscular dose, with a booster every
2 yr and has a protective efficacy of 70–80%.
35

36. 10.References
1.Nelson text book of pediatrics,19
th
ed.
2.Nelson essentials of pediatrics, 5
th
ed.
36

37. Typhus
37

38. Typhus
•Classification
–murine typhus
–epidemic typhus
•Etiology
•Rickettsia typhi - the cause of murine typhus
•Rickettsia prowazekii - the cause of epidemic typhus.
•The genomes of both R. typhi and R. prowazekii share
considerable genetic identity.
•Transmission
–R. typhi is transmitted to humans by fleas
–R. prowazekii is transmitted in the feces of body lice
•virulence
–Louse-borne or epidemic typhus is the most virulent of all rickettsial
diseases, with a high case fatality rate even with treatment.
–Murine typhus is moderately severe and perhaps 1 of the most
under-recognized infections in the world.
38

39. Epidemic Typhus (Rickettsia prowazekii)
Etiology
–Humans are considered the principal or only reservoir of R.
prowazekii, the causative agent of epidemic or louse-borne typhus,
and its recrudescent form, Brill-Zinsser disease.
–Another reservoir has recently been identified in flying squirrels,
implying that a sylvatic cycle with small rodents and their
ectoparasites also exists.
–The rickettsia is the most pathogenic of the genus, and multiplies to
very large intracellular quantities before mechanical rupture of
infected endothelial cells.
–R. prowazekii and all Rickettsia species are recognized as a genetic
relative of the eukaryotic mitochondrion.
39

40. Epidemiology
–The infection is characteristically seen in winter or spring or during
times of poor hygienic practices associated with crowding, war,
famine, extreme poverty, and civil strife.
–Most cases of louse-borne typhus in the developed world are
sporadic, but outbreaks have been identified in Africa like Ethiopia
40

41. Transmission
–Human body lice (Pediculus humanus subspecies corporis) become
infected by feeding on rickettsemic persons.
–The ingested rickettsiae infect the midgut epithelial cells of the lice
–The organisms are then passed into the feces,
–which in turn are introduced into a susceptible human host through
•abrasions or perforations in the skin,
•through the conjunctivae, or
• rarely through inhalation of dried infected louse excreta present
in clothing, bedding, or furniture.
•The lice die from the rickettsial infection within 2 weeks but
desiccated dead lice and fecal materials remain infectious
for much longer
41

42. Clinical manifestation
–Mild or severe in children.
–The incubation period is usually <14 days
–The typical clinical manifestations include
– fever
–severe headache
–abdominal tenderness
–rash in most patients
–However, investigation of recent African outbreaks has shown
• A lower frequency of rash (25%)
• A high frequency of delirium (81%)
•High frequency of cough associated with pneumonitis (70%).
–The rash is initially pink or erythematous and blanches.
–In ⅓ of patients, red, nonblanching macules and petechiae appear
predominantly on the trunk
–Primary epidemic typhus is fatal in 10% to 50% of untreated patients and
is more likely to be clinically severe or fatal in people with concurrent
malnutrition or disease
42

43. •Other clinical features are
–chills (82%)
–myalgias (70%)
– arthralgias (70%)
–anorexia (48%)
–nonproductive cough (38%)
–dizziness (35%)
–photophobia (33%)
–nausea (32%)
–abdominal pain (30%)
– tinnitus (23%)
–constipation (23%)
–meningismus (17%)
–visual disturbances (15%)
– vomiting (10%)
–diarrhea (7%)
43

44. •Estimates of case fatality rates range between 3.8% and 20% in
outbreaks.
•Brill-Zinsser disease
–is an unusual form of typhus that becomes recrudescent months to
years after the primary infection, thus rarely affecting children.
44

45. Diagnosis
•The most sensitive and rapid assays are polymerase chain
reaction (PCR) amplification of rickettsial DNA from whole
blood or buffy coat fraction, from biopsies of the rash
45

46. Treatment
–Treatment must be instituted before diagnosis is confirmed
–The treatment of choice is doxycycline (2.2 mg/kg/dose bid PO or IV,
maximum 200 mg/day).
–Alternative treatments include
•Tetracycline (25–50 mg/kg/day divided every 6 hr PO, maximum
2 g/day), or
•Chloramphenicol (50–100 mg/kg/day divided every 6 hr IV,
maximum 3 g/day).
–Therapy should be continued for a minimum of 5 days and until the
patient has been afebrile for at least 3 days to avoid relapse
•Doxycycline as a single 200 mg oral dose (4.4 mg/kg if <45
kg) is also efficacious
46

47. Prevention
–Immediate destruction of vectors with an insecticide is important in
the control of an epidemic.
– For epidemic typhus, antibiotic therapy and delousing measures will:
•interrupt transmission
•reduce the prevalence of infection in the human reservoir
•diminish the impact of an outbreak
–Dust containing excreta from infected lice is stable and capable of
transmitting typhus, and care must be taken to prevent its inhalation
–Infection confers solid protective immunity
–However, recrudescence may occur years later with Brill-Zinsser
disease, implying that immunity is nonsterile
–No licensed vaccines for epidemic typhus are available
47

48. Relapsing fever
48

49. Arthropod-borne infection characterized by recurrent episodes of fever
It is caused by spirochetes of the genus Borrelia, a fastidious
microorganism transmitted to humans by lice or ticks
Classification
Epidemic relapsing fever, or louse-borne fever,
caused by Borrelia recurrentis and is transmitted from person to
person by Pediculus humanus, the human body louse.
Endemic relapsing fever, or tick-borne fever
caused by several species of Borrelia and is transmitted to humans
by Ornithodoros ticks
49

50. Epidemic relapsing fever
After ingestion of an infective blood meal by the louse, the spirochetes
penetrate its midgut, migrate to and multiply within the hemolymph, and
remain viable throughout its life span of several weeks.
Human infection occurs as a result of crushing lice during scratching,
facilitating entry of infected hemolymph through abraded skin.
50

51. Endemic relapsing fever
–Endemic relapsing fever, or tick-borne fever, is caused by several
species of Borrelia and is transmitted to humans by Ornithodoros
ticks.
•Borrelia hermsii and Borrelia turicatae are the common species
in the western United States, and Borrelia dugesi is the major
cause of disease in Mexico and Central America.
–After ingestion of an infective blood meal, spirochetes invade all
tissues of their arthropod hosts, including the salivary glands and
reproductive tract, which permits transovarian passage of infected
spirochetes and perpetuates arthropod infection of successive
generations.
–Human infection occurs when saliva, coxal fluid, or excrement is
released by the tick during feeding, thereby permitting spirochetes
to penetrate the skin and mucous membranes.
51

52. •EPIDEMIOLOGY.
–Louse-borne relapsing fever
•tends to occur in epidemics, often in association with typhus
•Epidemics are associated with war, poverty, famine, and poor
personal hygiene
•This form of relapsing fever occurs more commonly during the
winter
•The major endemic focus of the disease is the highlands of
Ethiopia
–Endemic relapsing fever
•Ornithodoros ticks, which transmit endemic relapsing fever, are
–distributed worldwide
–prefer warm, humid environments and high altitudes
–found in rodent burrows, caves, and other nesting sites
–Rodents are the principal reservoirs
–Infected ticks gain access to human dwellings on the rodent
host
52

53. PATHOLOGY AND PATHOGENESIS.
–The cyclic nature of relapsing fever is explained by the ability of
Borrelia organisms to continually undergo antigenic (phase)
variation
–Multiple variants evolve simultaneously during the first relapse, with
1 type becoming predominant
–Spirochetes isolated during the primary febrile episode differ
antigenically from those recovered during a subsequent relapse
–During febrile episodes, spirochetes enter the bloodstream, induce
the development of specific immunoglobulin M (IgM) and IgG
antibody, and undergo agglutination, immobilization, lysis, and
phagocytosis
–During remission, Borrelia spirochetes may remain in the
bloodstream, but spirochetemia is insufficient to produce symptoms
– The number of relapses in untreated patients depends on the
number of antigenic variants of the infecting strain
53

54. Clinical manifestations
Relapsing fever is characterized by periods of fever lasting 2–9
days, separated by afebrile periods of 2–7 days.
Louse-borne disease has:
a longer incubation period
longer periods of pyrexia
fewer relapses
longer remission periods than tick-borne disease
The incubation period of tick-borne disease is usually 7 days
with a range of 2–18 days.
Each form of relapsing fever is associated with sudden onset of
high fever, lethargy, headache, photophobia, nausea,
vomiting, myalgia, and arthralgia
54

55. Cont…
Symptoms which occur later include abdominal pain, a
productive cough, and mild respiratory distress
 Bleeding manifestations may occur and include epistaxis,
hemoptysis, hematuria, and hematemesis
A diffuse, erythematous, macular, or petechial rash may
develop over the trunk and shoulders
Rash is more common in louse-borne fever (25%), occurring
almost exclusively during the end of the primary febrile
episode, and lasts for 1–2 days
55

56. Cont…
–Lymphadenopathy, pneumonia, and splenomegaly may occur
–Hepatic tenderness associated with hepatomegaly is a common sign,
with jaundice in half of affected children
–Central nervous system manifestations may be the principal feature
of late relapses in tick-borne disease (lethargy, stupor, meningismus,
convulsions, peripheral neuritis, focal neurologic deficits, and cranial
nerve paralysis)
–Severe manifestations include myocarditis, hepatic failure, and
disseminated intravascular coagulopathy
56

57. Cont…
–The initial symptomatic period characteristically ends with a crisis in
2–9 days, marked by abrupt diaphoresis, hypothermia, hypotension,
bradycardia, profound muscle weakness, and prostration
–In untreated patients, the first relapse occurs within 1 wk, followed
by usually 3 up to 10 relapses
–Symptoms during each relapse becoming milder and shorter as the
afebrile remission period lengthens
57

58. Diagnosis
–Diagnosis depends on
•Bemonstration of spirochetes in thin or thick blood smears
stained with Giemsa or Wright's stain
•Blood culture
–During afebrile remissions, spirochetes are not found in the blood
–Leukocytosis (with a left shift) and a markedly elevated erythrocyte
sedimentation rate are typical
58

59. Treatment
•Non Drug treatment - Delousing
•Drug treatment – first line:
–Procaine penicillin 25,000-50,000 units
•Check blood film after 12 hours of treatment. If negative,
give tetracycline 250 mg TID for three consecutive days. If
the blood film remains positive, repeat the same dose of
procaine penicillin and continue with tetracycline later as
described above
59

60. Cont…
–For children >8 yr of age and young adults, tetracycline (500 mg PO
every 6 hr) for 10 days
–Single-dose treatment with tetracycline (500 mg PO) or
erythromycin is efficacious in adults
–In children <8 yr of age, erythromycin (50 mg/kg/day divided every 6
hr PO) for a total of 10 days
–Penicillin and chloramphenicol are also effective.
–Resolution of each febrile episode either by natural crisis or as a
result of antimicrobial treatment is usually accompanied within 2 hr
by the Jarisch-Herxheimer reaction, which is associated with clearing
of the spirochetemia.
60

61. Jarisch-Herxheimer reactions
•Occur within two hours of antibiotic administration; thus, observation for
several hours after treatment is recommended
•Cannot be prevented by prior administration of corticosteroid
•Symptoms and signs include rigors, fever, and hypotension and in severe
cases, significant arterial hypotension with heart failure and pulmonary
edema may supervene
•Proinflammatory cytokines, especially tumor necrosis factor (TNF)-alpha,
interleukin (IL)-6 and IL-8, have been implicated in the pathogenesis of this
process
•The mortality rate from JHR in LBRF is approximately 5 percent
•Some patients have survived the crisis or JHR, only to die suddenly later that
day or the next, perhaps from an arrhythmia
•Both penicillin and tetracycline can induce JHR but penicillin therapy appears
to cause a more prolonged reaction
•Nonsteroidal anti-inflammatory medications and, in severe instances, intravenously
administered fluids have been used for treatment of this reaction.
61

62. Prognosis
–With adequate therapy, the mortality rate for relapsing fever is <5%
and for TBRF is less than 2%
–The mortality rates for untreated LBRF and TBRF are in the ranges of
10 to 70 percent and 4 to 10 percent, respectively
–A majority of patients recover from their illness with or without
treatment after the appearance of anti-Borrelia antibodies
–In patients who remain febrile after treatment, consider other
concomitant infections like typhus
–Poorer prognostic features include:
•Stupor or coma on admission
•Diffuse bleeding
•Myocarditis
•Poor hepatic function
•Bronchopneumonia
•Co-infection with typhus, typhoid, or malaria
62

63. Prevention
–No vaccine is available
–Avoidance or elimination of the arthropod vectors.
–Good personal hygiene
–Delousing of persons, dwellings, and clothing
–Maintaining rodent-free dwellings for tick-borne disease
–Giving prophylactic doxycycline for 4 days after a tick bite
63