Meningitis

By Abaynesh A.(MD)
Meningitis
 Classification: based on
- Etiology
- Duration
Meningitis
 Etiology
- Bacterial(pyogenic) meningitis
- Tuberculous meningitis
- Viral meningitis
- Cryptococcal meningitis
- Syphilitic meningitis
- Carcinomatous meningitis
- SLE meningitis
- Parasitic meningitis
Meningitis
 Duration:
- Acute meningitis
- Sub acute meningitis
- Chronic meningitis
Acute Bacterial Meningitis

 Bacterial meningitis is an acute purulent

infection within the subarachnoid space
 Menigoencephalitis:

- Meninges
- Subarachnoid space
- Brain parenchyma
Etiology
 Streptococcus pneumoniae (~50%)
 N. meningitides (~25%)
 Group B streptococci (~15%)
 Listeria monocytogens (~10%)
 H. influenzae <10%
 Gram negative bacilli
 Group B Streptococcus(S.agalactiae)
 Staphylococcus aureus /coagulase negative

staphylococcus
 Factors
- Age
- Immune status
- Settings
- Weather conditions
S. pneumoniae
 The most common cause of meningitis in adults
>20 years of age
 Predisposing factors:
- Pneumococcal pneumonia
- Pneumococcal sinusitis or otitis media
- Alcoholism, diabetes, splenectomy,
- Hpogammaglobulinemia, complement
deficiency
- Head trauma with basilar skull fracture and
CSF rhinorrhea.
 Mortality remains ~20% despite antibiotic therapy
Neisseria Meningitides
 Accounts for 25% of all cases adult bacterial
meningitis

 For up to 60% of cases in children and young

adults between the ages of 2 and 20

 Petechial or purpuric skin lesions may occur

Cont…..
 Obligate human Gram-negative diplococcus

 Exclusively human disease

 Normally located in the mucous membrane of

the upper respiratory tract

 Invasive isolates - encapsulated and express

pili
Cont……
 Different serogroups (A, B, C, 29-E, H, I, K, L,
W-135, X, Y, and Z)

 Serogroups A, B, and C account for more than

90 per cent of all invasive isolates

 Less than 10% of clinical isolates are from

serogroups W-135 and Y
Cont…….
 Developing countries
- Incidence approaches 10 to 25 per 100 000
inhabitants per year
- Serogroup A dominate the isolates of large
epidemics
 Industrialized countries

- Infection presents as single cases or in

small clusters
- Sero group B
Predisposing factors for invasive
disease
 Lack of protective antibodies

 Antibodies against serogroups A, C, W-135,

and Y capsule polysaccharides are
bactericidal

 Serogroup B polysaccharide induces a weak,

transient IgM response that is not protective
Defects in the complement system

 Increase susceptibility to meningococcal

infections

 The commonest are absent or malfunctioning

properdin or late complement components
C5 to C9

 Recurrent meningitis
Defects in the mannan-binding lectin

 Mannan-binding lectin is a calcium-

dependent, opsonizing, acute-phase protein

 Low level increased susceptibility

Nasopharyngeal colonization

 Upper respiratory tract mucosa is the natural

habitat of N. meningitides

 It spreads from person to person by droplets and

direct mucosal contact

 Most colonizing meningococci are non-

pathogenic

 Only a small minority of those colonized with

virulent strains will develop invasive disease
Invasive infection

 Invasive disease occurs after acquiring the

virulent strain in the upper respiratory tract

 Most are carriers for up to 7 weeks

 N. meningitides adheres to specific structures

on the epithelial cells in the nasopharynx

 They reach sub mucosal tissue and via

capillaries and gain access to the circulation
Manifestations
 Meningitis

 Meningococcemia

 Meningococcemia with meningitis

Meningococcal meningitis
 More than 50 per cent of all cases of systemic
meningococcal infections

 Presence of multiple petechia and symptoms

of meningitis supports a diagnosis of
meningococcal meningitis
Meningococcemia
 Fulminant meningococcal septicemia (Waterhouse–Friderichsen
syndrome) characterized by

- Persistent circulatory failure

- Coagulopathy leading to thrombosis and

extensive hemorrhage ,gangrene of the
extremities

- Impaired renal, adrenal, and pulmonary

function
 There is very rapid microbial proliferation in the circulation

generating large amounts of bacterial lipopolysaccharides in a

few hours
H. influenzae type b
 Meningitis has declined dramatically since the
introduction of the Hib conjugate vaccine

 H. influenzae causes meningitis in

unvaccinated children and adults
Enteric gram-negative bacilli
 Chronic and debilitating diseases such as
diabetes, cirrhosis, alcoholism ,chronic
urinary tract

 Neurosurgical procedures, particularly

craniotomy
Group B streptococcus(S.agalactae)
 Neonates

 >50 years of age, particularly those with

underlying diseases
L. monocytogens
 Neonates (<1 month of age)

 Pregnant women

 Individuals >60 years

 Immunocompromised individuals of all ages

 Infection is acquired by ingesting foods:

- contaminated coleslaw, milk, soft cheeses
- several types of "ready-to-eat" foods
- uncooked hotdogs
Staphylococcus aureus and
coagulase-negative staphylococci
 Invasive neurosurgical procedures shunting
procedures for hydrocephalus

 Intrathecal chemotherapy
Pathophysiology

 Colonize the nasopharynx by attaching to

nasopharyngeal epithelial cells

 Bacteria are transported across epithelial cells in

membrane-bound vacuoles to the intravascular space

 Bacteria are able to avoid phagocytosis because of the

presence of a polysaccharide capsule

 Blood borne bacteria can reach the intraventricular

choroid plexus, directly infect choroid plexus epithelial
cells, and gain access to the CSF
Cont……
 Pathophysiology of bacterial meningitis is a
direct consequence of elevated levels of CSF
cytokines and chemokines

 TNF and IL-1 increase the permeability of the

blood-brain barrier and resulting in vasogenic
edema

 Adherence of leukocytes to capillary endothelial

cells increases the permeability of blood vessels
Cont…..
 Neutrophil degranulation results in the release of toxic
metabolites that contribute to cytotoxic edema, cell injury,
and death

 The subarachnoid exudate of proteinaceous material and

leukocytes obstructs the flow of CSF through the
ventricular system

 Diminished the resorptive capacity of the arachnoid

granulations in the dural sinuses

 Obstructive and communicating hydrocephalus and

concomitant interstitial edema
Cont…..
 The combination of interstitial, vasogenic,
and cytotoxic edema leads to raised ICP and
coma

 Cerebral herniation results from the effects

of cerebral edema, hydrocephalus ,dural
sinus or cortical vein thrombosis
Clinical Presentation
 Classic clinical triad of meningitis is fever,
headache, and nuchal rigidity

 A decreased level of consciousness occurs in

>75% of patients - lethargy to coma

 Nausea, vomiting, and photophobia

 Seizure
Signs of increased ICP
 Deteriorating or reduced level of consciousness

 Papilledema

 Dilated poorly reactive pupils

 Sixth nerve palsies

 Decerebrate posturing

 Cushing reflex (bradycardia, hypertension, and irregular respirations)

 The most disastrous complication of increased ICP is cerebral

herniation
Laboratory
 CSF

 Blood cultures

 Empirical antimicrobial therapy initiated

without delay
Cerebrospinal fluid
 Increased opening pressure>180mmH2O

 Increased WBC 10-10,000/mm predominance neutrophil

 Increased protein>45mg/dl

 Decreased glucose <40mg/dl/CSF/serum glucose<0.4

 Gram stain …..>60%

 Culture---80%

 Gross appearance- color - bloody-SAH

- Turbid- bacterial-pyogenic
Latex agglutination - S pneumonena
- N menigitidis
- H .influnezea type B
- group B steptococcus
 Limulus lysate—gram negative meningitis
 PCR
Contraindications for LP
 Papille edema

 Focal neurological deficit

 Bleeding diathesis( severe thrombocytopenia)

 Infection to LP site

 Increased ICP

 Head trauma

 Cardiorespiratory compromise
DDx- pyogenic meningitis
 Viral meningitis
 Tbc meningitis
 SAH
 AFI
 Cerebral malaria
 Cryptococcal meningitis
 Syphilitic meningitis
 SLE meningitis
 Carcinomatous meningitis
 Viral Menigoencephalitis
 Focal supportive CNS infections-empyema-sub/epidural
- brain abscess
 Chemical meningitis- tumor rupture,
Empirical therapy
Preterm and neonate(<1 month)
ampicillin + cefotaxime
 Infants 1-3 months

ampicillin +cefotaxime or ceftriaxone

 Immunocompetent children> 3months and

adults
cefotaxime or ceftriaxone +
vancomycin
 Adult>55 or any age with alcoholism,
debilitating
ampicillin + cefotaxime or ceftriaxone
+ vancomycin

 Nosocomial meningitis , posttraumatic, post

neurosurgical procedures ,neutropenic
ampicillin +ceftazidime + vancomycin
Treatment for N.Meningitidis
 Pre hospital
- start benzyl penicillin in suspected cases of
meningococcal infection

- Open IV line with NS

 Antibiotic treatment
- Adequate doses of benzyl penicillin,
cefotaxime, ceftriaxone, or chloramphenicol

- No Jarisch–Herxheimer reaction

- Seven days of treatment is adequate to

eradicate sensitive meningococci
Supportive treatment
 Volume treatment

 Inotropic support
- Dopamine, dobutamine, noradrenaline, and
adrenaline are used

 Corticosteroid therapy
- controversial

 Ventilatory support
Vaccination

 Capsule polysaccharide vaccine (A, C, Y, and W)

 The serogroup A polysaccharide vaccine is immunogenic from

6 months of age

 Serogroup A infection

- Infants of less than 24 months should receive two

doses with at least a 1-month interval

- Above 2 years should receive one dose

 For serogroup C infection, one dose should be given from 18

months
Antibiotic prophylaxis
Close contacts
 With rifampicin at 10 mg/kg, maximum dose

600 mg every 12 h for 48 h

 Azithromycin 500 mg po stat

 Ceftrixone 250 mg IM stat

Duration treatment
 5-7 days-N menigitides

 14 days- S .pneumonea

 21 days- L. monocytogen
- gram negative
Dexamethasone

 Dexamethasone 10 mg Iv 20 minutes before

the first dose of an antimicrobial agent

 The same dose was repeated every 6 hours

for 2-4 days
Complications(meningitis)
 Decreased intellectual function

 Memory impairment

 Seizures

 Hearing loss and dizziness

 Gait disturbances

 Focal neurologic deficit - vasculitis

 Hyponatremia
Prognosis

 Mortality 3–7% for H. influenzae, N.meningitidis, group B streptococci

 15% for L. monocytogenes

 20% for S. pneumoniae

 Predictive of increased mortality and poorer

outcomes:
- Decreased CSF glucose concentration [<2.2
mmol/L (<40 mg/dL)] and

- Markedly increased CSF protein concentration [>3g/L

(> 300 mg/dL)]
 Poor prognostic signs

- Decreased level of consciousness on admission

- Onset of seizures within 24 h of admission

- Signs of increased ICP

- Young age (infancy) and age >50

- The presence of comorbid conditions including shock and/or

the need for mechanical ventilation

- Delay in the initiation of treatment

Acute Viral Meningitis
 Present with headache, fever, and signs of
meningeal irritation

 The headache of viral meningitis is usually frontal

or retroorbital and associated with photophobia

 Nuchal rigidity is present in most cases

 Constitutional symptoms like malaise, myalgia,

anorexia, nausea and vomiting, abdominal pain,
and/or diarrhea
 Often have mild lethargy or drowsiness

 If the patient has :

- Profound alterations in consciousness
- Seizures or focal neurologic signs

 Are not typical of viral meningitis and

suggest the presence of encephalitis
Etiology

 The most important agents

- Enterviruses

- HSV type 2 (HSV-2)

- Arboviruses

- HIV
Laboratory Diagnosis

 CSF Examination
- The total CSF cell count in viral meningitis is
typically 25–500/mL
- lymphocytic pleocytosis
- A normal or slightly elevated protein [0.2–0.8
g/L (20– 80 mg/dL)]
- A normal glucose concentration
- A normal or mildly elevated opening pressure
(100–350 mmH2O)
Cont…..
 Organisms are not seen on Gram's or acid-
fast stained smears or India ink preparations
of CSF

 PCR

 VIRAL CULTURE

 SEROLOGY
Acute Viral Meningitis: Treatment
 Treatment primarily symptomatic

 Use of analgesics, antipyretics, and antiemetics

 Fluid and electrolyte status should be monitored

 Hospitalization may not be required in

immunocompetent patients with:
- No focal signs or symptoms no significant
- Alteration in consciousness
Drugs
 Oral or intravenous acyclovir for HSV-1 or 2

 Pleconaril for Enteroviral

 For cases of severe EBV or VZV infection

famciclovir, Val acyclovir for a total course of
7–14 days
Cryptococcal meningitis
 Caused by Cryptococcus neoformans

 A yeast-like fungus

 C. neoformans is frequently found in soils

contaminated with avian ,pigeon droppings
Cont…….
 C. neoformans is the leading infectious cause of
meningitis in patients with AIDS

 It is the initial AIDS-defining illness in ~2% of

patients
 Generally occurs in patients with CD4+ T cell
counts <100/L

 Cryptococcal meningitis is particularly common in

patients with AIDS ~20% of patients
Pathogenesis

 Cryptococcal infection is acquired by inhalation of

aerosolized infectious particles

 Cryptococcal infection is acquired in childhood

 Inhalation of C. neoformans can be followed by

clearance of the organism or establishment of the
latent state
Clinical manifestations
 The course is sub acute or chronic

 Presented with fever, nausea, vomiting,

altered mental status, headache, and
meningeal signs

 The incidence of seizures and focal

neurologic deficits is low

 Visual loss
Cont……
 Classic characteristics of meningeal irritation,
may be absent in cryptococcal meningitis

 Patients may develop cryptococcomas and

cranial nerve involvement

 One-third of patients also have pulmonary

disease
Cont…….
 Uncommon manifestations of cryptococcal infection
include
- Skin lesions that resemble molluscum
contagiosum,
- Lymphadenopathy,
- Palatal and glossal ulcers
- Arthritis
- Gastroenteritis
- Myocarditis
- Prostatitis

 The prostate gland may serve as a reservoir
for smoldering cryptococcal infection

 Pulmonary cryptococcosis presents as cough,

increased sputum production, and chest pain
Diagnosis
CSF Analysis :
 Opening pressure may be markedly elevated

 CSF analysis Protein = 30–150 mg/dl

 Decreases in glucose

 WBC = 0–100 /mm3 (monocyte)

 Culture = positive 95–100%

 Indian ink = positive 60–80%

 Cryptococcal Ag > 95 % sensitive and specific

Therapy for Cryptococcosis

 Has three phases:

- Induction

- Consolidation

- Maintenance
Induction phase(2 weeks)
 Option A. High dose fluconazole- Fluconazole 600 mg

twice daily alone

 Option B. Amphotericin B + fluconazole: Amphotericin

0.7-1 mg/kg/day + fluconazole 800 mg/day

Consolidation phase (8 weeks)

 Option A. Fluconazole 800 mg/day

 Option B. Fluconazole 400-800 mg/day

Cont…….
Maintenance treatment (or secondary prophylaxis)
 Fluconazole 200 mg daily

 Discontinuation :

- When patients are stable and adherent to ART

- Anti-fungal maintenance treatment for at

least one year

- CD4 cell count of greater than or equal to 200

cells/ mm3 (two measurements six months apart)
Cont……..
 Management of increased ICP
- Daily serial LP(20-30 ml)
- CSF shunting

 Role of dexamethasone
- No beneficial effect
- ICP is mainly decreased CSF absorption
Tuberculous meningitis
 TB meningitis results from the hematogenous
spread of primary or post primary pulmonary
disease

 From the rupture of a subependymal tubercle into

the subarachnoid space

 In >50% evidence of old pulmonary lesions or a

miliary pattern is found on chest radiography
Manifestations
 The disease often presents as sub acute or
chronic forms

 Headache and slight mental changes after a

prodromal of weeks of low-grade fever,
malaise, anorexia, and irritability

 TB meningitis may evolve acutely with severe

headache, confusion, lethargy, altered
sensorium, and neck rigidity
Cont……
 Typically, the disease evolves over 1–2 weeks, a course
longer than that of bacterial meningitis

 Paresis of cranial nerves (ocular nerves in particular) is a

frequent finding

 Multiple cranial nerve palsies in basal meningitis

 The involvement of cerebral arteries may produce focal

ischemia

 The ultimate evolution is toward coma, with hydrocephalus

and intracranial hypertension
Diagnosis
 The CSF reveals:
- High leukocyte count (up to 1000/µl)
with a predominance of lymphocytes

- Protein content of 1–8 g/L (100–800 mg/dL);

- Low glucose concentration (hypoglychorachea)

 But any of these three parameters can be within

the normal range
Cont……
 AFB are seen on direct smear of CSF sediment in up
to one-third of cases

 Culture of CSF is diagnostic in up to 80% of cases

and remains the gold standard

 Polymerase chain reaction (PCR) has a sensitivity of

up to 80%, but rates of false-positivity reach 10%

 Imaging studies (CT and MRI) may show

hydrocephalus and abnormal enhancement of basal
cisterns or ependyma
Treatments
 Neurologic sequele are documented in 25% of
treated cases

 Start Anti TB immediately

 Adjunctive glucocorticoids may experience

faster resolution of CSF abnormalities and
elevated CSF pressure
Cont……..
 Adjunctive dexamethasone 0.4 mg/kg/day given IV
and tapering by 0.1 mg/kg per week until the
fourth week

 Followed by 4 mg/d given by mouth and tapering

by 1 mg per week until the fourth week

 Significantly enhanced the chances of survival

Syphilitic meningitis
 Two forms:
- Meningeal syphilis

- Meningovascular syphilis
Diagnosis
 CSF for pleocytosis (>5 white blood
cells/mm3)

 Increased protein concentration (>45 mg/dL)

 VDRL reactivity

 The CSF VDRL test is highly specific but is

insensitive and may be nonreactive even in
cases of symptomatic neurosyphilis
Cont…….
 FTA test on CSF is reactive far more often than the
CSF VDRL test in all stages of syphilis

 FTA reactivity may reflect passive transfer of serum

antibody into the CSF

 A nonreactive CSF FTA test may be used to rule out

neurosyphilis
Treatment
 Crystalline penicilline 4million IU IV Q4hrs for
10-14 days or

 Procaine penicillione 2.4 million IU IM

+
probenicide 500mg QID for 10-14 days
Brain Abscess
 A brain abscess is a focal, suppurative infection
within the brain parenchyma, typically surrounded
by a vascularized capsule

 Cerebritis - non encapsulated brain abscess

Predisposing conditions

 Otitis media

 Mastoiditis

 Paranasal sinusitis

 Pyogenic infections in the chest or other body sites

 Penetrating head trauma

 Neurosurgical procedures

 Dental infections
Etiology
A brain abscess may develop

 By direct spread from a contiguous cranial

site of infection

 Following head trauma or a neurosurgical

procedure

 As a result of hematogenous spread from a

remote site of infection
 Hematogenous abscesses account for 25% of
brain abscesses.

 Hematogenous abscesses are often multiple

 Multiple abscesses often (50%) have a

hematogenous origin
Stages of Brain Abscess
 The early cerebritis stage (days 1–3) :
- Is characterized by a perivascular infiltration of
inflammatory cells
- Marked edema surrounds the lesion

 In the late cerebritis stage (days 4–9)

- Pus formation leads to enlargement of the
necrotic center
- A thin capsule of fibroblasts and reticular fibers
gradually develops, and the surrounding area of
cerebral edema becomes more distinct
 The third stage, early capsule formation (days
10–13)

- Characterized by the formation of a capsule

- This stage correlates with the appearance

of a ring-enhancing capsule neuroimaging
studies
Cont…..
 The final stage, late capsule formation (day 14 and
beyond)
- Defined by a well-formed necrotic center surrounded by
a dense collagenous capsule

- The surrounding area of cerebral edema has

regressed, but marked gliosis with large numbers of
reactive astrocytes has developed outside the capsule

- This gliotic process may contribute to the development

of seizures as a sequelae of brain abscess
Clinical Manifestation
 The classic clinical triad
- Headache
- Fever, and
- Focal neurologic deficit

 The most common symptom in patients with

a brain abscess is headache, occurring in
>75% of patients
Cont……..
 Fever is present in only 50% of patients at the
time of diagnosis, and its absence should not
exclude the diagnosis

 The new onset of focal or generalized seizure

activity is a presenting sign in 15–35% of patients

 Focal neurologic deficits including hemiparesis,

aphasia, or visual field defects are part of the
initial presentation in >60% of patients
Treatment
 Optimal therapy of brain abscesses involves a
combination of:
- High dose parenteral antibiotics
- Neurosurgical drainage

 Empirical therapy of community-acquired brain

abscess in an immunocompetent patient

- Third or Fourth-generation cephalosporin

(e.g., cefotaxime, ceftriaxone, or cefepime) +
- Metronidazole
Cont……..
 Patients with penetrating head trauma or
recent neurosurgical procedures:

- Ceftazidime + Vancomycin OR

- Meropenem plus Vancomycin

Cont……..
 Medical therapy alone is be reserved for patients

- Small abscesses (<2–3 cm)

- Nonencapsulated abscesses (cerebritis), and

- Patients whose condition is too tenuous to allow

performance of a neurosurgical procedure

 All patients should receive a minimum of 6–8 weeks

of parenteral antibiotic therapy
Cont…….
 Prophylactic anticonvulsant therapy because of the
high risk (35%) of focal or generalized seizures

 Anticonvulsant therapy is continued for at least 3

months after resolution of the abscess
THANK U!
Malaria

By Abaynesh A.(MD)
 Definition
 It is a protozoan diseases transmitted by the bite of
female Anopheles mosquito
 It can also be transmitted by blood transfusion and
transplacentally
 Human infections are caused by six species of the
genus plasmodium
- P. falciparum
- P. vivax
- P. malariae
- P. ovale curtisi
- P. ovale walliri
- P. knowlesi
 Severe and fatal malaria are due to P. falciparum
 Epidemiology
GLOBAL Epidemiology grew
 At Risk
- More than 40% of the world population
 Cases
- 300 to 500 million clinical cases / year
 Deaths
- About 1-2 million per year
- 80 to 90% of deaths occur in sub-Saharan Africa
- 90% of deaths are U5 children and pregnant mothers
- LBW, pre-term delivery, cerebral malaria, and sever malarial
anemia are
major causes of deaths

 Cognitive impairment, behavioral changes, spasticity, epilepsy are

among the sequels of malaria in children

 Malaria is not only a disease of poverty but is also a contributor of

poverty
 MALARIA IN ETHIOPIA

 Risk: more than 50 million people live in

malaria risk area (70% of land )
 Cases: 9 million cases per year, with
additional 6 million cases in epidemic year
 Death during outbreak: more than
115,000/yr
 Contributes to 20% death in Children U5
 Malaria in Ethiopia is unstable
 About 60% are due to P. falciparum and
40% are due to P. vivax
 More than 20 million ITN distributed
 ENDEMICITY

❖ Assessed by splenomegaly and

asymptomatic parsitemia rate in children 2-
9 yrs
 Holoendemic: >75%
 Hyperendemic: 51-74%
 Mesoendemic: 10-50%
 Hypoendemic: <10%
 Transmission of malaria depends on the
density, feeding (biting) habits, and
longevity of the anopheles mosquito.

 The intensity of malaria transmission is

measured by the Entomologic Inoculation
Rate (EIR) which is the number of
inoculations of malaria parasites received
by one person in one year
 Intensity of Malaria transmission

 A. STABLE TRANSMISSION
- transmission of malaria occurs throughout the
year
- EIR >10 per year
- partial immunity acquired, disappears during
pregnancy and when leaving the area
- acute and severe disease confined to young
children
- adolescents and adults rarely suffer clinical
disease
 B. Unstable transmission
- EIR fluctuate throughout the year (1-5
EIR/Yr)
- No partial immunity acquired
- All age groups affected
- Epidemics can occur when inoculation
rates
increase
 Life Cycle
Pre-patent period
 period from inoculation to appearance of
merozoits from the liver
Incubation period
 period from inoculation to appearance of
clinical symptoms
❖ for P. falciparum: 7-30 days
 Mosquito inoculates sporozoites
 Sporozoites will infect the liver within ½ to 2
hrs
 Sporozoites undergo multiple nuclear division
without cytoplasmic division to produce
hepatic schizonts (Hepatic schizogony)
 Hepatocytes burst to produce merozoites
 P. vivax, P. ovale may remain in the
hepatocytes as hypnozoites to cause disease
later in life
 Merozoites invade the RBC
- P. vivax: receptor is Duffy blood group Ag
- P. falciparum: glycophorin
 In the RBC the parasites feed on hemoglobin
 Initial form: ring form which is a vacuole then
become a trophozoite
 The trophozoite undergoes asexual nuclear
division to produce schizonts
 Degradation product of the HB forms the
malaria pigment which is Hemozoin.
 schizonts causes lysis of RBC and each releases
about 8-24 merozoites which infects other RBC
 After a few days some of the merozoites
transform into male or female gametocytes.
These are necessary for sexual reproduction of
the parasite.
 Generally at least two schizogonous cycles
must be completed before gametocytes appear
 Mosquito picks up during feeding female and
male gametocytes
 In the mosquito gametes undergo fertilization
to form the zygote (sexual reproduction )
→ookinte →oocyte
→ sporozoite
 The incubation period is variable
- P. falciparum: 7-9days
- P. vivax and ovale: days to years
 The rupture of the hepatocytes is not
associated with any symptoms but burst of
the RBC triggers fever, chills, muscle ache
and malaise
 Parasitized RBCs are removed by spleen
causing splenomegaly.
 Only P. falciparum causes potentially fatal
complicated and sever malaria
 Cytoadherence:
-RBCs produce membrane knobs which mediate
adhesion of the RBCs to endothelial cells in the
venules and arterioles and sequestration of
RBCs with
mature schizonts
 Infected RBCs stick to uninfected RBCs causing
rosette formation among themselves
 Infected RBCs irregular in shape, less deformable
and more antigenic
 Cytoadherence and rosetting lead to sequestration
of RBCs in the vital organs
- sequestered parasites continue to grow out of
reach of
spleen
 Cause obstruction of microcirculation in vital organs
leading to derangement of functions

 Anemia in malaria
- lysis of infected RBC’s by the parasite
- splenic sequestration infected RBS
- less deformability of uninfected RBC’s
- bone marrow suppression
 Immunity in malaria
 The specific immune response to malaria
following repeated infections confers
protection from hyperparasitemia and
disease but not from infection in adults
(premonition)
 Immunity is species and strain specific
 Maternal antibody transferred to new born
confers protection against severe disease
in the few months of life
 The immunity wanes with in months after
leaving malaria endemic area
 Uncomplicated malaria

- Symptomatic malaria without signs of severity or

evidence of vital organ dysfunction
- commonly presentation is nonspecific like lack
of
sense of well- beingness, muscle aches,
headache,
fatigue
- less common paroxysms of chills(ብርድ ብርድ
ማለት), rigor, fever and sweating
- tertian malaria: vivax, ovale, falciparum
- quartan malaria: malaria
- anemia, mild jaundice, splenomegaly,
hepatomegaly
 Management of uncomplicated
malaria
 Reliable and complete history (including
travel history)
 Complete Physical examination and clinical
assessment
 Parasitological testing (use of microscopy)
 Other laboratory investigations to aid
diagnosis and to rule out other medical
conditions resembling malaria.
 Blood Film
-Thick blood smear: initial test
- Detect the presence of parasite
- High sensitivity
- Thin blood smear: confirmatory test
- High specificity, low sensitivity
- Determination of plasmodium species
- Parasites are visible in RBCs since
morphology of
erythrocyte is preserved
- Evaluation of parasite and erythrocyte
morphology
 P.falciparum : Coartum(artemether and
lumefantrine) :4 tabs po BID for 3 days
 P. vivax, and malaria: chloroquine d 10 mg
base/kg po immediately (Day 1), followed by
10 mg base/kg po at 24 hours (Day 2), and
5mg base/kg po at 48 hours (Day 3)(4,4,2
tabs)
 Mixed infection: Coartum and single dose
Premaquine(.25mg/kg max 15 mg)
Diagnosing severe malaria
 Taking a reliable history

 Complete physical examination

Parasitological testing (use of microscopy)

 Other laboratory investigations to aid

diagnosis and rule out other infections
resembling malaria
 Clinical features
 Prostration(መውደቅ)
 Impaired consciousness or un-rousable
coma
 Respiratory distress (acidotic breathing)
 Multiple convulsions
 Circulatory collapse or shock(ድንጋጤ)
 Pulmonary edema or difficulty in
breathing
 Bleeding tendency/abnormal bleeding
 Jaundice
 Haemoglobinuria
 Laboratory findings
Severe anemia (hemoglobin <5g/dl,
haemocrit < 15%)
 Hypoglycemia (<2.2 mmol/L or 40 mg/dL)
 Acidosis (bicarbonate <15 mmol/L)
 Hyperlactatemia (>5 mmol/L)
 Hyperparasitemia (>4%) (non-immune
person)
 Renal impairment (creatinine >3mg/dl)
Treatment of severe malaria
❖First line treatment for severe malaria at
the health center and hospital level is
either:
 IV or IM artesunate (preferred) OR
ተመራጭ
• IM artemether (alternate) ORተለዋጭ
• IV quinine infusion (if artesunate or
artemether is not available) OR

 IM quinine (if artesunate is not

available).
 ARTESUNATE IV/IM
Dosing schedule:
1. Give three parental doses over 24 hrs
2. Give parental doses for a minimum of
24 hrs once started irrespective of the
patients’ ability to tolerate oral
treatment earlier
Artesunate 2.4 mg/kg per dose
- Day 1 - Dose 1: on admission(0 hr)
- Dose 2: 12hrs later
- Day 2 - Dose 3: 24hrs after first dose
 When the patient tolerates oral therapy, a
full course of oral ACT(3 days) should be
started to complete the treatment
 Until the patient is able to take oral
medication continue parenteral
treatment(once daily dose) for a maximum
of 7days
 A course of injectable artesunate should
always be followed by a 3 day course of
ACT
 Artemether injection
 Artemether injection is given at:
- Day 1: 3.2 mg/kg
- Day 2: 1.6 mg/kg
- Day 3: 1.6 mg/kg
 Then if the condition of the patient
improves, will be followed by full dose ACT
 IV quinine infusion
 Loading dose: 20mg dihydrochloride salt/kg
diluted in 10ml isotonic fluid/kg IV infusion over 4
hours followed by 8 hours
 Maintenance dose :10mg salt/kg over 4 hours

 Each dose of parenteral quinine must be given

as a slow, rate controlled infusion (usually
diluted in 5% dextrose and infused over four
hours).

 For all patients with severe malaria, IV quinine

infusion should be given at least for the first 48
hours
 IM quinine
 Quinine dihydrochloride can be given in
the same dosages by IM injection in the
anterior thigh (not in the buttock)

 The dose of quinine should be divided

between two sites – half the dose in
each anterior thigh

 If possible, for IM use, quinine should be

diluted in normal saline to a
concentration of 60–100mg salt/ml
General management of patient
with severe malaria
 A = airway: In the unconscious or convulsing
patient, it is imperative that the airway is free of
obstructions.
 B = breathing: Check that the patient is
breathing by looking for chest movements and
listening for breath sounds; and support
breathing by giving oxygen.
 C = circulation: Feel hands and check for
capillary refill, check, monitor and record vital
signs, i.e. blood pressure, pulse, respiratory rate.
 In addition, support circulation by giving IV
fluids preferably the plasma expanders.
 Correct hypoglycemia
-1 ml/kg of 50% dextrose diluted with an
equal volume of NS(1ml/kg saline)IV
- 5 ml/kg of 10% dextrose by slow IV
infusion
 A body temperature of greater than
38ºC
- Paracetamol 1g po PRN
- Remove the patient’s clothes and start
tepid
sponging and fanning
 Control convulsions:
- Correct hypoglycemia
-If convulsions continue for more than 5
minutes, a slow IV injection of diazepam (0.15
mg/kg of body weight, maximum of 10 mg
for adults)
 Consider the need for blood transfusion.
Indication for blood transfusion:
- Severe anemia(hematocrit<15% )
- If the patient’s life is threatened by anemia-associated
acidosis,
shock or the parasitemia is so high that you can predict a
critical
drop
- If the patient has spontaneous bleeding
Fluid electrolyte and acid base disturbances:
 Hypovolaemia: - Low jugular venous pressure,
- Postural hypotension and
- Oliguria with high urine specific gravity.
 Acidosis: can be due to a relative shortage of oxygen in tissues
occupied by sequestered parasites.
 This shortage of oxygen is made worse when there is hypovolaemia
and/or severe anemia
 This lack of oxygen forces tissues to obtain energy by other
biochemical pathways not dependent on oxygenone result of this is
the release of
lactic acid, leading to metabolic acidosis
 Acidosis usually presents as
- Deep breathing (not necessarily rapid) with in drawing of the
bony
structures of the chest wall, in the absence of localizing chest
signs.
 Perfusion is improved by correcting hypovolaemia.
Acute renal failure:
 It is worsened by hypovolemia and hypotension
 . It is highly preventable if fluid balance and blood
pressure is maintained.
 If a patient has oliguria, first correct fluid deficit and
 try to correct blood pressure, however if there is
persistent oliguria (<17 ml/hour) despite adequate
correction of dehydration or hypotension, renal
failure is present or imminent.
 Hiccup may be an indicator of advanced renal
failure.
 Management: Correct dehydration and maintain
fluid balance, maintain normotension, monitor JVP,
do peritoneal dialysis.
 Pulmonary edema and Adult Respiratory
Distress Syndrome (ARDS):
 Clinical presentation:
- Hyperventilation (rapid breathing)
- Crackles are present on auscultation, and
- Pink frothy sputum (severe cases).
 Management:
- Position patient upright (sitting position),
- Give oxygen therapy;
- Give diuretics, e.g. furosemide 40 mg IV.
 If no response increase dose progressively to
maximum 6mg/kg/day: assess the need for
intubation and mechanical ventilation
 Recrudescence(ያልተጠናከረ)
- Is the recurrence of asexual parsitemia after treatment of the
infection with
the same infection that caused the original illness.
-This results from incomplete clearance of parsitemia due to
inadequate or
ineffective treatment.
 Relapse
- The recurrence of asexual parsitemia in P. vivax and P. ovale
malaria deriving
from persisting liver stages.
- occurs when the blood stage infection has been eliminated but
hypnozoites
persist in the liver and mature to form hepatic schizonts.
 Recurrence(ተደጋጋሚነት)
- The recurrence of asexual parasitemia following treatment.
- This can be caused by a recrudescence, a relapse or a new
 Prevention and control
1. Prompt diagnosis and treatment of cases
2. Chemoprophylaxis
3. Vector control program
- Insecticide treated bed nets (ITN,LLITN)
- DDT
- Environmental interventions
4. Epidemic detection and control
Thank U!
 Acute febrile illnesses
For 3rd Year PHO students
Dr.Kibretu. B(MD)
October, 2019G.C
Outline

 Introduction
 Epidemiology, clinical feature ,Dx and Rx

◦ Typhoid fever
◦ Typhus
◦ Relapsing fever
AFI

 Fever a common complaint encountered in the

emergency department the differential diagnosis of
which is numerous.

 How do you define fever?

Typhoid fever

 Enteric fever

 is a systemic disease characterized by fever and

abdominal pain and caused by dissemination of S.
typhi or S. paratyphi.
Epidemiology

 S. typhi and S. paratyphi serotypes A, B, and C—have

no known hosts other than humans.

 Food-borne or waterborne transmission results from

fecal contamination by ill or asymptomatic chronic
carriers.

 Health care workers infected after exposure to

infected patients or during processing of clinical
specimens and cultures.
Con’t…
 The incidence is
◦ highest (>100 cases per 100,000 population
per year) in south central and Southeast Asia

◦ medium (10–100 cases per 100,000) in the rest

of Asia, Africa, Latin America, and Oceania
(excluding Australia and New Zealand); and

◦ low in other parts of the world .

Con’t…

 Worldwide there are an estimated 22 million cases

of enteric fever, with 200,000 deaths annually.

 A high incidence of enteric fever correlates with

poor sanitation and lack of access to clean
drinking water.

 In endemic regions, enteric fever is more common

in urban than rural areas and among young
children and adolescents.
Con’t…
 Risk factors include
◦ contaminated water or ice
◦ flooding
◦ food and drinks purchased from street vendors
◦ raw fruits and vegetables grown in fields fertilized
with sewage
◦ ill household contacts
◦ lack of hand washing and toilet access, and
◦ evidence of prior Helicobacter pylori infection .
Con’t…

 It is estimated that there is one case of

paratyphoid fever for every four cases of typhoid
fever, but

 The incidence of infection associated with S.

paratyphi A appears to be increasing, this
increase may be a result of vaccination for S.
typhi.
classic presentation
• Classic reports described the characteristic stages
of typhoid fever in untreated individuals

• In the 1st wk of illness,

• rising ("stepwise") fever and bacteremia develop
• While chills are typical, frank rigors are rare
• Relative bradycardia or pulse-temperature dissociation
may be observed.
• In the 2nd wk of illness,
• abdominal pain develops and “rose spots” (faint salmon-
colored macules on the trunk and abdomen) may be seen.
• During the 3rd wk of illness

 Hepato-splenomegaly, intestinal bleeding, and perforation

due to ileocecal lymphatic hyperplasia of the Peyer's
patches may occur,

 Together with secondary bacteremia and peritonitis.

Septic shock or an altered level of consciousness may
develop
Clinical picture

 The incubation period for S. typhi averages 10–14

days but ranges from 3–21 days, depending on
the: inoculum size and the host's health and
immune status.

 Fever and abdominal pain—are variable

 While fever is documented at presentation in >75%

of cases, abdominal pain is reported in only 30–
40%.
Con’t…

 The most prominent symptom is prolonged fever

(38.8°–40.5°C; 101.8°–104.9°F), which can
continue for up to 4 wks if untreated.

 S. paratyphi A causes milder disease than S.

typhi, with predominantly GI symptoms.

 Early physical findings of enteric fever include

◦ rash ("rose spots"30%), hepatosplenomegaly (3–6%),
epistaxis, and relative bradycardia at the peak of high
fever (<50%).
Con’t…

 Rose spots make up a faint, salmon-colored,

blanching, maculopapular rash located primarily
on the trunk and chest.

◦ is evident in 30% of patients at the end of the 1st wk and

resolves without a trace after 2–5 days.

◦ Salmonella can be cultured from punch biopsies of these

lesions.

◦ The faintness of the rash makes it difficult to detect in

highly pigmented patients.
Con’t…
 The development of severe disease (which occurs in
10–15% of patients) depends on

o host factors (immunosuppression, antacid therapy,

previous exposure, and vaccination),

o strain virulence and inoculum, and

o choice of antibiotic therapy.

Con’t…
 Neurologic manifestations occur in 2–40% of
patients and include
◦ meningitis,
◦ Guillain-Barré syndrome,
◦ neuritis, and
◦ neuropsychiatric symptoms (described as
"muttering delirium" or "coma vigil"), with
picking at bedclothes or imaginary objects.
Complications

 GI bleeding (10–20%) & intestinal perforation (1–

3%)

 most commonly occur in the 3rd & 4th wks of

illness

 result from hyperplasia, ulceration, and necrosis

of the ileocecal Peyer's patches at the initial site
of Salmonella infiltration.
Rare complications
 DIC , hepatitis
 pancreatitis
 hepatic & splenic abscesses and granulomas
 endocarditis, pericarditis, myocarditis,
 orchitis, glomerulonephritis, pyelonephritis and
 HUS
 severe pneumonia
 arthritis, osteomyelitis, &
 parotitis.
Con’t…

 Up to 10% of untreated patients with typhoid fever

excrete S. typhi in the feces for up to 3 months,

 1–4% develop chronic asymptomatic carriage,

shedding S. typhi in either urine or stool for >1
year.

 Chronic carriage is more common among women,

infants, and persons with biliary abnormalities or
concurrent bladder infection with Schistosoma
haematobium.
Diagnosis

 The definitive DX of enteric fever requires

◦ the isolation of S. typhi or S. paratyphi from
blood, bone marrow, other sterile sites, rose
spots, stool, or intestinal secretions.

 The sensitivity of blood culture is only 40–80%,

probably because of high rates of antibiotic use
in endemic areas and the small quantities of S.
typhi (i.e., <15 organisms/mL) typically present
in the blood.
 Con’t…

 Bone marrow culture is 55–90% sensitive, &, unlike

that of blood culture, its yield is not reduced by up to
5 days of prior antibiotic therapy.

 Culture of intestinal secretions can be positive despite

a negative bone marrow culture.
Con’t

 If blood, bone marrow, and intestinal secretions are

all cultured, the yield is >90%.

 Stool cultures, while negative in 60–70% of cases

during the 1st wk, can become positive during the
3rd wk of infection in untreated patients.
 Con’t….

 Leukopenia and neutropenia are detectable in 15–

25% of cases.

 Leukocytosis is more common among children,

during the first 10 days of illness, and in cases
complicated by intestinal perforation or secondary
infection.

 Other nonspecific laboratory findings include

moderately elevated LFTs & muscle enzyme levels.
Con’t…
 Several serologic tests, including the classic Widal
test for "febrile agglutinins,"

 PCR and DNA probe assays to detect S. typhi in

blood have been identified but have not yet been
developed for clinical use.
Treatment

 Prompt administration of appropriate antibiotic

therapy prevents severe complications of enteric
fever and results in a case-fatality rate of <1%.

 For treatment of drug-susceptible typhoid fever,

fluoroquinolones are the most effective class of
agents, with cure rates of 98% and relapse and
fecal carriage rates of <2%


Con’t…
 The 1–5% of patients who develop chronic carriage
of Salmonella can be treated for 4–6 wks with an
appropriate oral antibiotic.

 Rx with oal amoxicillin, TMP-SMX, ciprofloxacin, or

norfloxacin is 80% effective in eradicating chronic
carriage of susceptible organisms.

 However, in cases of anatomic abnormality (e.g.,

biliary or kidney stones), eradication often requires
both antibiotic therapy and surgical correction.
Prevention
 Two typhoid vaccines are commercially available:

◦ (1) Ty21a, an oral live attenuated S. typhivaccine (given on

days 1, 3, 5, and 7, with a booster every 5 years); and

◦ (2) Vi CPS, a parenteral vaccine consisting of purified Vi

polysaccharide from the bacterial capsule (given in 1 dose,
with a booster every 2 years).
Con’t…
 The minimal age for vaccination is 6 years for
Ty21a and 2 years for Vi CPS.

 Currently, there is no licensed vaccine for

paratyphoid fever.

 Hygiene
Rickettsial disease
 The members of the family responsible for human
disease in the tropics are:
◦ Orientia tsutsugamushi, mite, the causative organism of
scrub typhus (tsutsugamushi disease in Japan)

◦ the typhus group (TG) of the genus Rickettsia, containing

R.prowazeckii, the agent of classic epidemic or louse-borne
typhus, and R. typhi, which causes murine or flea-borne
typhus; and

◦ The spotted fever group (SFG) Rickettsia,are mostly

transmitted from rodents and other animals by ticks, except
for R. akari (mites) and R. felis (fleas).

◦ Q fever transmitted by tick

Typhus
 Typhus fevers are caused by the rickettsiae
bacteria and transmitted by arthropod (e.g. flea,
mite, tick) bites.

 When arthropods bite a victim, they leave the

rickettsaie bacteria behind.

 Scratching the bite opens the skin to the bacteria,

allowing them to enter the bloodstream.

 Within the blood stream, the bacteria grow and

replicate.
Con’t…

 Types of typhus and carriers:

 epidemic/louse-borne typhus (caused by

Rickettsia prowazekii) carried by the body-louse

 murine typhus (caused by R. typhi) carried by

the rat or cat flea.

 scrub typhus (caused by Orientia

tsutsugamushi) carried by mites.
Endemic typhus
 Is caused by R .typhi

 Fleas acquire R. typhi from rickettsemic rats and

carry the organism throughout their life span.

 Nonimmune rats and humans are infected when

rickettsia-laden flea feces contaminates pruritic
bite lesions; less frequently, the flea bite transmits
the organism
Con’t…
 Transmission also may occur via inhalation of
aerosolized rickettsiae from flea feces.

 Infected rats appear healthy, although they are

rickettsemic for 2 wks.

 Globally, endemic typhus occurs mainly in warm

(often coastal) areas throughout the tropics and
subtropics.

 Patients seldom recall exposure to fleas, although

exposure to animals such as cats, opossums, and
rats is reported in nearly 40% of cases.
Clinical feature
 The incubation period averages 11 days (range, 8–
16 days).

 Headache, myalgia, arthralgia, nausea, and malaise

develop 1–3 days before onset of chills and fever.

 The duration of untreated illness averages 12 days

(range, 9–18 days).
Con’t…
 Rash is present in only 13% of patients at presentation
(usually 4 days after onset of fever),

 appearing an average of 2 days later in half of the

remaining patients and never appearing in the others.

 The initial macular rash is often detected in the axilla

or the inner surface of the arm.

 Subsequently, the rash becomes maculopapular,

involving the trunk more often than the extremities; it
is seldom petechial and rarely involves the face,
palms, or soles.
Con’t…..
 A rash is detected in only 20% of patients with
darkly pigmented skin.

 35% of patients have a hacking, nonproductive

cough, and 23% of patients who undergo chest
radiography have pulmonary densities due to
interstitial pneumonia

 pulmonary edema, and pleural effusions

 Bibasilar rales are the most common pulmonary

sign.
Con’t…
 Less common clinical manifestations include
abdominal pain, confusion, stupor, seizures,
ataxia, coma, and jaundice.

 Complications may include respiratory failure,

hematemesis, cerebral hemorrhage, and hemolysis.

 Greater severity is generally associated with old

age, underlying disease, and treatment with a
sulfonamide; the case-fatality rate is 1%.
Diagnosis
• PCR, or cross-adsorption serologic studies of acute-
and convalescent-phase sera

 immunohistochemical method for identification of

typhus group-specific antigens.

 Clinical laboratory studies may reveal

◦ anemia and leukopenia early in the course,
◦ leukocytosis late in the course,
◦ thrombocytopenia, hyponatremia, hypoalbuminemia,
mildly increased serum hepatic aminotransferases,
and prerenal azotemia.
Treatment

 doxycycline (100 mg bid orally for 7–15 days) on

the basis of clinical suspicion.

 Ciprofloxacin provides an alternative if doxycycline

is contraindicated.
Epidemic typhus
 Is tranmitted by the human body louse (Pediculus
humanus corporis).

 Lice acquire R. prowazekii when they ingest blood from

a rickettsemic patient.

 The rickettsiae multiply in the midgut epithelial cells of

the louse and are shed in the louse feces.

 during its blood meal it deposit the feces ; the patient

auto-inoculates the organisms by scratching.
Con’t…
 The louse is killed by the rickettsiae and does not
pass R. prowazekii to its offspring.

 wars and disasters poor hygienic conditions and

usually in impoverished cold areas.

 Brill-Zinsser disease is a recrudescent illness

occurring years after acute epidemic typhus,
probably as a result of waning immunity.
Clinical features
 incubation period of 1–2 weeks

 the onset of illness is abrupt, with prostration,

severe headache, and fever rising rapidly to 38.8°–
40.0°C (102°–104°F).

 Cough is prominent, occurring in 70% of patients.

 Myalgias are usually severe.

Cont…
 A rash begins on the upper trunk, usually on the
fifth day, and then becomes generalized, except
the face, palms, and soles.

 Initially, this rash is macular then it becomes

maculopapular, petechial, and confluent.

 The rash often is not detected in black skin; 60% of

African patients have spotless epidemic typhus.
Con’t…
 Photophobia, with considerable conjunctival
injection and eye pain, is common.

 The tongue may be dry, brown, and furred.

 Confusion and coma are common.

 Skin necrosis and gangrene of the digits as well as

interstitial pneumonia may occur in severe cases.
Con’t…
 Patients with untreated infections develop renal
insufficiency and multiorgan , neurologic
manifestations .

 Overall, 12% of patients with epidemic typhus have

neurologic involvement.
Diagnosis
 Serologic or immunohistochemical diagnosis of a
single case or by detection of R. prowazekii in a
louse found on a patient.

 Cross-adsorption indirect fluorescent antibody

(IFA) studies can distinguish R. prowazekii and R.
typhi infections.
Treatment
 Doxycycline (100 mg/d, bid) is administered orally or
—if the patient is comatose or vomiting—
intravenously.

 Although under epidemic conditions a single 200-

mg dose has proved effective, treatment is generally
continued until 2–3 days after defervescence.

 Pregnant patients should be treated with either

chloramphenicol early in pregnancy or, if necessary,
doxycycline late in pregnancy.
Prevention

 Prevention involves control of body lice.

 Clothes should be changed regularly, and

insecticides should be used every 6 weeks to
control the louse population.
Relapsing Fever

Outline
 Epidemiology, Clinical feature, diagnosis and
treatment of
◦ Relapsing fever
Relapsing fever

 is an illness characterized by recurring episodes

of fever and nonspecific symptoms

 is transmitted by the bite of an Ornithodoros

tick , after the bite of a tick or the human body
louse (Pediculus humanus).

 LBRF is also known as epidemic relapsing fever

Etiology and pathogenesis
 Borreliae are helical or wavy motile spirochetes
whose length ranges from 3 to 25 m and whose
width is usually 0.2–0.3 m.

 Borreliae are transmitted to humans by

◦ exposure to the bite of an infected Ornithodoros
tick (TBRF) or
◦ to the hemolymph of an infected human body
louse (LBRF) or feces of louse.
Con’t….

 LBRF is caused by Borrelia recurrentis,

 whereas TBRF is caused by a variety of

Borrelia species.
◦ For example, B. hermsii is
transmitted by the tick O. hermsi,
and B. turicatae is transmitted by O.
turicata
Epidemiology
 Caves ,houses, cabins, and cowsheds have been
implicated as sources of infection

 because of tick-infested rodent nesting where humans

come into contact with diurnal rodents and their ticks.

 eastern sub-Saharan Africa, B. duttonii is more prevalent

 TBRF has been detected (albeit less commonly) in

northern Africa where B. hispanica and B. crocidurae
have been identified.
Con’t…
 LBRF is relatively well described in East Africa.

 Outbreaks have been reported in Sudan and

Ethiopia.

 Reports of disease in the highlands of Ethiopia have

included many documented cases, despite a recent
decline, more cases have occurred in male than in
female patients..
Clinical feature

 The mean incubation period is 7 days for TBRF

(range, 4–18 days or longer) and 8 days for LBRF
(range, 5–15 days; sometimes a shorter period in
North Africa).

 Alteration of sensorium, abdominal pain, and

vomiting are common.

 Diarrhea may develop in 25% of cases.

Cont’d

 Jaundice; CNS involvement; petechiae on the

trunk, extremities, and mucous membranes;
epistaxis; and blood-tinged sputum are more
likely in LBRF
Cont….
 Uncommon manifestations
◦ include iritis,
◦ acute respiratory distress syndrome,
◦ uveitis, iridocyclitis,
◦ myocarditis, and splenic rupture.

 Neurologic findings may include

◦ signs of meningitis with or without CSF
abnormalities,
◦ seizure,
◦ focal deficits, hemiplegia, paraplegia, paresthesias,
psychosis, hallucinations, and delirium.
Con’t…
 Certainspecies of tick-borne Borrelia
◦have been reported with particular frequency in cases
with neurologic complications (B. duttonii and B.
turicatae).

 Headache, dry cough ,eye pain, dizziness, arthralgia

,nausae, vomiting ,abdominal pain ,diarrhea, rash
dysuria, hepatosplenomegally ,conjunctival injection.

A history of travel, place of residence, and animal

exposures is useful when patients have these fever
patterns.
Con’t….

 The average duration fever of in the first episode of

TBRF is 3 days (range, 12 h to 17 days).

 In contrast, the average duration of fever in the

first episode of LBRF is 5.5 days (range, 4–10 days).

 Subsequent relapsing febrile episodes are typically

of shorter duration.
 average time between the first episode and the first
relapse is 7 days for TBRF and 9 days for LBRF.

 During afebrile intervals, the patient may have

symptoms (e.g., malaise) or may feel well
Diagnosis
 Laboratory confirmation is made by the detection
of spirochetes from blood during a febrile episode.

 During asymptomatic interval it not detected in the

blood by microscopy

 Spirochetes also may be visualized by direct or

indirect immunofluorescent staining and
fluorescence microscopy.
Con’t…

 A dark-field microscope may be used to observe

spirochetes in the blood.

 Polymerase chain reaction (PCR) and monoclonal

antibody can be used to determine the species of
Borrelia.
Con’t…

 Serologic confirmation of TBRF is demonstrated by

a fourfold rise in antibody titer

 The most reliable method—the recombinant GlpQ

assay
Treatment
 Single-dose therapy is generally recommended for
LBRF, while a 7- 10-day course is usually used for
TBRF.
Cont…

 Children <8 years of age and pregnant women with

relapsing fever should be treated with penicillin or
erythromycin.

 Monitoring of patients for JHR reaction for the first

12 h after the first dose of antibiotic is
recommended
Complication
 Moderate to severe thrombocytopenia is a typical
finding in acute TBRF.

 Bleeding complications, such as

◦ epistaxis, purpura, hemoptysis, hematemesis, bloody
diarrhea, hematuria, subarachnoid and cerebral
hemorrhages, splenic rupture, and retinal hemorrhage, are
more common with LBRF.

 spontaneous abortion, premature birth, or neonatal

death.
Cont…
 The Jarisch-Herxheimer reaction is an acute
exacerbation of symptoms that may occur on initial
treatment of relapsing fever with an effective antibiotic.

 During this reaction, spirochetes disappear rapidly from

the circulation and there is massive cytokine release.

 Is unpredictable

 the reaction is common in LBRF treated with

tetracycline.
Con’t…

 Symptoms of the JHR often include

◦ hypotension, tachycardia, chills, rigors, diaphoresis, and
marked elevation of body temperature.

 The reaction typically begins within 1–4 h of the

first dose of antibiotic.

 should be transferred to an intensive care unit for

close monitoring of fluid balance, arterial and
central venous pressure, and myocardial function.
Prognosis

 Death is more likely if relapsing fever is acquired

from a louse rather than a tick.

 Nutritional status may play a significant role in

outcome.

 Two Borrelia species associated with a relatively

high fatality rate from relapsing fever are B.
recurrentis (louse-borne) and B. duttonii (tick-
borne).
Prevention
 Prevention of TBRF includes
◦ the avoidance of rodent- and tick-infested dwellings as
well as infested natural sites, such as animal burrows or
caves.

◦ Wearing clothing that protects the skin and applying insect

repellents such , can prevent transmission of disease by
hard ticks and possibly by soft ticks in some settings (e.g.,
in caves or—as a partial measure of protection—during
sleep).
Cont…

 promoting personal hygiene (e.g., bathing) and

systematic delousing (e.g., application of
permethrin to clothing). Laundering or disposal of
infested clothing and bedding is another important
measure.

 Control of epidemics may involve widespread

antibiotic use.
Thank U For Your Attention!!!!
 HIV/AIDS and
Principles of ART
Common
Opportunistic
Infections

By Abaynesh A.(MD)
 AIDS was first recognized in the United
States in the summer of 1981
 Human immunodeficiency virus (HIV) was

isolated from a patient with

lymphadenopathy in 1983
 In 1984 it was demonstrated clearly to be

the causative agent of AIDS

 Common in developing countries
Etiology
 HIV is the etiologic agent of AIDS
 It belongs to the family of human retroviruses
(Retroviridae) and the subfamily of lentiviruses
 The four retroviruses known to cause human
disease belong to two distinct groups:
-Human T lymphotropic viruses
- HTLV-I
- HTLV-II
- Human immunodeficiency viruses
- HIV-1
- HIV-2
Anatomy of the HIV Virus

 Gp120 Envelope Protein

 Gp41 Envelope Protein
 P17 matrix protein
 P24 Capsule Protein
 Reverse Transcriptase
 The Lipid Membrane
Effect on immune system
 CD4 cell depletion and dysfunction
 Lymphoid tissue destruction
 CD8 cell dysfunction
 B cell abnormality
 Thymus dysfunction
 Auto immune dysfunction
 Gradual reduction in number of circulating
CD4 cells inversely correlated with the viral
load

 Any depletion in numbers of CD4 cells

renders the body susceptible to
opportunistic infections

 Lymphatic tissue (spleen, lymph nodes,

tonsils/adenoids) main reservoir of HIV
WHO Clinical staging
 Stage I
- Asymptomatic
- Persistent generalized lymphadenopathy
 Stage II
- Moderate unexplained weight loss( <10% of presumed or
measured
body weight)
- Recurrent URTIs
- Herpes Zoster
- Angular chelitis
- Recurrent oral ulceration
- Papular pruritic eruption
- Fungal nail infection
- Seborrhoeic dermatitis
Stage III

 Unexplained severe weight loss(>10% of presumed or

measured body weight
 Unexplained chronic diarrhea(>1 month)
 Unexplained persistent fever(> 1 month)
 Persistent oral candidiasis
 Oral hairy leukoplakia
 Pulmonary TB
 Severe bacterial infections (such as pneumonia,empyema,
pyomyositis,bone or joint infection, meningitis, bacteraemia)
 Unexplained Anaemia (Hgb <8 g/dl), Neutropaenia (<0.5 x
109/l) and/or Chronic Thrombocytopaenia (<50 x 109/l)
 Acute necrotizing ulcerative stomatitis, gingivitis or
periodontitis
Stage IV
 HIV wasting syndrome
 Pneumocystis (jirovecii) pneumonia
 Recurrent severe bacterial pneumonia
 Chronic herpes simplex infection
 Esophageal candidiasis
 Extrapulmonary TB
 Kaposi sarcoma
Stage IV

 CMV infection
 Central nervous system Toxoplasmosis
 HIV Encephalopathy
 Extrapulmonary cryptococcosis
 Disseminated non tuberculous mycobacterial

infection
 Progressive multifocal leukoencephalopathy
 Chronic cryptosporidiosis
 Chronic Isosporiasisz
Stage IV

 Disseminated Mycosis
 Recurrent septicemia
 Lymphoma (cerebral or B-cell non-Hodgkin)
 Symptomatic HIV-associated nephropathy

or cardiomyopathy
 Recurrent septicemia (including

nontyphoidal Salmonella )
 Invasive cervical carcinoma
 Atypical disseminated leishmaniasis
Opportunistic Infections
Respiratory System
 URTIs (Upper Respiratory Tract Infections)
- Pharyngitis
- Sinusitis
- Otitis media
 LRTIs (Lower Respiratory Tract Infections)
- Pneumonia
- Tuberculosis
- Pneumocystis pneumonia
 Others
- Kaposi Sarcoma
- Lymphoma
- LIP
CD4 Correlates with respiratory
diseases

CD4 count/mm Respiratory diseases

Any CD4 count URI
Bacterial Pneumonia
TB
Lymphoma
Non specific interstitial pneumonia
CD4 count <200 PCP
TB often disseminated
Cryptococcus pneumonia
Bacterial pneumonia often with bacteremia or
sepsis

22
1
CD4 count/mm Respiratory diseases

CD4 count < 100 Bacterial pneumonia (* Pseudomonas

aeruginosa)
Toxoplasmosis
Kaposi Sarcoma
CD4 count < 50 MAC
CMV
Fungal infections

22
2
 Tuberculosis
 Is caused by Mycobacterium tuberculosis
complex (M. tuberculosis, M. bovis, M.
africanium)
 TB disease can occur at any stage of HIV
disease (at any level of Immunity)
 At early stage it presents with typical
presentation
 At late stage the presentation is more
atypical and extra pulmonary
(disseminated)
 A case of TB in an a positive person is
staged in Stage 3 or 4
 TB/HIV Link
Effect of HIV on TB Effect of TB on HIV
 HIV increases:  TB increases HIV
- Susceptibility to be infected with
Tuberculosis
replication and leading
- The risk of progression to TB disease &
to increased viral load
- The incidence and prevalence of TB
 This results in more
 The life time risk of HIV positive individuals rapid progression of
who develop TB is 20-37 times greater HIV disease
than HIV negative individuals.
 HIV is the strongest risk factor for

progression from latent to active TB

Reactivation)
Diagnosis of TB in HIV infected
people
 Diagnosis of TB is challenging in HIV positive individuals

 Standard TB diagnostic approaches and clinical

algorithms should be followed to guide the diagnosis of
TB in PLHIV

 Clinical assessment:
- Thorough clinical evaluation of the patient:
- Current cough
- Fever
- Weight loss and
- Night Sweats
XPert MTB/RIF Test (GeneXpert Test):
 Detects MTB complex DNA in

- Sputum
- Pleural fluid,
- Lymph node aspirate or tissue,
- CSF,
- Gastric fluid and
- Tissue other than lymph node
 The assay detects MTB and Rifampicin resistance
 It is recommended as an initial diagnostic test for all

presumptive TB cases (individuals with TB symptoms)

among HIV infected people.
AFB microscopy:
 It is indicated for HIV infected presumptive TB cases when access to

XPERT MTB/RIF test is limited.

 The recommendation for AFB microscopy is 2 spot tests with in 1 hour

Chest radiography:
 It plays a significant role in shortening delays in diagnosis of TB in

PLHIV
 It can also be an important entry point to diagnose non-tubercular

chest diseases, which are common among HIV positives

Sputum culture:
 Sputum culture is the gold standard for the diagnosis of tuberculosis

in general.
 In patients with XPert negative results, sputum culture may be

indicated as part of the diagnostic procedure for people living with HIV
if clinical suspicion persists
Extra pulmonary TB diagnostic
approaches in HIV positive patients.
Lymph Node TB
 2Cm or more in size,
 Asymmetrical/localized
 Painless swelling
 Firm/fluctuated
 Cervical location
 Patient with weight loss, night sweats, fever
 Diagnosis -LN Aspirate for AFB has 85%

yield, if not possible to do FNAC of LN, start

anti-TB
Pleural effusion
 Unilateral effusion
 Aspirate of fluid is clear and straw colored

and clots on standing in a tube without

anticoagulants or
 Pleural fluid analysis shows protein >30g/L

& >50% lymphocytes

 Patients with weight loss, night sweats,

fever, or evidence of TB elsewhere

 Start anti-TB as soon as possible
Tuberculosis Meningitis
 Patients with weight loss, night sweats, fever
 Cerebrospinal fluid clear with high protein, low glucose

and lymphocytes
 Cryptococcal antigen (or Indian Ink and fungal culture)

negative in CSF
 Evidence of TB elsewhere
 Admit patient, start anti-TB with steroids as soon as

possible.
 Start treatment for cryptococcal meningitis based on

clinical or lab evidences.

 Note: GeneXpert test has to be conducted on CSF

specimen as an initial diagnostic test as much as possible

Pericardial Effusion
 Hemodynamically significant pericardial effusion
 Often with pleural effusions
 Lung fields clear and intrathoracic lymphadenopathy
 Usually patients with weight loss, night sweats, fever
 90% of Pericardial Effusions in HIV positive patients

in high-TB burden areas is due to TB

 CXR, Echocardiogram or chest ultrasound
 Pericardiocentesis, and pericardial biopsy
 Routine TB Workup
 Start anti-TB as soon as possible
Disseminated TB
 Patients with weight loss, night sweats,

fever and cough

 Abnormal CXR (which can include military

pattern)
 Large spleen/liver
 Anemia
 Start anti-TB treatment (add antibiotics if

critically ill)
TB of the Spine
 Pain over localized area
 Children/adolescents –often thoracic

vertebrae
 Adults frequently lumbar vertebrae
 Spinal imaging (e.g. X-Ray, MRI)
 FNA of vertebral lesions and /or paraspinous

abscesses when feasible

 When to start the ART after
the TB treatment

 Antituberculosis treatment should be

initiated first, followed by ART as soon as
possible within the first 8 weeks of treatment
 The HIV-positive TB patients with profound
immune-suppression (such as CD4 counts
less than 50 cells/mm3) should receive ART
immediately within the first two weeks of
initiating TB treatment
Bacterial Pneumonia
 It can occur in immune-competent individuals, but
incidence of bacteremia accompanying pneumonia
is increased
 Bacterial pneumonia occurs during the whole

spectrum of HIV disease, but tends to be more

severe and recurrent as the CD4 counts drops
significantly.
 In addition pneumonia can concomitantly present

with sinusitis and/or bacteremia.

 If not treated promptly, extra pulmonary

complications like empyema, meningitis,

pericarditis, hepatitis and arthritis can follow.
Bacterial Pneumonia
 Common etiological agents:
- Streptococcus pneumoniae
- H. Influenzae
 Clinical presentation
 Symptoms and signs
- Abrupt onset with fever and chills
- Cough with Purulent sputum
- Dyspnea, Tachypnea and Pleuritic chest pain
- Abnormal physical signs of systemic infection and
consolidation
 Chest X-ray: confirming the diagnosis of pneumonia.
Treatment
For none severe pneumonia :
 Amoxicillin 1000mg TID for seven days or
 Erythromycin 500 mg QID or
 Doxycycline 100 mg BID or
 Azithromycin 500 mg PO per day for three

days or
 Clarithromycin 500 mg twice daily for seven

days.
 Admission to manage as inpatient if the patient
has severe pneumonia:
- Tachypnea (RR>30)
- Cyanosis,
- Hypotension,
- Altered mental status,
- Multilobar involvement and
- Age>70 years
 Ceftriaxone 1-2 gm IV once a day plus
Erythromycin 500 mg oral or IV four time a day
Pneumocystis Pneumonia
 Pneumocystis pneumonia is caused by Pneumocystis
jiroveci formerly known as pneumocystis carini
pneumonia (PCP)
 It commonly occurs when patients have significant

immune suppression (CD4<200cells/mm3 or CD4

percentage < 14%).
Clinical manifestation :
 Typical clinical presentations are characterized by

insidious onset of:

- Low grade fever,
- Dry cough, and
- Dyspnea exacerbated by exertion
Physical examination:
- Fever
- Tachypnea
- Tachycardia and
- Scattered rales in the lungs
 But examination of the lungs can appear

normal in some patients

Diagnosis:
 Presumptive diagnosis of PCP is based on

clinical judgement
 Typical chest X-ray findings revealing a perihilar

interstitial infiltration with tendency to spread

outwards
 Note that the chest X-ray can be normal in 20%

of patients.
 Definitive diagnosis of PCP is based on

demonstration of the organism from an

induced sputum sample
Treatment
 Use Trimethoprim 15-25 mg/Kg, three or four times daily for 21
days
 Alternative regimens for mild to moderate cases of PCP

include:
1. Clindamycin 600 mg qid plus primaquine 15 mg bid
or
2. Clindamycin 600 mg qid plus dapsone 100 mg daily.

 Consider spontaneous pneumothorax in patients with sudden

deterioration in clinical condition.

 In severely ill patients with marked respiratory distress and

extensive chest Xray findings, prednisolone has to be given
simultaneously
Prednisolone
Adult Children

Day 1-5 80 mg po/day 1 mg/kg

Day 6-11 40mg po/day 0.5 mg/kg

Day 12-21 20mg po/day 0.25 mg/kg

Evolution after treatment

 Improve slowly
 Usually better after 1 week
 If no improvement then, suspect another

infection
 Always continue with secondary

prophylaxis, relapse up to 40% in 3 months

if no prophylaxis
 N.B patient can develop PCP while on

primary prophylaxis - breakthrough PCP

Management of Gastrointestinal Opportunistic Diseases

 The GI OI diseases commonly manifest with:

- Diarrhea
- Nausea and vomiting
- Dysphagia and odynophagia
 Most common organisms:

- Isospora belli
- Cryptosporidium
- Shigella and salmonella
- CMV etc.
 Dysphagia and
odynophagia
 Dysphagia (difficulty in swallowing) and odynophagia
(painful swallowing) are symptoms of esophagitis
 Most common causes :
- Candida
- HSV
- CMV, and
- Aphthous ulcers
 If thrush is associated with dysphagia, odynophagia,
and/or retrosternal pain, consider oesophageal candidiasis
 Thrush or oropharyngeal candida is characterized by
white, painless, plaque-like lesions on the buccal surface
and/or tongue
Diagnosis:
 Is frequently made on clinical grounds
 Upper GI endoscopy with or without biopsy or contrast imaging

Treatment:
 Dysphagia and/or odynophagia are treated as oesophageal candida on
clinical grounds
 Patients are empirically treated with Fluconazole in presumptive

oesophageal candida
 Drug of choice: Fluconazole 200 mg(3mg/k/day in children) PO daily for 14

days
 Alternatively, ketoconazole 200 mg(3-6mg/kg/day daily in children) twice

daily for 4 weeks.

 Risk of recurrence after completing treatment may be high

 If diagnosis suggests HSV eosophagitis use acyclovir 400mg po five times

per day for 14 to 21 days

ORAL HAIRY LEUKOPLAKIA (OHL)

 Non-removable
Caused by EBV  Vertical white/gray
replication in the patches/folds on
epithelium of the lingual lateral margins
(+/- dorsal or ventral
surface of the tongue
surface of tongue)
 Not painful
 No treatment
 Sign of immune
suppression

25
1
Oral Thrush
Candida albicans is  60% of patients per
an endogenous yeast year with CD4 < 100
 10-20% associated
with oesophageal
candidiasis
 White painless
plaques on the buccal
or pharyngeal mucosa
or tongue surface that
can easily be scraped
off

25
2
Clinical presentations:

 Thrush:
◦ pseudomembranous (classical) > 80%,
◦ atrophic,
◦ erythematous
 Angular cheilitis (perleche)
 Median rhomboid glossitis

25
3
Pseudomembranous
thrush

25
4
Atrophic thrush

25
5
Angular cheilitis

25
6
Treatment for Oral
Candidiasis
 Nystatin 500,000 IU q 6H
◦ Sucked and retained in the mouth for 20 minutes
◦ Until 48 hours after symptoms resolve

 Miconazole oral gel

 Clotrimazole oral lonzenges 10 mg 5x/d until
resolution

25
7
Aphthous Stomatitis
 Usually painful & self-limiting
 Minor: < 1 cm
 Major: > 1 cm, deep
 May prevent oral intake!
 Start with topical steroids (Triamcinolone oral
paste) or suspension with tetracyclines / nystatin,
hydrocortisone, lidocaine
 For refractory cases: systemic steroids:
prednisone 40 mg daily for 1 week
 Analgesics

25
8
Aphthous stomatitis

25
9
Diarrhea
 Diarrhea is defined as passing more than
three loose or watery stools/day
 It may be:

- Acute or chronic,
- Persistent or intermittent
 Delay in treatment can result in fluid loss

and hemodynamic instability

 Chronic diarrhea may also lead to

nutritional deficiencies and wasting

Causes :
Opportunistic or pathogenic organisms,
such as:- Viruses (including HIV),
- Bacteria,
- Protozoa,
- Fungi,
- Helminthic,
- Non-infectious causes and drugs
Laboratory evaluation:
 Stool microscopy including modified acid fast
stain
 Stool culture when indicated (optional)
Management:
 Correction of fluid loss (ORS or IV fluid
therapy)
 Patients with severe dehydration are
admitted for intravenous fluid administration.
Treatment of specific enteric
pathogens
Agent Cd4 Symptom Diagnosis Treatment
E.Hystolitica Any Bloody Stool Metronidazo
stool, colitis microscopy le
Giardia Any Watery Stool Metronidazo
diarrhea microscopy le
Cryptospori <150 Watery Modified ART
dium diarrhea AFB
Isospora beli <100 Watery Modified TMP-SMX
diarrhea AFB
Microsporidi <50 Watery Giemsa Albendazole
um diarrhea stain
CMV <50 Watery/bloo Tissue Ganciclovir
dy biopsy
diarrhea ,
colitis
 Patients with bloody diarrhea but repeatedly
negative stool results: empirical treatment
with ciprofloxacin or norfloxacin
Symptomatic treatment:
 In adults use anti-diarrheal agents
Loperamide 4mg stat then 2mg after each
bowel motion or Diphenoxylate 5mg QID
Visceral Leishmaniasis
 VL is a systemic parasitic illness, transmitted primarily by the
phlebotomine sand fly from animal or human reservoirs.
 In HIV patients, VL represents reactivation of latent infection with
Leishmania parasite
 Clinical features: - Unexplained fever,

- Splenomegaly and
- Pancytopenia (anaemia, leucopenia and
thrombocytopenia)
Diagnosis:-
 Parasitological diagnosis: Isolation of the organism from material
taken from reticuloendothelial tissue and examined with Giemsa,
Wright’s or Leishmanial stain.
 Immunological diagnosis • Antibody detection

• Leishmanial test is negative

Treatment:
 Ambisome40mg/kg, require longer treatment and more liable to relapse.
Peri-anal problems
 Acute or Chronic peri-anal problems include:
- Recurrent peri-anal abscesses,
- Chronic peri-anal fistula,
- Peri-anal herpes (severe, persistent and extensive), and
- Perianal warts

Treatment :
 Peri-anal abscess may extend depending on the immunological status
of the patient; therefore early treatment is mandatory to avoid this
and more serious morbidity.
 If patients require surgical incision, it should be done promptly on first
visit, or referral made if the surgery is unavailable.
 Otherwise, broad spectrum antibiotics such as amoxacillin-clavulanic
acid (augmentin) alternatively amoxacillin or ampicillin must be
administered in sufficient dose for at least 10 days
 Palliative care including Sithz baths and analgesics
Sexually transmitted infections and cervical cancer

 There is a synergy between HIV and sexually

transmitted infections (STIs) and they frequently coexist.
◦ Mostly they are asymptomatic
◦ Asymptomatic STIs can cause complications, be transmitted to
sexual partners and enhance HIV transmission
 Cervical cancer is a preventable disease and is curable if
diagnosed and treated early.
 Women living with HIV have a higher risk of pre-cancer
and invasive cervical cancer.
 The risk and persistence of HPV infection increases with
low CD4 count and high HIV viral load.
 All women with HIV should therefore be screened for
cervical cancer
Common HIV Associated Dermatologic
Problems
 Herpes zoster
 Mucocutaneus Herpes simplex
 Warts (Condyloma accumunata & Labial)
 Molluscum Contagiosum
 Impetigo
 Secondary syphilis
 Eosinophilic folliculaites
 Tinea
 Balanitis

26
8
 Cryptococus skin lession
 Bacilary angiomatosis
 Cutaneous lishmaniasis
 Scabis
 Seboric Dermatites
 Kaposi sarcoma
 Pappular pruritic eruption
 Fixed drug reactions
 Psoriasis

26
9
 Herpes Zoster
 Painful and vesicular with dermatomal
eruption with dermatomal distribution

 Etiology – reactivation of varicella zooster

virus

 When healed scar will remained

Treatment
 Analgesic: Potent analgesics including
carbamazepin and amitriptylin
 Acyclovir 800mg 5X per day for 7 days and

it should be started within 72hours

 When there is ocular involvement

(ophthalmic zoster) use parental and Local

Acyclovir with mydriatic agents

27
2
Herpes Simplex(HSV1)

 Painful and vesicular lesion around mouth or

genitalia

 Clinical Feature: Ulcerating, covers large

parts of genitals and surrounding skin
Herpes simplex
 Local antiseptics to
avoid superinfection
 Oral acyclovir
◦ 400 mg PO TID for 10
days

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4
Chronic Mucocutaneous
HSV

27
5
Chronic Mucocutaneous Herpes Simplex:
treatment

 Acyclovir 400 mg PO
TID minimum 10 days
but it can extend untill
resolution
 Consider higer dose 800
mg TID in advanced
immuno-suppresion
 Analgetics
 Suppressive therapy if
>6 recurrences/year
(acyclovir 200 mg 2x/d)
 Keep clean (hygiene
care)

276
Molluscum contagiosum

 Occurs when CD4 is

below 200
 First line treatment is
ART

Clinical Feture: Papule with typical

central umbilication (often with some
white cheesy material in the dimple)
27
7
Condyloma accuminata
 Caused by HPV
Clinical Presentation :
Grape like fungating lesions Transmitted by direct
contact, usually through
sexual intercourse,
sometimes by infected
hands
 Transmission is also possible
from mother to child during
childbirth
 Excessive growth occurs in
immuno-suppressed patients
 Check syphilis serology to
exclude Condylomata lata
 Women with genital warts
should have a Pap smear
27
8
Treatment of Condylomata
accuminata

 Podophyllin 10-25% solution.

 Protect the skin surrounding the
warts with petroleum jelly
 Apply podophyllin carefully to the
warts with the back of a matchstick
for 3 consecutive days per week.
Repeat weekly until cleared. Leave
on for 4 to 6 hours then wash off
with water and soap.
 Podophyllin is contra-indicated in
pregnancy!
 Examine partners and perform
syphilis serology
 Cryotherpay and surgical debulking

27
9
Impetigo
 Erythematous
small papule
limited to few
lesions coalescing
in to crusted
plaques
 Ethiology:
- Streptococus
pyogenus
- Stphylococus aurus
Treatment
:topical
antibiotis
,amoxacilline for
extensive disease

28
0
Secondary Syphilis
 Consider Secondary
Syphilis in HIV infected
petients with
dermatologic problem

 Skin
manifestation can
have any morphology

 Can involve palm and

face

28
1
Treatment of Secondary syphilis

Benzathin penicillin 2.4 MIU IM

weekly for 3 weeks
or
Erythromycin 500 mg po QID
for 4 weeks

28
2
Tinea
 Severe form is common in HIV infected
patient
 Aetiology: Dertmatophytes
 Starts at higher CD4 counts
 Clinical presentations

◦ Tinea cruris
◦ Tinea pedis
◦ Tinea corporis
 Diagnosis based on clinical findingns

28
3
Tinea Pedis
 Interdigital itching,
scaling, fissures
and maceration,
sometimes redness

28
4
Tinea Cruris

Red scaly patch on

inner thigh with
sharply demarcated
borders

28
5
Tinea corporis
Circular erythematous
scaling that spreads
with central clearing
(“ringworm”)

28
6
Diagnosis and Treatment
of Tinea
 Diagnosis based on clincial findings
 Clotrimazole 1% cream BID
 Ketoconazole 2% cream daily
 Miconazole cream 2% BID
 For refractory, chronic or extensive disease:

griseofulvin can be considered

28
7
Cryptococcal Skin Lesions
 Common in advanced
immunocompromised
patients, when CD4 is less
than 100
 Aetiology: Cryptococcus
neoformans
 Nodular, papular, follicular
 Always rule out CNS
involvement
◦ Sign of disseminated
cryptococcosis
 May resemble molluscum!
 Usually on face, neck, scalp

28
8
Cryptococcus Diagnosis and
treatment
Diagnosis : extraction of
the lesion and indian ink
Treatment
 If negative LP: fluconazole

400 mg/d PO for 8 weeks.

 Then 200mg/day for

continued secondary
prophylaxis
 If positive LP, see

neurology chapter for

managment

28
9
Scabies

 Small red papules, intensely pruritic, especially at

night
 Sometimes superficial tunnel (where female mite
lays eggs) between fingers, volar aspect of wrist,
axillae, thighs, buttocks, genitals, feet, breast, peri-
umbilical 29
0
Classical Scabies
Treatment

•Topical benzylbenzoate, 3 days on body (except

scalp)
•Chlorpheniramine
•Treatment of family
•Treatment of clothes and bed sheets 29
1
Norwegian Scabies
 Severe form, in
immunocompromis
ed host
 Thick, grey
keratoses and
crusts develop on
the hands, elbows,
knees and ankles
and to rest of body
 Scales and crusts
show thousand of
mites isolate!

29
2
Norwegian Scabies
 Use ivermectin (200
μg/kg) if available (3-12
mg). If not available,
prolonged topical
treatment
 Keratolytics need to be
applied to remove the
thick crusts: salicylic
acid 5-10%
 Consider antibiotics for
superimposed infections

29
3
Papular Pruritic Eruption (PPE)
 Common in HIV infected
patients
 Occurs at early stage of
disease progression
 Ethiology: Unknown
 Hyperpigmented papules
and nodules with severe
itching.
 Most frequently on
extensor side of arms and
legs
 Often ulcerations and
scars because of
scratching
29
4
PPE Diagnosis and
Treatment
 Diagnosis: Clinical
 Treatment
◦ Potent topical
steroids
◦ Calamine lotion
◦ ART
◦ Antihistamines

29
5
Management of Opportunistic
Diseases of the Nervous System
Neurological complications in HIV patients
may be due to: -
 HIV(HIV encephalopathy)
 OIs (Toxoplasmosis, cryptococcal

meningitis)
 Neurosyphilis
 Malignancies (primary CNS lymphoma)and
 Drugs (e.g. EFV, etc)
Toxoplasma gondii
Encephalitis
 It is caused by the protozoan Toxoplasma
gondii.
 Disease appears to occur almost exclusively
because of reactivation of latent tissue cysts.
 Primary infection occasionally is associated
with acute cerebral or disseminated disease.
 Sero-prevalence varies substantially in
different communities; in Ethiopia, general
prevalence is about 80%.
Clinical Manifestations
 The most common clinical presentation of T.
gondii infection is
- Focal encephalitis with
- Headache
- Confusion, or motor weakness and
- Fever
 If untreated results in seizures, stupor, and

coma
Diagnosis
 HIV-infected patients with TE are almost uniformly seropositive
for anti-toxoplasma immunoglobulin G (IgG) antibodies

 The absence of IgG antibody makes a diagnosis of toxoplasmosis

unlikely but not impossible

 Anti-toxoplasma immunoglobulin M (IgM) antibodies usually are

absent

 Definitive diagnosis of CNS toxoplasmosis requires:

- A compatible clinical syndrome
- Identification of one or more mass lesions by CT, MRI, or
other radiographic testing; and
- Detection of the organism in a clinical sample
 In the absence of imaging support, empirical
treatment is justified when patients present
with focal neurological findings and the CD4
count is < 200 cells μL.
 With empirical treatment for toxoplasmosis,
nearly 90% of patients will demonstrate
clinical improvement within days of starting
therapy
 Radiological evidence of improvement is
usual after 14 days of treatment.
Treatment
 1st line regimen in the Ethiopian context is:
Trimethoprim/sulfamethoxazole 80/400,
oral, 4 tablets 12 hourly for 28 days,
followed by 2 tablets 12 hourly for 3 months
in adults
 Secondary prophylaxis: use co-trimoxazole

960mg daily
 Alternative regimen
I. Sulfadiazine, 1-2 gm p.o.q 6h for six weeks or 3
weeks after resolution of lesion, PLUS
 Pyrimethamine Loading dose of 200 mg once,

followed by: Pyrimethamine 50-75 mg/day :

PLUS
 Folinic acid (Leucovorin): 10-20 mg/d OR
II. Pyrimethamine and Folinic Acid (Leucovorin):
PLUS
 Clindamycin: 600 mg q 6 hrs
 Adjunctive corticosteroids for patients with:
- Radiographic evidence of midline shift
- Signs of critically elevated intracranial pressure
or
- Clinical deterioration within the first 48 hours of
therapy
 Dexamethasone (4 mg every six hours) and is

generally tapered over several days and

discontinued as soon as possible
 Anticonvulsants should be administered to patients

with a history of seizures

Cryptococcal infection

 Most HIV-associated cryptococcal infections are

caused by Cryptococcus neoformans
 Cryptococcosis commonly presents as a

subacute meningitis or meningoencephalitis

with fever, malaise, and headache.
 Classic meningeal symptoms and signs, such as

neck stiffness and photophobia, occur in only

one-quarter to one-third of patients
 Some patients experience encephalopathic

symptoms, such as lethargy, altered mentation,

personality changes, and memory loss
Diagnosis
 LP and CSF analysis: -
- Opening pressure may be markedly elevated.
- CSF analysis - Protein= 30-150 mg/dl
- WBC =0-100 /mm3 (monocyte)
- Culture =positive 95-100%
- Indian ink =positive 60-80%
- Cryptococcal Ag > 95 % sensitive
and
specific
 If it is not possible or contraindicated to do LP, serum

cryptococcal antigen can be used for diagnosis

Management
 Requires hospitalization and evaluation by physician Phases of
management:
1. Induction phase (2 weeks)
- Option A. High dose fluconazole- Fluconazole 600 mg
twice daily alone
- Option B. Amphotericin B + fluconazole: Amphotericin 0.7-1
mg/kg/day + fluconazole 800 mg/day
2. Consolidation phase (8 weeks)
- Option A. Fluconazole 800 mg/day
- Option B. Fluconazole 400-800 mg/day
3. Maintenance treatment (or secondary prophylaxis) -
Fluconazole
200 mg daily
Additional Points about
Cryptococcal Meningitis
1. Management of elevated Intracranial
pressure (ICP):
2. Discontinuation of maintenance treatment

(secondary prophylaxis)
3. Timing of ART initiation
Management of elevated
intracranial pressure (ICP):
 Daily serial LP should be done to control
increased ICP by drawing 20-30 ml of CSF
based on patient’s clinical response

 Signs of ICP include headache, altered mental

status, meningismus and changing in hearing
or vision should be closely monitored

 There is no role for acetazolamide, mannitol, or

corticosteroids to reduce intracranial pressure.
Discontinuation of maintenance
treatment
 When patients are stable and adherent to
ART and anti-fungal maintenance treatment
for at least one year and

 Have a CD4 cell count of greater than or

equal to 200 cells/mm3 (two measurements
six months apart)
Timing of ART initiation
 Immediate ART initiation is not recommended in
HIV-infected patients with cryptococcal meningitis
due to the high risk of IRIS, which may be life-
threatening.
 ART initiation should be deferred until there is
evidence of a sustained clinical response to anti-
fungal therapy
 After 2-4 weeks of induction and consolidation
treatment with amphotericin B-containing regimens
combined with fluconazole, or
 After 4-6 weeks of induction and consolidation
treatment with high-dose oral fluconazole regimen
Poor prognostic signs

 Extra CNS manifestation(especially

pulmonary)
 Altered mental status
 Low CSF WBC count less than 20cells/µl
 High CSF cryptococcal antigen titer
Peripheral Neuropathies
 Peripheral neuropathies are among the most common
causes of painful legs in HIV infection
 Causes : - Complication of HIV infection itself

- Drug therapy
- Metabolic or Organ dysfunction
- Nutritional deficiencies.
 Distal symmetrical sensory polyneuropathy is the most

common
 The neuropathies associated with HIV can be classified as:

- Primary, HIV-associated
- Secondary causes related to medications(ddI,d4T,INH),
OIs or organ dysfunctions
Diagnosis
 Clinical picture presenting with pain, tingling
sensations, paresthesia or numbness
 Physical examination can reveal:
- Depressed or absent ankle reflex
- Decreased sensitivity to different modalities of
sensation
- Difficulty in walking
 The feet and sometimes the hands are involved in
symmetrical distribution
 Electro diagnostic studies: including
electromyography (EMG) and nerve conduction
studies (NCS)
Treatment
 Avoid the offending agent if identified
 Substitute or switch drugs such as d4T/DDI when the

neuropathy is severe
 Remove other drugs associated with peripheral neuropathy

 Supplement vitamin intake for all patients including

concomitant administration of pyridoxine with INH

 Adjuvants for pain management (such as Amitriptyline,

carbamazepine) indicated for patients with pain and

paresthesias.
Monitoring of events
 Recognize presence of peripheral neuropathy
 Asses severity at each clinical visit
 Avoid drugs causing neuropathy
Primary CNS lymphoma

 Alterations in consciousness or cognition,

hemiparesis or aphasia (40%), seizures
(15%) or cranial neuropathies (5 -10%)
 Difficult to distinguish from cerebral

toxoplasmosis even with CT scan

 Empiric treatment for cerebral

toxoplasmosis
 If no improvement REFER for brain radiation
 The role of adjuvant chemotherapy is

undefined

31
5
CT Scan- Primary CNS Lymphoma

31
6
Metastatic Lymphoma
 Less common
 Clinical presentation:
 Systemic lymphoma (usually Non-Hodgkin's) may
lead to neurological dysfunction in AIDS patient
(meningeal or skull base involvement)
 Cranial neuropathy and headache are common

 Diagnosis: CSF cytology > malignant cells

31
7
Anti Retroviral
Therapy(ART)
 Classes of ARVDs:
- Reverse transcriptase inhibitors
- Nucleotide ~ (NRTIs)
- Non-nucleotide~ (NNRTIs)
- Protease inhibitors
- Entry Inhibitor
Fusion Inhibitor
Chemokine Receptor Antagonist
Attachment Inhibitor
- Integrase Inhibitor
Reverse Transcriptase Inhibitors
(NRTI)
 NRTIs
- Block the RT enzyme (RNA dependent DNA
polymerase) by mimicking the bases that make
up DNA
 Non-Nucleoside Reverse Transcriptase Inhibitors :

- They stop HIV replication by binding directly

onto reverse transcriptase
- Bind at a different location (allergenic site) than
the active site
 Nucleoside Reverse Transcriptase Inhibitor (NRTI)
- Zidovudine(AZT,ZDV)
- Stavudine (d4T)
- Didanosine (ddI)
- Lamivudine (3TC)
- Emtricitabine (FTC)
- Abacavir (ABC)
- Zalcitabine (ddC)
 Nucleotide analogues
- Tenofovir (TDF)
 Non-Nucleoside Reverse Transcriptase
Inhibitor (NNRT)
- Nevirapine (NVP)
- Efavirenz (EFV)
- ETRAVIRINE (ETR)
Protease Inhibitors (PIs)
 Block the function of the protease enzyme
 Prevent proper cleavage of viral proteins
 Prevent maturation of newly produced virus
 Protease Inhibitors
- Saquinavir (SQV)
- Ritonavir (RTV)
- Indinavir (IDV)
- Nelfinavir (NFV)
- Amprenavir (APV)
- Lopinavir (LPV)
- Atazanavir (ATV)
 Fusion Inhibitors
- Enfuvirtide (T-20)
 Integrase Inhibitors

- Raltegravir (RAL)
- Dolutegravir
 CCR5 Blockers

- Maraviroc (MVC)
ARVD selection for
combination
ARVDs with
 Similar mechanism of action
 Similar side effect

 Antagonistic effect

will not be chosen together

 We have 1st line regimen for treatment naïve patients,

and 2nd line drugs for those with treatment failure.

 Ethiopian Guidelines for adults and adolescents

First Line Regimen (2NRTIs + 1NNRTIs)

While in
Second Line Regimen (2/3NRTIs + 1PI)
Firs Line Regimen
Preferred 1st line regimen

◦TDF+3TC+DTG or TDF+3TC+EFV

Alternative 1st line regimens

◦TDF/3TC/NVP
◦ZDV+3TC+EFV
◦ZDV+3TC+NVP
◦ABC/3TC/EFV
Second Line Regimen
 Second line regimen is a combination
ARVDs given for patients who had prior 1st
line ART experience

 The first line regimen either has failed or

caused serious side effect

 Drugs used as second line rigimen are:

2NRTIs + 1 PI
Target population Preferred second-line regimen
Adults and If AZT was used in TDF + 3TC + LPV/r or
adolescents (≥10 first-line ART ATV/r
years)a If TDF was used in AZT + 3TC + LPV/r or
first-line ART ATV/r
If TDF+3TC+DTGb AZT + 3TC + ATV/r or
used in first-line LPV/r
HIV and TB co- If rifabutin is not Same NRTI backbones
infection available as recommended for
adults and adolescents
plus double-dose
LPV/r (that is, LPV/r
800 mg/200 mg twice
daily) or standard LPV
dose with an adjusted
dose of RTV (that is,
LPV/r 400 mg/400 mg
Treatment Failure
 Clinical failure
 Immunologic Failure
 Virologic Failure
Treatment Failure
Clinical failure Adults and adolescents New or recurrent clinical
event indicating severe immunodeficiency (WHO
clinical stage 4 condition and certain WHO clinical
stage 3 conditions (pulmonary TB and severe
bacterial infections) may also indicate treatment
failure) after 6 months of effective treatment

Immunologic Adults and adolescents

failure CD4 count at or below 250 cells/mm3 following
clinical failure or
Persistent CD4 levels below 100 cells/mm3.

Virologic failure Viral load above 1000 copies/ml based on two

consecutive viral load measurements in 3 months,
with enhanced adherence support following the first
viral load test.
THANK YOU!
Sexually Transmitted
Infections

Debre Markos University

Dr.Wallelign Demissie
 Sexually Transmitted
Infections
Objectives
 Understand what STIs are
 Overview of epidemiology of STIs
 Common sexually transmitted infections
 Approaches to STIs

33
3
 Are infections which are mainly transmitted by
unprotected sexual intercourse while they can also
be transmitted by blood transfusion mother-to-child
etc.
 STIs are serious and common problems worldwide.
There are more than 20 types.
 Many of these are curable with effective
treatment, but continue to be a major health
problem for an individual and the community at 33
4
 Although there is little information on the incidence and prevalence
of STIs in Ethiopia, the problem of STIs is generally believed to be
similar to that of other developing countries.
 According to 2011 EDHS,1percent of each Ethiopian women and
men reported having had an STI in the past 12 months before the
survey.
 3% of women and 2% of men reported having had an abnormal
genital discharge
 1% of each women and men had a genital sore or ulcer in the 12
months preceding the survey
 These figures might be underestimations 33
5
 Approaches to STIs

1. Etiologic Approach
2. Clinical Approach
3. Syndromic Approach

33
6
1. Etiologic Approach
Focuses on identifying the causative agents using
laboratory tests and giving treatment targeting to
the pathogen identified
 it avoids over treatment
 Satisfies patients who feel not properly attended
to
 can be used to screen asymptomatic patients

33
7
 Drawbacks of Etiologic
Approach
 Identifying the 30 or more STI causative agents
requires skilled personnel and sophisticated lab
equipment.
 Testing facilities usually not available at primary
health care level where a large number of patients
seek care for STI.
 Lab tests are expensive ,time consuming and ,results
may not be reliable
 Delay in treatment and reluctance of patients to wait33
8
 2. Clinical Approach
 Uses clinical experience to identify symptoms which
are typical for a specific STI, then giving treatment
targeted to the suspected pathogen.
 saves time for patients
 reduces lab expenses

33
9
Drawbacks of Clinical
Approach
 Requires high clinical skill
 Mixed infections overlooked
 Does not identify asymptomatic infections

34
0
 3. Etiologic Approach
 Identification of clinical syndrome and giving
treatment targeting all the locally known pathogens
which can cause the syndrome
 Complete STI care offered at first visit
 simple, rapid and inexpensive
 Patients treated for possible mixed infections
 Accessible to a broad range of health workers
 Curtails unnecessary referral to hospitals
34
1
 Urethral Discharge
Syndrome
 Is the presence of abnormal secretions from the distal part of the
urethra and it is the characteristic manifestation of urethritis.
 Is accompanied by burning sensation during micturition.
 Person with urethral discharge can also have increased frequency
and urgency of urination and itching sensation of urethra.
 There are two major causes of this syndrome:
Neisseria gonorrhea and chlamydia trachomatis
 Most of the time urethral discharge is caused due to mixed infection
by these two organisms.
 Some of the other causes of this syndrome are mycoplasma
genitalium,trichomonas vaginalis and ureaplasma urealyticum. 34
2
 The urethritis caused by N.gonorrhea has usually an
acute onset with profuse and purulent discharge.
 C.trachomatis has sub-acute onset with scanty
mucopurulent discharge.

34
3
 Management

-ceftriaxone 250mg IM stat/spectinomycin 2gm IM stat

+
Azithromycin 1gm po stat/doxycycline 100mg po BID for
7 days/tetracycline 500mg QID for 7
days/erythromycin 500mg po QID for 7 days in cases
of contraindications for tetracycline

34
4
Note
 Patients should be educated on
-Risk reduction
-Treatment compliance
-Proper and consistent use of condom
-Partner notification and management
-Importance of HIV testing
-Abstinence from sex till all symptoms resolve
34
5
Some patients may complain of persistent or recurrent burning
sensation on urination,with or without discharge due to
 Inadequate treatment or poor compliance
 Re-infection
 Persistent urethritis after doxycycline based treatment might be
caused by doxycycline-resistant M.genitalium
 T.vaginalis is also known to cause urethritis in men
 Infection by drug-resistant organisms

NB—address these factors in cases of recurrence and persistence

34
6
Treatment of Persistent/Recurrent
Urethritis Syndrome

1. Retreat with initial regimen

-If non-compliant or re-exposure occurs ,retreat with the
initial regimen with due emphasis on drug compliance
and/or partner management
2. Cover M.Genitalium and T.Vaginalis
-If compliant with the initial regimen and re-exposure can
be excluded ,the recommended drug in ethiopia is
Metronidazole 2gm po stat/tinidazole 1gm po once
for 3 days+azithromycin 1gm orally in a single dose 34
7
 Genital Ulcer Syndrome
 Genital ulcer is an open sore or a break in the
continuity of the skin or mucous membrane of the
genitalia as a result of sexually acquired infections.
 Commonly caused by viruses and bacteria.
 It facilitates transmission of HIV more than other
STIs because it disrupts continuity of skins and
mucous membranes significantly.

34
8
Etiology

 Herpes Simplex Viruses

 Treponema Pallidum
 Haemophilus Ducreyia
 Chlamydia Trachomatis
 Klebsiella Granulomatis

34
9
 Most cases of genital herpes are caused by HSV-2.
 According to a study conducted in 2001 HSV-2 alone
was the leading cause of GUS in both males and
females constituting 44% and 76% of the cases
respectively.
 Moreover dual infection with other genital ulcer
pathogens was found in 52% of males and 78% of
females.
35
0
 Common Clinical Manifestations

-Constitutional symptoms such as fever, headache, malaise and

myalgia
-Recurrent painful vesicles and irritations
-Shallow and non-indurated tender ulcers
-Common sites in males are glans penis,prepuce,and penile
shaft
-Common sites in females are vulva,perineum,vagina and cervix
-Painless indurated ulcer-chancre
-Regional LAP
35
1
Treatment

Non-vesicular
-Benzathine penicillin 2.4M units IM stat/doxycycline 100mg BID
for 14 days
+
Ciprofloxacin 500mg po BID for 3 days/erythromycin 500mg po
QID for 7 days
+
Acyclovir 400mg po TID for 10 days/200mg po five times a day for
10 days

35
2
Vesicular,multiple or recurrent genital ulcer
-Acyclovir 200mg five times a day for 10 days/400mg
po TID for7 days
Recurrent infection
-Acyclovir 400mg po TID for 7 days

35
3
Vaginal Discharge
Syndrome
 Physiologically women have vaginal discharge which is white
mucoid,odorless and non-irritant thin or thick based on
menstrual cycle.
 There is individual variation in the amount of normal vaginal
discharge.
 Abnormal vaginal discharge which is STI related is abnormal
in color ,odor and amount.
 In other words it is abnormal when a woman notices a
change in colour ,odor and amount accompanied by pruritus.

35
4
Etiology

-Neisseria gonorrhea
-Chlamydia trachomatis
-Trichomonas vaginalis
-Gardnerella vaginalis
-Candida albicans
Nb-bacterial vaginosis –gardnerella vaginalis-is the
leading cause of vaginal discharge in ethiopia followed
by candidiasis ,trichomoniasis,gonococcal and
chlamydia cervicitis in that order 35
5
Clinical Manifestations

The classical manifeststion is discharge from the vagina

which can be
-Thin homogenous whitish discharge with fishy odor
-Thick,profuse,malodorous,yellow-green,frothy,itchy
-Purulent exudate from the cervical os
-White,thick and curd-like discharge coating the walls of
the vagina
-Vulvo-vaginal pruritus,irritation of
vulva,dyspareunia,dysuria,and frequency of urination 35
6
The following are the common risk factors for
development of vds
- Multiple sexual partners in the last three months
- New sexual partner in the last three months
- Ever traded sex
- Age below 25 years
The presence of one or more risk factors suggest
cervicitis.
35
7
Treatment

Risk assesment positive

Ceftriaxone 250mg IM stat/spectinomycin 2gm IM stat
+
Azithromycin 1gm po stat/doxycycline 100mg po BID for 7 days
+
Metronidazole 500mg po BID for 7 days
If discharge is white or curd-like add clotrimazole vaginal pessary
200mg at bed time for 3 days.
note- the preferred regimen is Ceftriaxone 250mg IM stat
+
Azithromycin 1gm po stat
+
Metronidazole 500mg po BID for 7 days

35
8
Lower Abdominal Pain/PID
 Is a clinical syndrome resulting from ascending infection
from the cervix and/or vagina.
 It comprises a spectrum of inflammatory disorders of the
upper female genital tract including any combination of
endometritis , salpingitis, tubo-ovarian abscess and pelvic
peritonitis.
 The inflammation may also spread to the liver, spleen or
appendix.
 The vast majority of PID with or without pelvic abscess
improves with antibiotics alone and the fever usually
35
9
Etiology

 It is frequently polymicrobial
 The commonest pathogens associated with PID
which are transmitted sexually,are C.trachomatis
and N.gonorrhea.

36
0
 Clinical manifestations
361

 Lower Abdominal Pain  Fever,nausea,vomiting

 Abnormal Vaginal  Cervical Tenderness
Discharge  Adnexal Tenderness
 Inter-menstrual or Post-  Rebound Tenderness
coital Bleeding  Adnexal Mass
 Dysuria
 Backache
Treatment

For outpatient
Ceftriaxone 250mg IM stat/spectinomycin 2gm IM stat
+
Azithromycin 1gm po stat/doxycycline 100mg po BID for 14
days
+
Metronidazole 500mg po BID for 14 days
The preferred regimen comprises ceftriaxone,azithromycin
and metronidazole.
36
2
For inpatient
Ceftriaxone 250mg IM/IV/spectinomycin 2gm IM BID
+
Azithromycin 1gm po daily/doxycycline 100mg po BID
for 14 days
+
Metronidazole 500mg po BID for 14 days

36
3
 Indication for Inpatient Treatment

-Uncertain diagnosis
-Surgical emergencies such as appendicitis and ectopic
pregnancy can not be excluded
-Pelvic abscess is suspected
-Patient is pregnant
-The patient is unable to follow or tolerate an outpatient
regimen
-Patient has to respond to outpatient regimen
-PID in HIV patients
36
4
 Scrotal Swelling Syndrome
-N.gonorrhea
-C.Trachomatis
-T.pallidum

36
5
 Clinical Manifestations

-Pain and swelling of the scrotum

-Tender and hot scrotum on palpation
-Edema and erythema scrotum on palpation
-Dysuria
 It is important to exclude other causes of scrotal
swelling like testicular torsion,trauma,and incarcerated
inguinal hernia as they may require urgent referral for
proper surgical evaluation and management
36
6
 Treatment
Ceftriaxone 250mg IM stat/spectinomycin 2gm IM stat

+
Azithromycin 1gm po stat/doxycycline 100mg po BID for 7
days/tetracycline 500mg QID for 7 days/erythromycin 500mg
po QID for 7 days

36
7
 Inguinal Bubo Syndrome(Swollen Glands)

-Is defined as swelling of inguinal lymph nodes as a

result of stis.
-It should be remembered that infections on the lower
extremities or in the perineum could produce
swelling of the inguinal lymph nodes.

36
8
 Etiology
-Chlamydia Trachomatis(l1,l2,l3)
-Klebsiella Granulomatis(donovanosis)
-Treponema Pallidum
-Haemophilus Ducreyia

36
9
 Clinical manifestations

-Constitutional symptoms of fever,headache and pain

-Tender unilateral or bilateral lymphadenopathy forms
a classical –groove sign-in the inguinal area.
-Fluctuant abscess formation which coalesce to form
mass-bubo

37
0
 Treatment

Ciprofloxacin 500mg po BID for 3 days

+
Doxycycline 100mg BID for 14 days/erythromycin 500mg
po QID for 14 days
 If patient has genital ulcer,add acyclovir 400mg TID orally
for 10 days
Note –surgical incisions are contraindicated rather aspirate
pus with hypodermic needle through the healthy skin

37
1
 Neonatal Conjunctivitis
-It is also called ophthalmia neonatorum
-Is an ocular redness ,swelling and drainage which can be
sometimes purulent due to pathogenic agents or irritant
chemicals occurring in infants less than 4 weeks of age
-In cases of neonatal conjunctivitis due to pathogenic agents ,the
neonates get the infections from their infected mothers
-It can cause loss of sight if it is not managed properly and
promptly
-If it is caused by sterile chemical irritants ,can resolve by itself
within 48 hours without any intervention 37
2
Etiology
-N.gonorrhea
-C.trachomatis
-S.pneumonia
-H.influenza
-S.aureus

37
3
 Clinical manifestations
-Red and edematous conjunctivitis
-Edematous eyelids
-Discharge which may be purulent
-Orbital cellulitis

37
4
 Prevention
 The best way of managing neonatal conjunctivitis Is
preventing it from happening
 Wiping the baby’s both eyes with dry and clean cotton cloth
as soon as the baby is born
 Apply 1% tetracycline eye ointment into the eyes of the
newborn infant
 Properly open the eye of the infant and place the ointment on
the lower conjunctival sacs and avoid placing on the eyelids

37
5
 Treatment
Ceftriaxone 50mg/kg IM stat maximum dose of
125mg/spectinomycin 25mg/kg IM stat maximum dose
75mg

+
Erythromycin 50mg/kg orally in four divided doses for 14
days

Note –TTC is used as prophylaxis for neonatal conjunctivitis

but not for treatment

37
6
Leishmaniasis

37
7
Outline

 Leishmaniasis
 Life Cycle of Leishmania Parasite
 Visceral Leishmaniasis
 Cutaneous Leishmaniasis
 Investigations and treatment

37
8
 Leishmaniasis
 Leishmaniasis is a zoonotic disease caused by protozoa, which

belong to the genus Leishmania.

 Mode of transmission is by the bite of phlebotomites (sand flies)

from animals to humans.

 It has two major clinical forms: cutaneous and Visceral

leishmaniasis.

 Leishmania parasites are digenetic that need two hosts,the sandfly

and a mammalian host,to complete their lifecycle

 The transmission of leishmaniasis is either zoonotic,which includes

37
9
 Leishmania infections do not always equate with
clinical illness
 Most infections in immunocompetent individuals
remain asymptomatic

38
0
Life Cycle of Leishmania
Parasite
 The infected female sandflies inject matacyclic
promastigote to a susceptible mammalian host during a
blood meal
 Promastigotes in the skin are phagocytized by
macrophages and transform into amastigotes
 Amastigotes multiply in infected cells and depending
on the infecting leishmania species and/or the immune
status of the host,the parasite can get disseminated to
the viscera or remain at its site of inoculation
 This yields either the cutaneous or visceral form of
clinical manifestation
 When sandflies take blood meals from an infected
host ,they ingest macrophages infected with 38
1
 Visceral
Leishmaniasis(Kalazar)
 The two Leishmania species usually considered as responsible
for VL are L. donovani and L. infantum.
 The commonest species causing Visceral leishmanisasis in
Ethiopia is L. donovani.
 The epidemiology of visceral leishmaniasis in Ethiopia is
closely related to travel history to the North, North west and
south west parts of the country particularly areas closer to the
Ethio-Sudanese border.
 The disease is more prevalent in males and HIV infected
adults. 38
2
 VL should always be suspected when an individual
presents with prolonged fever from the endemic areas
 The diagnosis of VL relies on
clinical,serological,parasitological and molecular
findings
 The definitive diagnosis is demonstration of the
parasite in a tissue aspirate which is an invasive
procedure associated with risk of bleeding and severe
pain 38
3
 Clinical signs and symptoms associated with VL
include fever for more than two weeks, fatigue,
weakness, loss of appetite, malaise, epistaxis,
cachexia, abdominal pain, anemia, pancytopenia and
etc…
 Enlargement of lymph nodes,liver and spleen(as a
result of invasion of the reticuloendothelial system)

38
4
VL Case Definition

 A person who presents with fever for more than two

weeks and an enlarged spleen(splenomegaly) and/or
enlarged lymph nodes(lymphadenopathy),or either
loss of weight ,anemia,or leucopenia while living in a
known VL endemic area or having travelled to an
endemic area
 As the clinical presentation of VL lacks specificity a
definitive test is required to decide which patient
should be treated 38
5
Investigations

DX is established by the clinical presentation in

endemic areas and the demonstration of the
organisms in smears.
a. Complete blood count (CBC )
b. Parasite Detection-Visualization of the amastigote
form of the parasite by microscopic examination of
aspirates from lymph nodes, bone marrow or spleen
aspiration.
However, this technique remains restricted to referral
38
6
d. Antigen Detection Test-It is more specific than the
antibody-based immunodiagnostic test. Evaluation of
the performance of a urine latex agglutination (KATEX)
at the Indian subcontinent and East Africa has shown
that this test has a good specificity but only a low to
moderate sensitivity.
e. Molecular Techniques-Compared to the other
diagnostic techniques available, the molecular
approaches remain expensive and technically highly
38
7
Treatment
Non pharmacologic
- Supportive care including proper hydration and
nutritional therapy before and during the VL treatment

- Correct severe anemia with blood transfusion

- Closely monitor patient for cardiovascular toxicities of
VL treatment
Pharmacologic
A. Combination Therapy: Sodium Stibogluconate
(SSG) and Paromomycin
Sodium stibogluconate, 20mg/kg body weight/day IM
daily for 17d
+ 38
8
B. SSG monotherapy (In the absence of
paromomycin), Pentavalent antimonials can be used
in monotherapy.
SSG 20 mg/Kg/day is given IV (slow infusion over
5min) or IM in a single dose for 30 consecutive days.

38
9
C. Liposomal Amphotericin B 5mg/kg/day over a period of
6days
 NB-Liposomal Amphotericin B is recommended in those
patients with pregnancy, HIV-coinfection, severe illness,
severe anemia, severe malnutrition and extremes of
age (below 2 years or above 45 years).
 In special situations with severe risk factors for death at the
patient’s admission, antimonials toxicity has proved to be
very high and, therefore, LAmB is preferable if available for
these patients. 39
0
 Cutaneous Leishmaniasis
 Cutaneous Leshmaniasis in Ethiopia is caused by
Leishmania tropica or Leishmania aetiopica, which is
transmitted by phlebotomus.
 Before ulceration occurs, there appears dermal
infiltrates consisting of large histiocytes filled with
many leishmandonovan (L-D) bodies, while during
ulceration an influx of neutrophils occurs.
 Older lesions develop a tuberculoid infiltrate and at
this stage either the organisms are scant or absent. 39
1
Clinical features
 Cutaneous leishmaniasis (CL) is a disease of the skin and mucous membranes.
 There are different clinical forms of CL: localized CL, diffuse CL, and mucosal
leishmaniasis
 Cutaneous lesions - Occur mainly on exposed body parts (face, neck, arms, legs)
- May be single or multiple with regional lymph node enlargement
- Are usually painless
- If secondarily infected, they can be painful and itchy
1. Localized cutaneous leishmaniasis - Papule at the site of the bite (like an
insect bite)
 If papule persists, it develops into
 A small nodule - An ulcer with a fl at base and raised border

39
2
 Leishmaniasis recidivans is localized CL that is
characterised by a chronic solitary lesion that expands
slowly and often reoccurs.
 The lesion can continue for many years, causing severe
disfigurement
2.Diffuse cutaneous leishmaniasis
- Coalescence of papules and nodules to form plaques
- Chronic and very difficult to treat

39
3
Mucosal leishmaniasis
 Is the most severe form of CL, causing severe disfigurement and
mutilation of the face
 Nasal lesions cause discharge, bleeding, obstruction, deformity, and
destruction of cartilage with collapse of the nose
 Oropharyngeal lesions: difficulty chewing and swallowing, bleeding
gums, toothache, loose teeth, perforation of the hard palate
 -Involvement of mucosa can follow: o primary infection (with L.
major or L. donovani); or dissemination of cutaneous leishmaniasis;
or o treatment for visceral leishmaniasis (post-kala-azar dermal
leishmaniasis).

39
4
Investigations
 Demonstration of the parasite:
- microscopic identification of intracellular
amastigote in Giemsa-stained specimens from
lesions
- culture of extracellular promastigote on
specialized media

39
5
Treatment
Local treatment

- This needs to be adapted according to species, and the clinical

characteristics (site, size, number of lesions, whether open or nodular,
whether superinfected, and the immune status of patients).

- Local infiltration (1 to 5 intralesional injections, every few days or

weekly) with Sodium stibogluconate

Systemic treatment
 This is indicated for MCL and DCL
 First Line Paromomycin, 14–15mg (sulphate) /kg IM once daily for 20–
30 days.

39
6
Thank you!

39
7
Debre Markos University
School of Medicine
Helmenthiasis Lecture for 3rd Year Public
Health Officer Students
By: Dr. Zelalem T.(MD, GP)

39
8
Intestinal Nematodes (Round
worms)
 Associated with
◦ Poor fecal sanitation
◦ Contribute to malnutrition
◦ Decreases work capacity

39
9
Ascaris Lumbricoides(Round
worm)
 The largest intestinal nematodes ,can reach
up to 40cm in length

 Lives in the lumen of jejunum

 Each worm can produces up to 240,000 egg

per day
 Embryonated eggs –infectious form.

40
0
Cont’d….
 Maturation takes place in the soil
 Larva hatched in the intestine
 Invade the mucosae
 Migrate through the circulation to the lungs

=> alveoli => bronchus

 Swallowed => Intestine => Develop into

adult, then lives for 1 – 2 years

40
1
Transmission
 Fecal contaminated soil
 Poor sanitation
 Affects young children
 Transported by vegetables as means of

transmission outside endemic areas

40
2
Clinical Presentation
 Lung Phase
◦ Irritating cough – dry
◦ Burning substernal discomfort
◦ Fever (38.5oC)
◦ Eosinophilia
◦ Complication– Eosinophilic pneumonitis (Loffler’s
syndrome) => Round/oval pulmonary infiltrations.

40
3
Cont’d….
Intestinal Phase -> Heavy load due to worm
burden.

 Predispose to intestinal obstruction

◦ Perforation, intussusception or volvulus
◦ Biliary colick, cholecystits, cholangitis, pancreatits,
intrahepatic abscess

40
4
Diagnosis
 Demonstration of ova in stool

 Identification of adult worm

 CXR for complication

40
5
Ascaris lumbricoides egg in feces

40
6
Treatment
 The aim is to prevent complications
◦ Albendazole 400mg stat
◦ Mebendazole 500mg stat
◦ Pyrantel pamoate 11mg/kg stat maximum 1gm-
Safe in pregnancy.

40
7
Hook worm
 Etiology:
◦ A. duodenale
◦ N. americanus
 Ova changed to larva in soil.
 Larva penetrates the skin.
 Through bloods stream reach lungs.
 Swallowed => reaches the intestine and lives
for about a decade.

40
8
Clinical Presentation
 Pruritic maculo-papular dermatitis =>
ground itching
 Pneumonitis – milder degree.
 Epigastria pain – post prandial accentuation
 Diarrhea
 Iron def. anemia, hypoprotenemia
 Risk factors for diseases development:
◦ Worm burden
◦ Prolonged duration of infection
◦ Inadequate iron intake

40
9
Diagnosis
 Ova in the stool

 Hypochromic microcytic anemia

 Hypoalbuminemia

41
0
Treatment
 Albendazole 400mg as a single dose
 Mebendazale 100mg po BID for 3 days or

500mg stat
 Pyrantel pamoate x 3 days
 Iron supplementation
 Nutritional support

41
1
Strongyloidiasis
 Etiology: S. Stercoralis

 Replicates with in the human host =>

autoinfection

 In immuno-compromized host => become

invasive => Disseminate widely

 Can be fatal

41
2
Transmission
 Fecal contaminated soil

 Larva penetrates the skin

 Common in hot humid regions

41
3
Clinical Presentation
 Recurrent urticaria – buttocks & wrists
 Migration –”Larva currens” – Running larva
 Abdominal or epigastric pain aggravated by

food ingestion
 Nausea, diarrhea, Gl bleeding, mild chronic

colitis and weight loss

 Pulmonary symptoms – rare
 Eosinophilia - common

41
4
Disseminated form=> fatal
 GI, lung, CNS, Peritoneum, liver, kidney
 Risk of bacteremia increases-
◦ Gram negative sepsis
◦ Pneumonia
◦ Meningitis

 Complications are common with HTLV-I but

not with HIV.

41
5
Diagnosis
 Stool for larva
 Eggs are not detectable in stool

 Treatment
◦ Ivermectine-200mg/kg/d 1-2 days
◦ Albendazole 400mg po BID for 3 days
◦ Thiabendazle 1500mg po BID for 3 days

41
6
Rhabiditiform larva of
strongyloides stercoralis in
stool specimen

41
7
Trichuriasis (Whip-worm)
 An infection of the intestinal tract caused by
T. trichiura.
 Distributed worldwide, most abundant in the

tropics and subtropics.

 The parasites have a characteristic whip like

shape.
 The females are slightly longer than the

males, 35-50mm long.

41
8
Cont’d….
 Adult worms reside in the colon and caecum,
 Thousands of eggs are laid daily and pass

with the feces.

 They mature in the soil.
 Ingestion-infective eggs hatch in the

duodenum, releasing larvae that mature

before migrating to the large bowel.
 Adult worms may live for several years.

41
9
Clinical Feature
 Most infections are asymptomatic.
 Large worm burden, especially in children--

diarrhea of long duration, dysentery, mucoid

stools, abdominal pain and tenderness,
dehydration, anemia, weight loss and
weakness.
 Rectal prolapse may occur, particularly in

children.

42
0
Diagnosis and Treatment
 Detection of lemon-shaped whip worm eggs.
 Adult worms, about 3-5cm long, can be seen

on proctoscopy.
 Treatment:
 Mebendazole 500mg once or
 Albendazole 400mg as a single dose with

cure rates of 70–90%

42
1
Enterobiasis (Pinworm)
 An infection of the intestinal tract by the pin
worm E. vermicularis.
 Enterobiasis is found all over the world- more

common in temperate countries than tropics.

 E. vermicularis is a spindle-shaped parasite

of humans.

42
2
Cont’d….
 The gravid female worm migrates nocturnally out into
the perianal region and releases up to 10,000
immature eggs.
 The eggs are transmitted by hand-to-mouth
passage.
 The larvae hatch and mature entirely within the
intestine.
 Self-infection results from perianal scratching and
transport of eggs to the hands or nails and then to
mouth.
 Pinworm infections are very common among family
members.

42
3
Clinical Features
 The most common symptom is the intense
nocturnal pruritus ani- due to the cutaneous
irritation in the perianal region by the migrating
gravid females and the presence of eggs.
 Intense pruritus may lead to dermatitis, eczema
and severe secondary bacterial infections of the
skin.
 Pinworms may invade the female genital tract,
causing vulvovaginits and pelvic granulomas-
rare.

42
4
Diagnosis
 Eggs are not usually found in the stool
because they are released in the perineum.
 Clear cellulose tape to the perianal region in

the morning –increase yield of microscope.

 The tape is then transferred to slide to be

seen under a microscope.

42
5
Treatment
 Mebendazole 100mg PO BID for 3 days, or
 Albendazole 400mg as a single dose
 Pyrantel pamoate10mg/kg,
 Piperazine, 4g in a single dose.
 It is advisable to treat all household contacts

42
6
Cestodes
 Cestodes or tapeworms are segmented worms.
 The tapeworms can be divided into two.
 1.The definitive hosts are humans, these

include Taenia saginata, Diphyllobothrium,

Hymenolepsis and Dipylidium Canium.
 2.Humans are intermediate hosts, these are

Echinococcosis, Sparganosis and Coenurosis.

 Humans can be a definitive or intermediate

host to T.solium.

42
7
Taeniasis saginata
 Also called beef tapeworm- infection is
caused by the presence of the adult beef
tapeworm, T. Saginata, in the intestine of
humans.
 It is found all over the world- countries where

raw meat is ingested.

 Ethiopia is one of the heavily affected

countries.

42
8
Cont’d….
 T.Saginata is a large tapeworm usually 5-10
meters in length.
 Humans are the only definitive host.
 Eggs deposited on vegetation can persist for

months or years, until ingested by cattle.

 Embryo from cattle intestine migrates to the

muscle and transform into cysticercus.

 When eaten raw or undercooked, this infects

humans.

42
9
Cont’d…
 Clinical features : Usually asymptomatic. Often
detected when patients pass proglottids with stool or
alone.
 Proglottids are motile and this causes perianal

discomfort during discharge.

 Mild abdominal pain, nausea, anorexia and weight

loss can occur.

 Diagnosis: demonstrating eggs or proglottids in stool.

 Treatment: Treatment of choice is prazequantel 5 -10

mg/kg in a single dose or 600mg.

 Niclosamide as a 2 g single morning dose before

breakfast is an alternative

43
0
Taeniasis Solium
 It is caused by T.solium from eating raw or undercooked
pork.
 The adult tapeworm resides in the upper jejunum,
similar to T. saginata.
 Both the adult tapeworm and the larvae (Cysticerca)
infect people.
 Clinical features : Mostly patients are asymptomatic; but
they could have epigastric discomfort, nausea and
weight loss.
 When infected with cysticerica (cysticercosis), they are
distributed all over the body.
 The major manifestations come from the CNS with
seizures, headache, raised intracranial pressure, mental
changes etc.
43
1
Diagnosis and Treatment
 Diagnosis: detection of eggs or proglottides.
 Diagnosis is difficult in cysticercosis
 Treatment: Intestinal- a single dose of

prazequantel 5-10 mg/kg or 600 mg, this

treatment may be complicated by
development of CNS inflammation if
cysticercosis co-exist—prazequantel 15-
100mg/kg in 3 divided doses for 15-30 days
or Albendazole 15mg/kg/day for 8-28 days
plus high dose corticosteroids.

43
2
Hymenolepis nana (Dwarf
tapeworm)
 Dwarf tapeworm is 25-40mm in length by
1mm in breadth.
 It is distributed all over the world.
 This tapeworm doesn't require intermediate

host.
 Hatching of eggs occurs in the small intestine

where they penetrate the villus and become

cysticercoid.
 Eventually the parasites breakout in to the

lumen of the gut and reach maturity.

 Infection is prevalent in children.

43
3
Cont’d….
 Clinical features: Most infections are
asymptomatic.
 Severe infections may manifest with

abdominal pain, anorexia and diarrhea.

 Diagnosis:demonstration of the eggs in the

stool.
 Treatment: The treatment of choice is

praziquantel 25 mg/kg as single dose or

1800mg as a single dose.
 A course of niclosamide for 7 days is also

effective (2gm in 1st day then 1gm for 6

days). 43
4
Diphyllobothriasis (Fish tape
worm)
 Diphyllobothriasis is infection caused by adult D. latum.
 It is acquired from eating raw fish.
 It is mostly found in Europe and Northern hemisphere.
 It is the longest tapeworm reaching up to 25 meters.
 Clinical: patients could have abdominal pain, loss of appetite,

anorexia, nausea, diarrhea or loss of weight.

 Can cause megaloblastic anemia due to its vit B12 use.
 Diagnosis: demonstration of characteristic eggs in the stool.
 Treatment: Praziquantel 5-10 mg/kg once is very effective.
 Vitamin B12 deficiency should be treated if present.

43
5
Schistosomiasis
Trematodes-Platyhelminths
 Blood flukes
◦ S. mansonia
◦ S. japonicum
◦ S. Intercalatum
◦ S. mekongi
◦ S. hematobium
 Hepatic flukes
◦ Fasciola hepatica
 Intestinal flukes
◦ Fasciolopsis buski
 Lung flukes
◦ Paragonimus westermani

43
6
Transmission
 Definitive host=mammalian/human
◦ Adults initiate sexual reproduction

 Intermidiate host- Snails

◦ Asexual reproduction

43
7
Life cycle
 Ova hatch in water to miracidia
 Inside a Snail changed to Cercaria
 Caracara attach to the skin
 In the SC tissue transforms to schistosomula
 Migration through venous or lymphatic to reach
lung and liver
 Adults descend down to intestinal veins or visceral
veins
 Ova penetrates the wall by enzymatic secretion and
reaches the intestinal lumen or urinary tract

43
8
Epidemiology
 Infection starts at the age of 3-4 yrs.
 Peaks at 15-20 yrs.
 Decreases after the age of 40 yrs.
 S. mansoni endemic
◦ Nile valley- Sudan, Egypt
◦ Arabian peninsula
◦ Latin America-Brazil
 S. hematobium
◦ Middle east, Africa, Indian
 S. japonicum
◦ China, Indonesia, Phillipines

43
9
Pathogenesis
 Immune complex
◦ Cercarial associated dermatitis
 Humeral and cell mediated inflammation
◦ Katayama fever-serum sickness like
◦ Chronic schistosomiasis
 Cell mediated granulomatous formation and fibrosis-
Symmers-clay pipe-stem fibrosis

44
0
Risk factors
 Geographic location

 Exposure to fresh water bodies

 Local eating and drinking habits

44
1
Clinical presentation
 Depends on
◦ Intensity of infection
◦ Host factors-age, genetics
Three stages:
1. Swimmers itch
◦ 2-3 days after invassion
◦ Itchy maculopapular rash at the affected site
◦ Commonly seen with S. mansoni & S. japonicum
◦ Self limiting

44
2
2. Acute Schistosomiasis
 “Katayama fever”
 Occurs 4-8 weeks after skin invassion
 Fever, generalized LAP
 Hepatosplenomegaly
 Peripheral blood eosinophilia
 Occurs during worm maturation and at the

beginning of oviposition
 Benign. Death reported with heavy exposure

44
3
3. Chronic schistosomiasis
 Species dependent-(S. mansoni & S.
japonicum)
 Intestinal phase:
◦ Colicky abdominal pain
◦ Bloody diarrhea, fatigue, growth retardation
◦ Colonic polyposis
◦ Malabsorbtion

44
4
Cont’d….
 Hepato-splenic phase
◦ Hepatomegaly-granulomatous
◦ Pre-sinusoidal portal fibrosis leads to portal
hypertension and splenomegaly.
◦ Esophageal verices-bleeding is tolerable because of
normal liver function.
◦ Cirrhosis- if it is associated with viral hepatitis and
malnutrition

44
5
S. hematobium
 Dysurea, frequency, hematuria
 U/A:

◦ Blood, albumin, bacteria, sediments, cellular

metaplasia
 Urinary bladder granulomas leads to
obstructive uropathy, Squamous cell Ca-
hence it is a human carcinogen.

44
6
Cont’d…
 Pulmonary:
◦ Cough, fever, dyspnea
◦ Cor-pulmonale due to pul. Hypertension

 CNS-granulomatous depossion
◦ Epilepsy in S. japonicum
◦ Transvers myelitis in S. mansoni & S. hematobium

44
7
Diagnosis
 Travel hx and exposure to fresh water
bodies
 For Katayama
◦ Peripheral eosinophilia
◦ High Ab for schistosoma-FAST-ELISA
◦ Immuno electrotransfer blot(IETB)
◦ Stool or urine for ova
◦ Stool:
 kato thick smear –quantifcation
 Concentration method
◦ Rectal biopsy
◦ Ultrasound of the abdomen.

44
8
Treatment
 Phase 1.
◦ Topical to relief itching
 Phase 2.(Katayama fever)
◦ Anti schistosomal chemotherapy
◦ Immunosuppressant-steroid
◦ Supportive
 Phase 3.
◦ Chronic form- supportive and treatment of
complication
◦ Hepatic failure & varices

44
9
Cont’d….
 Chemotherapy
◦ Praziquantel 40-60mg/kg divided in 2-3 doses for
1 day
 Parasitological cure rate-85%
 Decreases egg counts by >90%

◦ Early hepatomegaly and bladder lesion resolve after

chemotherapy, fibrosis remained the same

45
0
Prevention
 Endemic areas:
◦ Sewage disposal, sanitation
◦ Health education
◦ Chemotherapy

 For travelers
◦ Avoid contact with fresh water bodies
◦ If exposed follow up visits

45
1
Filariasis
 Nematodes that dwell in SC tissue and
lymphatics
 Eight filarial species
 Lymphatic filariasis

◦ W. bancrofti, B. malayi, B. timori

 SC dwellers
◦ Onchocerca volvulus, Loa loa

45
2
Life cycle
 Transmission by mosquitoes or arthropodes

 Inoculates infective larvae

 Develops to Adults that circulate in the circulation

or SC tissue.

 Microfilaria formed –(stays for 3-36 months)

 Ingested by arthropode vector and develop to new

infective larva in 1-2 wks

45
3
Lymphatic Filariasis
 Reside in lymphatic channels or LN. It
remained viable for > 2 decades.
 W. bancrofti widely distributed , affects > 115

million people.
 Found in the tropics and sub tropics
 Common in Africa
 Human- the only definitive host.

45
4
Cont’d…
 Vector:
◦ Culex fatigans mosquitoes-urban
◦ Anapheline or aedean in rural

 B. malayi found in China, India, Indonessia,

Korea, Japan, Malaysia, Phillipin.

45
5
Pathology
 Inflammatory damage to the lymphatics by
adult worms (not by microfilaria).
 Lymphatic dilatation and thickening of
vessel wall.
 Incompetence of lymphatic valves.
 Lymphedema and chronic stasis changes.
 Granulomatous reaction following death of
worms with fibrosis.
 Complete lymphatic obstruction.

45
6
Clinical Presentation
 The most common manifestation:
◦ Asymptomatic microfilaremia, hydrocele,
acuteadenolymphangitis(ADL) and chronic
lymphatic disease.
 Early manifestations
◦ Microscopic hematuria or proteinuria
◦ Dilated, totuous limphatics – by imaging
◦ Scrotal lymphangiectasia by ultrasound

45
7
Cont’d….
 ADL (acuteadenolymphangitis)
◦ Fever – high grade
◦ Lymphatic inflammation
◦ Transient local edema
◦ Inflammation is retrograde – extending from the LN
draining the area
 In B. Malayi forms a local abscess – raptures
to the surface

45
8
 Cont’d…
 Both involves the upper and lower extremities
 Genital involvement is exclusively with W.

bancrofti infection
◦ Epididmitis
◦ Scrotal pain and tenderness

45
9
Cont’d….
 Dermatolymphangioadenities (DLA)
◦ High grade fever, chills, myalgia and head ache
◦ Edematous inflammatory plaques
◦ Vesicles, ulcers, hyper pigmentation
◦ History of trauma precedes
◦ Mimics cellulites

46
0
Cont’d…
 Chronic changes
◦ Brawny edema
◦ Early pitting
◦ Thickening of SC tissue and hyperkeratosis
◦ Fissuring and hyperplastic changes with super
infection
◦ Hydrocele- scrotal elephantiasis
◦ Chyluria- due to obstruction of retroperitoneal
lymphatics

46
1
Diagnosis
 Demonstration of micrifilaria in blood, body fluids, hydrocele
◦ Direct staining
◦ Concentration with centrifugation(knott’s technique)
◦ Adult worms are not accessible
◦ Microfilaria are lesser number (scarce) in the peripheral blood by
day and increase at night.
 Serology- Ag of W. bancrofti
◦ ELISA
◦ Rapid formation imino-cromatography
◦ Sensitivity =96-100%
◦ Specificity= 100%
 PCR for DNA
 High frequency U/S with Doppler
◦ Visualizes worms in the scrotum or female breast.
 Eosinophilia
 Increased IgE and antifilarial anti body

46
2
Cont’d….
 Difference from bacterial lymphangitis
◦ Ascending infection
◦ Filarial infection a retrograde extension.
 Active disease
◦ Microfilaremia
◦ Antigen positivity
◦ Detection of adult worms on ultrasound

46
3
Treatment
 Active infection
◦ DEC (Diethylcarbamazine)
◦ Has both micro and macro filacidal properties
◦ Dose-6mg/kg/d x 12days
◦ Albendazole – macro filaricidal efficacy
◦ Does – 400mg bid x 21days
 Adult worm carriers without microfilaria- need
◦ DEC
 Chronic complication
◦ Surgical correction of hydrocele
◦ It recurs

46
4
Prevention
 Impregnated bed nets.
 DEC – prophylaxis
 Mass distribution of chemotherapy annually

◦ Albendazole + DEC/Ivermectine

46
5
Onchocerciasis (“River
blindness")
 Caused by the filarial nematode Onchocerca
volvulus.
 Infection in humans begins with deposition
infective larvae on the skin by the bite of an
infected black fly.
 The larvae develop into adult in subcutaneous
tissue and form nodules.
 Infection is transmitted to other persons when a
female black fly ingests microfilariae from the
host’s skin and these microfilariae then develop
into infective larvae.

46
6
Clinical features and Diagnosis
 Has an incubation period of several months before
nodules appear.
 The subcutaneous nodules, onchocercomata, are the
most characteristic lesions of onchocerciasis.
 They usually appear on coccyx, sacrum, thigh and bony
prominences.
 The most frequent manifestations are pruritus and
rash.
 The skin lesions are characterized by wrinkling of skin
and epidermal atrophy that can more often lead to
hypopigmentation than hyperpigmentation.
 Eczematous dermatitis and pigmentary changes are
more common in the lower extremities.

46
7
Cont’d…
 Visual impairment is the most serious
complication and is due to intense inflammation
that surrounds the dying microfilaria.
 Early lesions are conjuctivitis with photophobia;

sclerosing keratitis occurs in minority of patients,

which leads to blindness.
 Inflammation in the interior eye cause iridocyclitis.
 Patients could have enlarged inguinal lymph

nodes (hanging groin).

 Heavily infected patients could have severe

wasting.

46
8
Diagnosis
 Diagnosis depends on demonstration of the
microfilariae in the skin snip or nodules.
 Microfilariae are rarely found in blood smear,

but may be seen in urine.

46
9
Treatment
 Ivermectin orally in a single dose of 150mg/kg,
yearly or semiannually is the treatment of choice but
no agent eradicates the adult worm.
 The drug has many advantages: no severe ocular

reaction and prevents blindness due to optic nerve

disease by 50%, inhibits the production of
microfilariae by adult female worms for some
months.
 Ivermectin is contraindicated if there is co-infection

with loa loa, in pregnant or lactating women and

children under the age of 5 years.
 Antihistamines should be given for the pruritus.

47
0
Prevention
 Avoiding black fly localities and by protective clothing.
 Repellents-only for short periods as they are washed

off by sweat.
 Control program (2 in Africa and one in America) have

covered over 99% of all population living in endemic

areas.
 The control of onchocerciasis today is based on 2

strategies:
◦ Vector control by spraying insecticides, used by West- Africa.
◦ Large scale Ivermectin chemotherapy is the main strategy
being used by Onchocerciasis Elimination Programme in the
Americas (OEPA) and African Programme for Onchocerciasis
control (APOC).

47
1
References
1. Internal Medicine, Lecture Notes for Health
Officers
2. Harrisons’ Principle of Internal Medicine 19th
edition
3. Ethiopian Treatment Guide Line 2014.

47
2
THANK YOU

47
3
Pneumonia

AWOKE SEID (MD)

47
4
pneumonia
 Definition :
 Pneumonia is an inflammatory condition of
the lung paranchyma—especially affecting
the microscopic air sacs (alveoli)—associated
with fever, chest symptoms, and a lack of air
space (consolidation) on a chest X-ray.

47
5
----pneumonia
Epidemiology:
 affects approximately 450 million people a year
and occurrs in all parts of the world.
 It is a major cause of death among all age groups
resulting in 4 million deaths (7% of the world's
yearly total).
 Death Rates are greatest in children <5, and adults

>75 years of age.
 occurs about 5X more frequently in the
developing world versus the developed world.

47
6
pathophysiology
 Bacteria typically enter the lung when airborne droplets
are inhaled, hematogenously disseminated, extend from
adjecent structure or those bacteria in parts of the URT
such as the nose, mouth, and sinuses can aspirated into
the alveoli.
 Once inside, bacteria may invade the spaces between cells

and between alveoli through connecting pores.

 This invasion triggers the immune system, neutrophils are

recruited.
 The neutrophils engulf and kill the offending organisms,

and also release cytokines, causing a general activation of

the immune system. This leads to fever, chills, and
fatigue.
47
7
------pneumonia
Classification:
 by where or how it was acquired:

community-acquired , aspiration , healthcare-

associated, hospital-acquired, and ventilator-
associated pneumonia.
 by the area of lung affected
 by the causative organism

47
8
----pneumonia.
Signs and symptoms:
-productive or non productive cough
-fever accompanied by shaking chills
-shortness of breath
-sharp or stabbing chest pain during deep
breaths
-confusion, and an increased respiratory rate
and some GI compliant

47
9
------pneumonia.

48
0
Community acquired pneumonia(CAP)
 Aetiology
-includes bacteria, fungi, viruses, and protozoa.
-new ones:the coronavirus responsible for severe
acute respiratory syndrome (SARS) and (MRSA).
-"typical" bacterial pathogens : S. pneumoniae, H.
influenzae, S. aureus and gram-negative bacilli
such as K. pneumoniae and P. aeruginosa.
-"atypical" organisms : include M. pneumoniae
and C.pneumoniae (in outpatients) and
Legionella spp.(in)
-virus may be responsible for up to 18% of cases.
48
1
-----CAP, aetiology
 S.pneumoniae isolated in nearly 50% of cases.
 10–15% of CAP are polymicrobial, a

combination of typical and atypical pathogens.

48
2
------CAP, aetiology.

48
3
-----CAP, diagnosis.
 History and P/E.
 sensitivity and specificity of the findings on P/E;

58% & 67%, respectively.

 CBC and CxR

-Gram's Stain, Culture of Sputum and antigen

-blood culture.
-PCR- use for research studies.

48
4
Chest X ray

48
5
 management
486

 The CURB-65 score is

useful for determining
the need for
admission in adults.
 score is 0 or 1

=home.
 2 =a short hospital

stay or close follow up

is needed
 3–5 hospitalization is

recommended.
-------management.
 In the UK, empiric treatmentwith amoxicillin is
recommended as the first line for CAP;
doxycycline or clarithromycin as alternatives.
 In USA, macrolides (such as azithromycin), and
doxycycline have replaced by amoxicillin.
 fluoroquinolones in uncomplicated cases is
discouraged due to concerns about S/E and
resistance.
 The duration of treatment has traditionally
been 7-10days, but increasing evidence
suggests that short courses (3-5days) are
equally effective. 48
7
---CAP treatment.
 Outpatient
*if no antibiotic in past 3 months:
-azithromycine/clarithromycine/doxicycline
*if antibiotic in <3 months or comorbidities:
-floroquinolones/high dose amoxa/amoxa-
clavulanate/iv ceftriaxone plus a
macrolide.

48
8
-----CAP
 Complications
-common: respiratory failure, shock and
multiorgan failure, coagulopathy, and
exacerbation of comorbid illnesses.
- others: metastatic infection(brain abscess or
endocarditis) , lung abscess, and complicated
pleural effusion.
-Lung abscess may occur in association with
aspiration or with infection caused by CA-
MRSA, P. aeruginosa, or (rarely) S.
pneumoniae.
48
9
 ----CAP
Follow-Up
-Fever & leukocytosis usually resolve within 2–4
days.
-physical findings may persist longer.
-radiographic abnormalities may require 4–12 wks
to clear
-follow-up radiograph can be done ~4–6 weeks .
-Young patients without comorbidity do well and
usually recover fully after ~2 weeks.

49
0
Health care associated pneumonia(HCAP )

 HCAP is defined as pneumonia that occurs in a non-

hospitalized patient with extensive healthcare contact:
-Intravenous therapy, wound care, or intravenous
chemotherapy within the prior 30 days
-Residence in a nursing home or other long-term care
facility
-Hospitalization in an acute care hospital for two or
more days within the prior 90 days.
-Attendance at a hospital or hemodialysis clinic within
the prior 30 days.

49
1
---------(HCAP)

 HCAP represents a transition between classic

CAP and typical HAP.
 MRSA in particular was more common in HCAP
than in traditional HAP/VAP
 patients receiving home infusion therapy or
undergoing chronic dialysis are probably at
particular risk for MRSA but may not be at
greater risk for Pseudomonas or Acinetobacter
than other patients who develop CAP.
 The Prognosis of HCAP is intermediate b/n that
of CAP & VAP and is closer to that of HAP.
49
2
Ventilator-Associated Pneumonia(VAP)

 Definition:
*VAP is pneumonia that occurs 48 to 72 hours
after endotracheal intubation.
 Etiology

-if VAP develops in the first 5–7 days of the

hospital stay, similar to severe CAP.
-if patients have other risk factors for HCAP,
MDR pathogens are a consideration.

49
3
------VAP

49
4
 ------VAP
 Epidemiology:
-Prevalence estimates vary between 6 and 52 cases
per 100 patients on MV.
-cumulative rate in those who remain ventilated for
30dys is as high as 70%.
 Pathogenesis:

1. colonization of the oropharynx with pathogenic

mo`s
2. aspiration of these organisms from the oropharynx
into the LRT, and
3. compromise of the normal host defense
mechanisms. 49
5
 -----VAP
 C/M:
-generally the same as in all other forms of
pneumonia.
-fever, leukocytosis.
-increase in respiratory secretions, and pulmonary
consolidation
-a new or changing radiographic infiltrate.
-tachypnea, tachycardia, worsening oxygenation.

49
6
 -----VAP
 Diagnosis
-clinical criteria can result in overdiagnosis of VAP:
(1) tracheal colonization with pathogenic bacteria in
patients with endotracheal tubes.
(2) other causes of radiographic infiltrates in pts on
MV
(3) other sources of fever in critically ill patients.
*ddx of VAP :atypical pulmonary edema, pulmonary
contusion, alveolar hemorrhage, hypersensitivity
pneumonitis, ARDS, and pulmonary embolism.

49
7
 ----VAP
 Treatment
 No Risk Factors for MDR Pathogens:

-Ceftriaxone (2 g IV q24h) OR
-Moxifloxacin (400 mg IV q24h), ciprofloxacin (400
mg IV q8h), or levofloxacin (750 mg IV q24h) OR
-Ampicillin/sulbactam (3 g IV q6h)
 If Risk Factors for MDR Pathogens

-Ceftazidime or cefepime plus

-Gentamicin or tobramycin or Ciprofloxacin or
levofloxacin plus
-Linezolid (600 mg IV q12h) or Vancomycin
49
8
------VAP.
Prognosis
-Crude mortality rates of 50–70%.
-Many patients with VAP have underlying diseases
that would result in death even if VAP did not
occur.

49
9
 Hospital-Acquired Pneumonia(HAP)
 Definition:
-HAP (or nosocomial pneumonia) is pneumonia that
occurs 48 hours or more after admission.
 HAP in nonintubated patients(both inside and

outside the ICU)is similar to VAP.

 higher frequency of non-MDR pathogens and the

better underlying host immunity in nonintubated

patients.
 Anaerobes more common in HAP(non

intubated)due to higher risk of macroaspiration.

 blood cultures are infrequently positive (<15% of

cases)
50
0
-------end

50
1
TUBERCULOSIS

Awoke Seid(MD)

502
Introduction:

 Currently, 95% of tuberculosis cases occur

in developing countries:
◦ where HIV/AIDS epidemics have the greatest
impact &
◦ where resources are often unavailable for proper
identification & Rx of these diseases.

503
Introduction:

 The WHO estimates:

◦ >8 million new cases of tuberculosis each year.
◦ ~ 3 million people die of the disease worldwide
each yr.
◦ > ⅓ of the world's population is infected with
M.tb.

504
Etiology.

◦ There are 5 closely related mycobacteria

 M. tuberculosis
 M. bovis
 M. africanum
 M. microti
 M. canetti.

505
Etiology……….

 M. tb is the most important cause of tb. disease in

humans.
 The tubercle bacilli are:
 non-spore-forming and acid fastness
 non-motile
 pleomorphic
 weakly gram-positive curved rods 2–4 μm long.
 obligate aerobes and slowly growing

506
Epidemiology

 Latent tuberculosis infection (LTBI)

◦ occurs after inhalation of infective droplet nuclei
containing M.tb
◦ Third of world population infected with MBT
◦ A reactive TST & the absence of clinical &
radiographic abnormalities are the hallmark
of this stage.

507
↑ed risk for progression from LTB to active tb.disease:

diabetes mellitus
 chronic renal failure
 malnutrition
 congenital or acquired immunodeficiency
 Infants & children ≤4 yr of age, especially <2

yrs
 Persons co-infected with HIV
 Persons with skin test conversion in the past

1–2 yr
 Persons who are immunocompromised

508
Transmission.

 Transmission of M. tuberculosis is:

◦ person to person
◦ usually by airborne mucus droplet nuclei
 Transmission rarely occurs by direct contact
with:
◦ Infected discharge or
◦ Contaminated fomite.

509
Transmission.

 The chance of transmission ↑es

when the patient has:
1. acid-fast smear of sputum
2. extensive upper lobe infiltrate or cavity
3. copious production of thin sputum
4. severe and forceful cough.
5. Environmental factors, especially poor air
circulation

510
Transmission………………

 Most adults no longer transmit the organism:

◦ Several days to 2 wks after

beginning chemotherapy.
◦ but some patients remain infectious for many
weeks.

 Young children with tb. rarely infect

other children/adults.
511
Pathogenesis…….

 The lung is the main way of portal of entry

 The tubercle bacilli multiply initially within alveoli & alveolar
ducts.
 The primary complex of tuberculosis includes:
◦ local infection at the portal of entry &
◦ the regional lymph nodes that drain the area

512
Pathogenesis……………

 Most of the bacilli are killed.

◦ some survive within non activated macrophages,
◦ which carry them through lymphatic vessels to the regional
LNs.


When the 10 infection is in the lung, the

hilar LNs usually are involved, although

an upper lobe focus may drain into para-
tracheal LNs.

513
Pathogenesis…….

 The tissue reaction in the lung parenchyma & LNs

intensifies over the next 2–12 wk.
 The parenchymal portion of the primary
complex often heals completely by:
◦ fibrosis or
◦ calcification
after undergoing caseous necrosis &
encapsulation.

514
Pathogenesis………….

 Occasionally, this portion continues to enlarge, resulting

in:
focal pneumonitis &
pleuritis.

 If caseation is intense,
the center of the lesion liquefies &
empties into the associated bronchus
leaving a residual cavity.

515
Pathogenesis…………….

 Partial obstruction of the bronchus caused by external

compression
may cause hyperinflation in the distal lung segment.

 Complete obstruction results in atelectasis.

 Inflamed caseous LNs can attach to the
bronchial wall & erode through it,
causing endobronchial tuberculosis or fistula
tract.

516
Pathogenesis…………..

 During the development of the 10 complex (Ghon

complex), the combination of:
◦ parenchymal pulmonary lesion &
◦ corresponding lymph node site
tubercle bacilli are carried to most tissues
through the blood & lymphatic vessels.

517
Pathogenesis……………..

 Although seeding of the organs of the respiratory

system is common, bacterial replication is more
likely to occur in organs with conditions that
favour their growth:
◦ the lung apices
◦ brain
◦ kidneys &
◦ Bones and others

518
Pathogenesis………….

 Disseminated tuberculosis occurs if:

◦ the number of circulating bacilli is large &
◦ the host cellular immune response is
inadequate.

519
Clinical manifestation:

 Productive cough of more than 2 wk

 Low grade fever
 Night sweet
 Weight loss and anoroxia

520
Clinical……………..

Extra-pulmonary tuberculosis

1.Tuberculous lymphadenitis
 The most common form.

 Often referred to as scrofula

 Most cases occur within 6-9 mo of initial
infection

 Disease is most often unilateral

521
 Systemic signs and symptoms other than a low-
grade fever are usually absent
 TST is usually reactive, but the CXR is normal in
70% of cases.
 Lymph node tuberculosis can resolve if left
untreated but more often progresses to
caseation and necrosis

522
 2. Tuberculosis of the spine or joints:
523

 Is the 2nd most common

form of childhood EPTB
 May occur within the 1st
few yrs following
primary infection
 The classic manifestation is
tuberculous spondylitis
with progression to Pott
disease
 3 Tuberculous (TB) meningitis
 Start initially with compliant of
progressive headach, fever,neck stiffness
and vomiting
 Later on

Changes in state of consciousness

and other complications

524
3 .Tuberculosis of the serous membranes

 TB pleurisy, pericardium &

peritonitis
Tb of GI, GU

525
Diagnosis of Paediatric TB

 To make the Dx of childhood TB with a fair degree

of accuracy the following tests are useful:

Tuberculin skin test (TST)

CBC,ESR,Gene Xpert
Chest radiograph
Sputum smear microscopy
HIV testing.

526
Drug-resistant
TB ???

Drug-resistant TB is a laboratory diagnosis.
 Drug-resistant TB should be suspected if:

1. Features in the source case suggestive of drug-resistant:

Contact with a known case of drug-resistant

TB

Remains sputum smear-positive after 3

months of Rx
History of previously treated TB

History of Rx interruption
527
 Drug-resistant TB
 Mono-resistant TB

◦ Resistant in vitro to one first-line anti-TB drug.

 Poly-resistant TB:
◦ Resistant in vitro to > 1 first-line drug, other
than both INH & RIF
 MDR:

◦ Resistant to at least both INH &

RIF.
528
Drug-resistant TB
 Extensive-drug resistant TB (XDR):

Resistance to at least RIF & INH, in addition to:

Any Fluoroquinolone &


At least one of the 3 following injectables used
in anti-TB Rx:

Capreomycin
kanamycin
Amikacin.

529
Principles of tuberculosis
treatment

1.Chemotherapy(anti Tb)
2.Nutritional rehabilitation
3.Health education
4.Family screening
5.Follow up

530
Category of TB patient for
registration on diagnosis
 New
 A patient who has definitely never taken anti-

TB drugs or who has taken anti-TB drugs for

less than one month.
 Relapse
 A TB patient who:
 a) previously received treatment and was declared
cured or treatment completed; and
 b) has once again developed bacteriologically positive
(by smear or culture) TB.

531
 Treatment after failure
◦ A patient who is started on a re-treatment regimen
after having failed previous treatment.
 Treatment after default
◦ A TB patient who returns to treatment,
bacteriologically positive, following
interruption of treatment for 2 months or
more.

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 Transfer in
◦ A TB patient who has been transferred from another
TB register to continue treatment.
 Other
◦ All TB patients who do not fit the above definitions.
◦ This group includes chronic cases (TB patients who
are sputum smear-positive at the end of a re-
treatment regimen).

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