Parasitology

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Parasitology

• Dr Hussien Bamashmous

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PROTOZOAOR

• METAZOA

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• PROTOZOA
  
• Protos first
  Zoon animal
• Phylum of animal kingdom which includes simplest
  animals
• most are unicellular
• some are colonial
• REPROPDUCTION
• usually asexual by fission
• some sexual reproduction

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• EXAMPLES OF PROTOZOAL DISEASE
• Malaria
• Amebiasis
• Giardiasis
• Trichomoniasis
• Toxoplasmosis
• Visceral leishmaniasis
• Pneumocystis carinii

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• METAZOA
• META after / beyond ZOON animal
• DIVISION OF THE ANIMAL KINGDOM THAT INCLUDES ALL
  MULTICELLULAR FORM
• They are either
• NEMATODES or CESTODES

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1- NEMATODES

• NEMA thread EIDOS form
• Nematohelminthes are either
• round, cylindrical, spindle shaped.
• Examples
• ENTEROBIASIS OXYURIASIS ( pin worm)
• ASCARASIS round worm
• ANCYLOSTOMIASIS hook worm
• TRICHINOSIS
• TRICHURIASIS whip worm

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2- CESTODES

• KESTOS GIRDLE
• Subclass of Cestoidae ? phylum
  
  
  
• 
  PLATYHELMINTHES
• EXAMPLES
• TAENIASIS tapeworms scolex segments
• 
  (proglottidis)
• VISCERAL LAVAR MIGRANS
• FILARIASIS
• BILHARSIASIS (schistosomiasis)

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MALARIAmal - aria
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MALARIA

• ESSENTIALS OF DIAGNOSIS
• Residence in or travel to an endemic area
• High fever, chills, headache
• Jaundice, vomiting, diarrhea
• Anemia, splenomegally
• Seizures, coma
• Malaria parasite in the blood smear

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• GENERAL CONSIDERATIONS
• Malaria kills 1,000,000 children/ year
• Resurgence is observed now
• Female Anopheline mosquito transmits the
  parasite
• Plasmodium Vivax (most common)
• P. Falciparum (most
  virulent)
• P. Ovale
  (similar to Vivax)
• P. Malariae

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• LIFE CYCLE
• INFECTED HUMAN BLOOD (GAMETOCYTES)
• Sucked by Anopheline mosquito
• In its stomach wall
• OOKINTE ? OOCYST ? MATURE OOCYST
• ? rupture ? SPORPZOITE ?
• to its salivary glands ? bite uninfected
  person
• In the uninfected person Sporozoites disappear
  within
• 1/2 hour from the circulation and infect the
  hepatocytes

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• HEPATIC PHASE ( PRE-ERYTHROCYTIC PHASE)
• about 2 weeks for all
• 3-5 weeks for P. Malarie
• Hypnozoites ? ONLY FOR P.VIVAX AND OVALE which
  is responsible for future relapses.
• Merozoites leave the liver thereafter to infect
  the RED BLOOD CELLS ERYTHROCYTIC CYCLE

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• ERYTHROCYTIC CYCLE (ASXETUAL CYCLE)
• ERYTHROCYTE HAEMOLYSIS
• METROZOITES ? TROPHOZOITES ?SCHIZONTS ?
  METROZOITES (which will be released by
  heamolysis)
• SYMPTOMS
• IMMATURE GAMETOCYTES
• MATURE GAMETOCYTS (male female)
• Sucked by mosquito
• REPEAT THE CYCLE

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• P. VIVAX ? affects young red cells ? ruptures ?
  symptoms X 48 hours
• P. MALARIAE ? old red cells ? symptoms X 72 hours
• P. FALCIPARUM ? all cells ? NO CLASSICAL TRIAD OF
  SYMPTOMS
• SURVIVAL (especially in endemic area)
• ? immunity
• ? intensity of the cycles

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• NO HEPATIC PHASE (pre- erythrocytic phase)
  with
• Blood transfusion
• Needle stick
• Congenital malaria
• Susceptibility varies genetically
• Partial resistance to infection with
• Hemoglobin S
• Hemoglobin F
• Thalassemia
• G6PD deficiency
• Maternal immunity protects the neonate despite
  placental infection
• Clinical findings varies according to
• strain
• host immunity

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PRESENTATION

• CLASSICAL TRIAD WITH P. VIVAX P. OVALE
• COLD STAGE
• AFTER ½ HOUR ? HOT STAGE
• AFTER 1-6 HOURS ? SWEATING

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• OTHER SYMPTOMS AND SIGNS
• Pallor and irritability
• Poor feeding
• Vomiting and diarrhea
• Jaundice
• Splenomegally
• Hepatomegally
• OLDER CHILDREN
• Headache and backache
• Myalgia
• Fatigue

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• IF UNTREATED RELAPSES STOPPED
• Within a year with P. Falciparum
• Within several years with P. Vivax
• May occur decades later with P. Malariae
• INFECTION DURING PREGNANCY
• Intrauterine growth retardation
• Preterm
• Congenital malaria

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• LABORATORY FINDINGS
• Multiple thick smears ? Giemsa stain
• Thin smear ? Wright stain
• In P. falciparum ? only ring form of Trophozoited
  Gametocytes are seen in peripheral smear.
• GAMETOCYTES MAY PERSIST FOR DAYS FOLLOWING
  ADEQUATE THERAPY

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• Complete Blood Count
• Normocytic normochromic anemia
• Leucopenia, leucoytosis
• Normal or low platelet count
• High retics
• LFT
• indirect and direct hyperbilirubinaemia
• mild transaminase elevation
• hypergammaglobinaemia
• Occasionally
• low complement
• positive rheumatoid factor
• positive ANA
• false positive VDRL

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• Differential diagnosis
• TUBERCLUSIS
• BRUCELLOSIS
• BORRELOSIS
• SQUENTIAL COMMON INFECTIONS
• HODGKENS DISEASE
• JUVENILE RHEUMATOID ARTHERITIS
• RAT BITE FEVER
• CAT-SCRATCH FEVER
• IDIOPATHIC PERIODIC FEVER
• TYPHOID FEVER
• MYCOPLASA PNEUMONIA

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• COMPLICATIONS AND SEQUALAE
• CHRONIC MALARIA SPECIALLY P. FALCIPARUM
• Anemia
• Deblitation
• Massive Splenomegaly (tropical splenomegally
  syndrome)
• MICROTHROMBOSIS AND ISCHAMIA
• Intestinal Tract ? bleeding and diarrhea
• Lung ? pneumonitis
• Brain ?diffuse edema, seizures,
  encephalopathy
• INTRAVASCULAR HAEMOLYSIS
• hemoglobinuria ? renal failure ( black water
  fever)
• CHRONIC P. MALARIAE
• nephrotic syndrome

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PREVENTION

• SPOROZOITES ? resistant to drugs
• CASUAL PROPHYLAXIS drugs which act on hepatic
  phase
• SUPPRESSION drugs which act on erythrocytic
  phase
• CHLOROQUINE safe in pregnancy
• CHLOROQUINE RESISTENCE ALL OVER EXCEPT
• Central America
• Haiti
• Panama
• Egypt
• Most of the middle east

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• IN RESISTENT-FREE AREA
• Cholorquine 5 m/kg of base max. 300 mg
  once/week.
• ONE WEEK BEFORE TRAVEL FOUR WEEKS
  AFTER RETURN
• IN CHLOROQUINE RESISTENT AREA
• Mefloquine (not if wt. is less than 15 kg)
• Maloprim pyrimethamine Dapsone
• Fansidar pyrimethamine Sulfdoxane
• FOR P.VIVAX P. OVALE
• 2 week course of primaquine phosphate
• SCREEN FOR G6PD BEFORE PRIMAQUINE
• INSECT REPELLENTS MOSQUITO NETTING (night)

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• TREATMENT
• New drugs has been discovered in the treatment
  of Malaria .
• They are called the (ARTEMESSININS).
• They are derived from a Chinese plant.
• Introduced in the market since 1996.
• They act as internal bomb inside the Malaria
  parasite using its own hydrogen peroxide.
• The best treatment is called ACT.
• ACT is combination of
• ARTEMESSININS and CHLOROQUINE.
• Unfortunately in the markets now in many
  countries there are mal-manufactured drugs with
  poor effectiveness and possibly emerging
  resistance.

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• Cont. TREATMENT
• CHLOROQUINE PHOSPHATE Drug of choice for
• Nonresistant P.Falciparum
• Most infections by other species
• Course of 3 days ERADICATES THE ERYTHROCYTIC
  PHASE
• Give orally 10m/kg (max 600mg) as initial dose
• 5 mg/kg 6 hours, 24 hrs 48 hrs
  later
• MEFLOQUINE
• effective but has neuropsychiatric side
  effects
• QUINIDINE GLUCONATE (parental)
• 10-14 mcg/kg as a loading dose
• then 0.02 mg/kg/min

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• CHLOROQUINE RESISTENCE MALARIA
• (P.O.)
• QUININE SULPHATE x 3 days PYRIMETHAMINE x 3
  days SULPHADIAZINE x 3 days
• QUININE SULFATE x 3 days TETRACYCLINE x 7 days
• (Parentral)
• QUININE DIHYDROCHLORIDE
• QUININE GLUCONATE

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• GENERAL MEASURES
• Hydration and fever control
• Blood and needle precautions
• Hospitalization with
• persistent vomiting
• severely ill
• Non-immune to P. Falciparum
• Iron and folate level
• Hepatitis and HIV screening (especially for
  drug users)

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• FOR CELEBRAL MALARIA
• Rule out other causes
• Anticonvulsants
• Parental antimalarial
• Control of cerebral edema
• Disferoxamine
• Steroids Contraindicated ( except with
  intravascular hemolysis)

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Giardiasis
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• Essentials of diagnosis
• Chronic relapsing diarrhea
• Flatulence, bloating, anorexia, poor wt. gain
• Absence of fever and blood in stool
• Presence of TROPHOZOITES in diarrhe or stool
• Cysts in formed stools

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• GENERAL CONSIDERATIONS
• In many areas most common protozoan in children
• Caused by GIARDIA INTESTINALS
• Water Drinking (contaminated water) in endemic
  areas
• Food-borne outbreaks do occur
• Incidence in DAYCARE NURSERIES up to 50
• Incidence in mental instituations
• The parasite resides in the duodenum and jujenum
  ? Inflamation subtotal villous atrophy

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Clinical findings

• Cyst ingestion trophozoites live
  non-invasively in the small intestine
• Symptoms develop in 1-3 weeks
• Diarrhea (soft)
• Steatorrhea mucus but no RBC / WBC
• Abdominal cramps
• anorexia, vomiting ? wt. lost
• The illness may last days to months or my relapse

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Laboratory findings

• CBC normal (no eosinophils)
• Fresh stool ve trophozoites
• Formed stool oval cysts
• Duodenal aspirate biopsy
• String test (Enterotest)
• Giardia antigen in stool

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• Differential diagnosis
• Toddlers diarrhea
• TB enteritis
• Chronic amoebiasis
• Other causes of steatorrhea.
• 
  
  

• PREVENTION
• Avoid unclean water and food stuffs
• Hand-washing is important
• Animals are not vectors
• Asymptomatic carrier ? identify and treat if
  needed

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Treatment

• Treat symptomatic day care center cases their
  contacts
• Drugs
• Furazolidine 2mg/kg X 6h X 7-10 days
• Metronidazole 5m/kg X 8h X 5-10 days
• Quinacrine HCL 2mg/kg X 8h X 5-10 days

• NB. giardiasis maybe self limiting and may
  relapse

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Leshmaniasis
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• General consideration
• Caused by protozoan of the genus leishmania
• Conveyed by female sand fly in which flagellate
  (proamistigote) develop
• In man ? in monocytes and macrophages ?
  amastigotes (leishmann-donovan bodies)

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• Visceral leishmaniasis (kala azar)
• In India ? man is the main host
• In Mediterranean ? dogs and foxes are main
  reservoirs
• Transmission by sandflies
• blood transfusion
• Multiplication by simple fission in monocytes
  macrophages in various organs ? huge
  hepatosplenomegally and lymphadenopathy
• Lishmania ? Malnutrition and Immune Suppression
  ? Intercurrent infections
• Tuberculosis

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• Clinical presentation
• Incubation period 1-2 months up to 10 years
• Insidious onset of fever
• Temperature is either remittent or intermittent
• Hepatosplenomegally
• Lymphadenopathy
• If untreated ? severe anemia and wasting
• Facial hyperpigmentation
• After therapy Dermal leshmaniasis,
• 
  Hypopigmentaed macules,
• Erythematous
  macules,
• Nodular
  eruption

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• Diagnosis
• Pancytopenia bone marrow suppression
  hypersplenism
• Immunoglobulin (esp IgG) albumin
• Aspirated and cultures from
• Bone marrow,
• liver spleen,
• lymph nodes
• ve Serology immunoflourescene
• C.F.T
• Leishmania skin test ? negative
• using killed proamstigotes

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Differential diagnosis

• Infective endocarditis
• Typhoid fever
• Brucellosis and tuberculosis
• Lymphomas
• Bilharizaisis
• Malaria

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Treatment

• Asia (India) ? good recovery
• Sudan east Africa ? more resistant
• Drugs used
• sodium stibogluconate
• pentavalent antimony compound
• IM or IV for 10 days,
• could be repeated after 10 days if needed days
  
• In resistant cases use
• Pentamidine Isethionate
• 2 hydroxy Stilbamidine
• Amphotericin B

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Prevention

• In endemic areas ? destroy stray dogs and foxes
• Sandflies should be combated by insecticides
  repellents
• No vaccine available

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Other types of leishmaniasis

• Leishmania of old world LESHMANIA TROPICA
  (ORIENTAL SORE)
• Geographical region
• Asia, India, North Africa, Arabia
• Vector sandfly,
• transmits the parasite from
  animal to man (ZOONOSIS)
• symptoms and signs
• incubation period 2-5 weeks up to years
• papule at the bite site (usually the face and
  limbs)
• ulceration of the papule ? scarring

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• Diagnosis
• Dry needle aspirate or skin slit smear ? ve for
  the organism
• Positive skin test
• Positive serology
• Therapy
• antimony compound reduces the scarring
• Resistant cases pentamidine amphotericin
• There is a vaccine for L.Tropica

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• Leishmania of the new world
• Leishmania Brazilliensis ? Espundia
• Leishmania Mexicana ? Chicleroulcer
• Leishmania peruviana ? Uta
• Geographical distribution south america
• Vector sandfly

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• Symptoms and signs
• Painful mucocutaneous ulcers or granulomas
• Nasolabial lesions (common)
• Lips, palate
• ? terrible suffering and disfigurment
• Diagnosis
• skin biopsy
• ve skin test
• serology
• Therapy
• Antimony compound
• Establishing espundia ? Amphotericin

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Brucellosis
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• IT IS A ZOONOTIC DISEASE CAUSED BY SPECIES
  BRUCELLA
• Brucella Melitensis goats and sheep
• Brucella Abortus cattle
• Brucella Suis swine
• Brucella Canis dogs
• Routes of infection in pediatrics
• Direct contact
• Inhalation of aerosols
• Ingestion of raw milk or milk products from
  infected animals
• Incidence could be decreased by
• Control of the disease in domestic animals
• Pasteurization of milk

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• Presentation in Children
• 50 acute disease
• Other 50 subacute disease
• Eitiology
• Brucella named for SIR DAVID BRUCE who first
  isolated the organism in 1887
• Epidemiology
• In industrialized countries ? occupational hazard
• In USA ? pediatric cases about 10
• In Arabia ? more

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• Endemic brucellosis
• caused by ingestion or raw milk, cream, butter,
  cheese or ice cream
• Organism my directly invade Eye, nasopharynx and
  genital tract
• Brucella can survive up to 3 weeks in
  refregerated garcass
• Endemic disease is maintained In Animals
  through excretion of large numbers of the
  organisms
• in genital secretions and milk with vertical
  and horizontal transmission
• Brucella causes ? abortion in Animals

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• Human to human transmission is Rare but may be
  caused by
• Blood transmission
• Bone marrow transplantation
• Transplacental
• Perinatal exposure

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Pathology and pathogenesis

• BRUCELLAE ? facultative intradellular parasite
• Capable of surviving and multiplying within
  phagocytes, red blood cells and many cell lines
• Nonspecific host factors triggered
• Agglutinins
• Polymorphs
• Complements
• ? Opsonization phagocytosis But Intracellular
  Killing Is Less Effective
• multiplications of the organism ? induction of
  immunity

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• Host responds by forming
• Specific antibodies
• IgM appears within 1 week and comes down by 3
  months
• IgG appears by 2-3 weeks and persists if
  untreated or partially treated
• Others like
• agglutinins
• opsonins
• precepitins
• C.F. antibodies

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• Brucella Variants are
• S. varient (smooth) more virulent
• resist
  intraleukocyte killing
• R. Varient (hard) less resistant
• All species of brucella produce
• Granuloma in the liver, spleen, l.nodes, bone
  marrow
• Granulomoatous inflammation of gall bladder
• Interstitial orchitis
• Endocarditis with vegetation
• Granuloma in myocardium
• Involvement of brain (neruobrucellosis),
• skin,
• bone

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Clinical manifestations

• Non specific Fever,
• Arthralgia and
  arthritis,
• Malaise,
• Weakness,
• Neurobrucellosis ?
  Depression
• Incubation period Few Days to Months
• The interval between onset of the Symptoms and
  Diagnosis 150 days (mean of 4 weeks
• Hepatosplenomegaly 30-40

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• Uncommon manifestations
• Osteomeyelitis (non-suppurative)
• Myocarditis
• Endocarditis
• Genitourinary
• Neonatal brucellosis

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Diagnosis

• History
• Examination
• Investigations
• CBC hemolysis,
• pancytopenia (hypersplenism)
• Bone marrow involvement with haemophagocytosis
  reported
• Acute disease before treatment
• Blood cultures ve up to 50
• Bone marrow cultures ve up to 90
• Serology (IgM IgG)
• - high titred serum prozone
• - Inhibition ? dilute with sera

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• Successful treatment
• Rapid decline of IgM
• IgG titer may persist for months or years
• High IgG titer ? persistent infection of relapse
• More sensitive test enzyme immuno assay
• Tissue biopsy (liver)

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Differential diagnosis

• Acute brucllosis
• Influenza
• Typhoid fever
• Infectious mononucleosis
• Tuberculosis
• Tularaemia
• Persistent brucellosis
• Malignant histocycosis
• Lymphomas
• Tuberculosis

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• Prevention
• Immunization of domestic herds
• Pasteurization of milk
• Periodic assessment of animals (slaughtering
  infected ones)
• Hunters should use caution in handling
  potentially infected animals

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• Treatment
• Treatment of choice is TETRACYCLINE in
  combination
• Doxycyline (orally)
• 5 mg/kg/day max 200m/day in 2
  divided doses
• (Plus)
• Streptomycin (IM)
• 30 mg/kg/day divided every 12 hours
• OR
• Gentamicin (IV)
• 5 - 7.5 mg/kg/day divided every 8 hours8h

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• For Children
• Trimethoprim sulfamethoxazole (orally )
• 10 - 12 mg/kg/day (Trimethoprim)
• (Plus)
• Rifampacin
• 15 - 20 mg/kg/day
• ( Duration of treatment 3 - 6 weeks )

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• Delay in Diagnosis
• High antigen load after treatment
• JARISH - HERXHEIMER like reaction ? Treated with
  Steroids if needed

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• Prognosis
• Untreated cases ? case fatality rate is 3
• Most deaths are due to specific organ involvement
  (as Endocarditis)
• Following treatment ? excellent prognosis
• Delayed diagnosis ? prolonged course
• Complete recovery may take up to 6 months
• Re-infection is uncommon
• Immune individuals if invadertently injected with
  the cattle vaccine ? local and mild systemic
  disease