UNIT 6

Diseases transmitted by arthropods

(vectors)
 Objectives
At the end of this chapter, the student will be able to:

o Describe what arthropod or intermediate vector-borne

disease means.

o identify the common vector-borne diseases.

o diagnosis and treatment of vector-borne diseases.

o Implement the common preventive and control methods

2
of vector-borne diseases.
 Introduction

Vector is any carrier of disease.

 ‘vector-borne diseases’ we restrict the word to those

invertebrate hosts (insects or snails), which are an

essential part of the life cycle of the disease organism

3
 Vector.....

Vector can be;

 Biological- the infectious agent requires a period of

multiplication/development before transmission
(extrinsic IP) ex. Malaria.
 Mechanical- directly infect to the host (no need of
extrinsic IP) ex. housefly

4
 Introd.....
Insect vectors usually acquire the disease organism by

sucking blood from infected persons, and pass it on, later,

by the same route.
Infection may enter through skin cracks or abrasions

either from infected faeces deposited when feeding, or

from body fluid
 The disease causing organism undergoes a period of

development inside the vector, and the time taken for this
5 is called the extrinsic incubation period.
 Vector borne diseases
1. Leishmaniasis

2.Malaria

3.Relapsing fever

4.Typhus

5.Yellow fever

6.Filariasis

7.Onchocerciasis
6
 1.Leishmaniasis

 Vector-borne zoonotic disease caused by genus leishmania

that is obligate intracellular protozoa

 Vectors – Phlebotomus and Lutzomyia
A unique disease with wide ranging (eg, cutaneous,
mucocutaneous & visceral)
Several parasite species with diverse characteristics
depending on geographic focus
Similar species could have different clinical spectrum and
severity of disease

7
Phlebotomus
Epidemiology of leishmania
Population at risk – 350 million

Over all world prevalence – 12million

Annual new case reports – 2 million

About 90 countries affected

More than 20 spp of leishmania identified

 Transmission
 By the bite of female sand flies.

Other route of transmission are via;

Blood

Shared needles

Blood transmission

Trans-placental spread

Via organ transplantation

10
Life cycle
Leishmania species produce widely varying clinical
syndromes ranging from self-healing cutaneous ulcers to
fatal visceral disease.
Depends on–Parasitic properties (Infectivity, pathogenicity and

Virulence)

These syndromes fall into three broad categories:

Cutaneous leishmaniasis (CL)

Mucosal leishmaniasis (ML)

Visceral leishmaniasis (VL)

12
 A. Cutaneous leishmaniasis (CL)

Caused by
 L. Tropica

 L. major, and

 L. Aethiopica

13
 An estimated 0.7 million to 1.3 m new cases

occur worldwide annually–

About one-third of CL cases occur in the

- Americas,

- Mediterranean basin

- Middle East and

- Central Asia countries.

14
 Cutan......

There are multiple ulcers

resulting from several sand
fly bites.
The edges of the ulcers are
raised

15
 B. Mucosal leishmaniasis
Presentation:

- Erythema and ulceration of the nares  Nasal septal

perforation and destructive inflammatory lesion 

- obstruction of pharynx/larynx and remarkable

disfigurement.

16
17
 C. Cutaneous and mucosal disease

 IP =Weeks - Months

 Start as a papule at the site of insect bite and evolve to nodules,

ulcer, plaque
 It may complicite with regional adenopathy, subcutaneous

nodules, lesion pain or pruritis, 20 bacterial infection

 The infecting spp, the location of lesion and the host immune

response determine the manifestation and chronicity of the lesion

 Most cases are reported from Bolivia, Brazil and Peru

18
 Diagnosis
Visualization of amastigote in Giemsa-Stained thin smear

from dermal scraping /biopsy specimen

Serology tests – insensitive

Indication for treatment

Persistent lesion ( > 6 months)

Lesions that are located over joints

Multiple lesions (> 5 to10 in number)

Large lesions (> 4-5cm)

19
 Treatment
Localized CL respond well but diffuse and MCL forms

are difficult to treat

IV/IM SSG therapy, Pentamidine, dapsone

Local/Topical therapy - Intralesional SSG therapy,

Heat therapy

 Cryo therapy

20
 D. Visceral Leishmaniasis
VL in 70 countries,

S. Asia 600,000 cases in 2006

East Africa 30,000 (mainly Sudan, Ethiopia)

Brazil 4,000

21
 Epidemiology in Ethiopia
Lowlands of Ethiopia with varying endemicity

N. West. - Metema and Humera, Wolkayit, Libo/Fogera

N. East – Ethio-Djibouti Awash Valley

S. West – Dawa, Genale, Woito, Konso, Omo, Gambella

Sudan border
 Risk of acquiring infection is determined by local sand fly

behavior and by the presence of an infected animal or

human reservoir.
22
 HIV-VL co-infection Ethiopia
VL- HIV co-infection rate at Humera

1998/99 – 18.5%

2006 – 40%

A Tigray retrospective review of 791 cases showed >4x CFR in

HIV + VL patients than VL without HIV

Libo – HIV /VL coinfection rate 15-18%

23-
+
 Visceral Leishmaniasis

 Kala- azar (Black fever in Hindu)

 caused by the L. donovani complex, which includes L.

donovani and L. infantum.

In the Old world, VL is caused by Leishmania donovani(in
regions of India, Pakistan, China and Africa) and
Leishmania infantum(in the Mediterranean region).
In the New World, VL is also caused by L. infantum (also
known as Leishmania chagasi or L. infantum chagasi),
which is found primarily in Brazil
 IP: Wks –Mo’s
24
 VL
 Zoonotic form, dogs as main reservoir, occurs in the

Mediterranean basin, China, the Middle East, and South-

America; cause is L. infantum
 The anthroponotic form, humans as reservoir, is caused

by L. donovani ; prevalent in East Africa and the Indian

subcontinent

25
 Clinical Presentation

 Often remains asymptomatic.

 Symptomatic cases: acute, sub acute or chronic course

 Fever, night sweats, weakness ,weight loss

 Cachexia, wasting, Pallor

 Nontender, soft massive splenomegaly + perisplenitis

26
 C/m...
 Hepatomegaly + LAP

 Darkening of face/ashen grey appearance

 Bleeding 20 to thrombocytopenia

 Susceptibility to 20 infection

 Pancytopenia (Anemia, Thrombocytopenia, Leukopenia,

Neutropenia)
 Marked eosinopenia, Reactive lymphocytosis, Monocytosis

 Hyper gammaglobulinemia(high level of anti body in blood)

27 Hypo albuminemia

 • A patient with visceral
leishmaniasis has a hugely
enlarged spleen visible through
the surface of the abdomen.
• Splenomegaly is the most
important feature of visceral
leishmaniasis.
28
 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

29
 Diagnosis of VL

Gold-standard: Demonstration of amastigotes in tissue

aspirates
Diagnostic sensitivity – Spleen - > 95%; Bone marrow 

70%, Lymph nodes  58%

DAT test: Anti- Leishmanial (titer) IgG sn >95%, sp >90%

Detection of Anti-rK39-Abs Sn 72%, Sp 82%

Culture

Isoenzyme and molecular techniques to differentiate species

30
Amastigotes (the tissue stage of Leishmania parasites) in a
Giemsa-stained impression smear
 Treatment
SSG 20mg/kg/d +paromomycine 15mg/kg/d Im for 17

days.
Sodium stibogluconate (SSG) 20mg/kg im for 30 days

Alternative: Amphotericin B 1mg/kg every other day for

30 days/total 15 doses.
 AmBisome 4mg/kg for 5-7 doses: 1-5days, 10th, 14 th

32
• AmBisome is the first-line treatment for VL in special

situations
- pregnancy,

- HIV-co-infection, severe illness, severe anemia,

- severe malnutrition and extremes of age (below 2 years or

above 45 years).
- antimonials toxicity

• has a relatively short treatment course and minimal side

effects; its main disadvantage is its high cost

 The objectives of VL treatment are to:

1. Reduce the parasite burden,

2. Prevent drug resistance,

3. Avoid toxic drug effects, and

4. Improve the clinical condition of patients and to

manage complications(anemia, malnutrition and

secondary infections)

34
 Prevention and control
 The avoidance of outdoor activities

 The use of mechanical barriers such as screens and bed

nets
 Wearing of protective clothing

 Application of insect repellent

 Treatment of cases

 Vector control and elimination of reservoir host (eg.

Domestic dogs)
35
 2.Malaria
 Acute Protozoan disease transmitted by the bite of infected

female anopheles mosquito

 Etiology: - Five species of the genus plasmodiaum

P. Falciparum

P. Vivax

P. Ovale

P. Malariae

P. Knowlesi

36 Reserver :human
 Transmission

1. By the bite of female anopheles mosquito.

2. Blood transfusion

3. Organ transplantation

4. Needle

5. Mother-to-child

37
 Life cycle
o Female anopheles mosquito bites human and injects

sporozoites.
o Sporozoites penetrate and produce tissue schizont in liver

cells.
o Merozoites released from liver cells and invade RBCs.

o Establishment of dormant forms (Hypnozoites) in liver

cells occur in p.vivax and P.ovale.

38
 Life...

Trophozoites in RBCs  schizonts with merozoite

formation  released merozoites infect new RBCs 

Formation of gametocytes  Mosquito bites infected
human and sucks gametocytes with blood fertilization
of gametocytes in mosquito entero epithelial cells
ookinette formation and moves out side of stomach
wall oocyte develops and forms sporozoites  oocyte
with many sporozoites rupture and sporozoites migrate to
salivary gland of mosquito  infected mosquito bites
39
another human.
40
 Con...

Incubation Period : vary

Pf: 7-14 days

Pv: 8-14

P. ovale: 8-14

P. malarie: 8-30 days

41
 Malaria Transmission pattern

Stable malaria transmission

 Transmission throughout the year

 Fairly uniform intensity of transmission with little variation over

the years
 Long- living and frequently biting mosquitoes present

 High immunity in the community due to intense transmission

 Young children, traveler's and pregnant women are

susceptible groups

42 Control of malaria is very difficult


 Trans....
Unstable Malaria transmission
• Uneven, non predictable, less intense transmission

• Liable to flare-up into dramatic epidemics

• Short lived and less frequently biting mosquitoes present

• Low immunity status of the community

• All age groups are frequently affected

• Control of malaria is much easier than stable malaria

•43 Commonest pattern of malaria transmission in Ethiopia

 Clinical features of Uncomplicated Malaria
Symptoms
Lack of sense of well being

Headache, Fever, sweating

Fatigue, Arthralgia, myalgia

Abdominal pain, diarrhea, Vomiting, anorexia

The classical malaria paroxysms of fever spikes, chills

and rigors

44
 c/m...
Signs
Fever, Tachycardia, Postural hypotension, Delirium

Pallor, Hepatosplenomegaly, mild Jaundice

45
 Diagnosis
 Clinical and epidemiological background

 Demonstration of the parasite by peripheral blood smear

 Thick and thin blood smear

 Thin blood film is methanol fixed; you can see intact RBC
with parasites inside it. species identification is
simple,percentage of RBC parasitized can be estimated
 Thick blood film, not methanol fixed, RBC are lysed during
staining, parasites are seen free from RBC
 Ab-based diagnostic stick /card test

46 - Remain positive for weeks after infection.

 Clinical diagnosis of malaria is made in a

patient who has fever or history of fever in

the last 48 hours and lives in malaria-
endemic areas or has a history of travel
within the last 30 days to malaria-endemic
areas
47
 Treatment of uncomplicated Malaria
P. Vivax /P. Ovale

Chloroquine 150 mg base; 4 tabs on 1st and 2nd days,

and 2 tabs on 3rd day

Premaquine 15mg po/d for 14 days for hepatic

hypnozoit clearance.
P. falciparum

Coartem (Artemether (20mg) – Lumefantrine (120mg))

combined tablets 4 tabs po bid for 3 days.

48
 Recrudescence or relapse
Recrudescence
occurs most often within days or weeks

parasites remain in the bloodstream undetected due to

ineffective treatment or host immunological response (or

both)
It is a result of continued survival or presence in the blood

of asexual forms of parasite because of no treatment or

inadequate treatment

49
P. falciparum is the usual cause
Relapses

occurs within weeks or months

It results from maturation of hypnozoites in the liver

with liberation of merozoites in to the blood

It varies according to the species & even according to the

group or strain
It can occur even three years after the primary infection

50
 Endemicity of malaria

Is determined by parasitemic rates or palpable spleen

rates in children 2-9 yrs of age
Hypo endemic - <10%

Mesoendemic - 11-50%

Hyper endemic - 51-75%

Holoendemic - > 75%

51
 Severe malaria

Older children and adults develop partial immunity after

repeated infections; these groups are thus at relatively low risk

for severe disease.
definition — acute malaria with high levels of parasitemia

(>5 %) and/or major signs of organ dysfunction.

- Young Children
- Visitors from non Endemic areas of any age
- Pregnant women
 Severe falciparum malaria
Signs Manifestations
Unarousable Failure to localize or respond appropriately to
coma/cerebral malaria noxious stimuli; coma persisting for >30 min after
generalized convulsion; GCS < 9

Acidemia/acidosis Arterial pH <7.25 or plasma bicarbonate level of

<15 mmol/L; venous lactate level of >5 mmol/L;
manifests as labored deep breathing, often termed
"respiratory distress"

Severe normochromic, Hematocrit of <15% or hemoglobin level of <50 g/L

normocytic anemia (<5 g/dL) with parasitemia level of >100,000/ L

Renal failure Urine output (24 h) of <400 mL in adults or <12

mL/kg in children; no improvement with
rehydration; serum creatinine level of >265 mol/L
(>3.0 mg/dL)
Pulmonary Non cardiogenic pulmonary edema, often aggravated by
edema/adult over hydration
respiratory distress
syndrome
Hypoglycemia Plasma glucose level of <2.2 mmol/L (<40 mg/dL)
Hypotension/shock Systolic blood pressure of <80 mmHg in adults (<50
mmHg in children 1–5 years); core/skin temperature
difference of >10°C; capillary refill >2 s

Bleeding/disseminated Significant bleeding and hemorrhage from the gums,

intravascular nose, and gastrointestinal tract and/or evidence of
coagulation disseminated intravascular coagulation

Convulsions More than two generalized seizures in 24 h; signs of

continued seizure activity sometimes subtle (e.g., tonic-
clonic eye movements without limb or face movement)
Hemoglobinuria Macroscopic black, brown, or red urine; not
associated with effects of oxidant drugs and red
blood cell enzyme defects (such as G6PD
deficiency)

Other
Impaired Unable to sit or stand without support
consciousness/arousable
Extreme weakness Prostration; inability to sit unaidedb

Hyperparasitemia Parasitemia level of >5% in non immune patients

(>20% in any patient including partially
immuned)
Jaundice Serum bilirubin level of >50 mmol/L (>3.0 mg/dL)
if combined with other evidence of vital-organ
dysfunction

Blood film must be positive for asexual form of P. falciparum and at least one
of the above to diagnose severe malaria.
 Treatment of severe malaria

Admit the patient

Maintain airway, breathing and circulation
Insert NG tube for feeding and medication

and urinary catheter/glove catheter for UOP

determination

56 Ensure nutrition and nursing care
First line treatment for severe malaria due to P. falciparum
IV or IM artesunate (preferred) OR

IM artemether (alternate) OR

IV quinine infusion (if artesunate is not available)

IM quinine (if artesunate is not available)

IV or IM artesunate has been shown to reduce significantly

(by about 35%) the risk of death from severe malaria

compared to IV or IM quinine.
Artesunate 2.4 mg/kg IV or IM(time = 0,12 hr,24 hrs) then

once a day for 5-7 days is the recommended treatment.

Start IV quinine 20mg/kg in 5% 500cc D/W to run over 4

hrs then 10 mg/Kg in 500cc D/W to run over 4hrs every 8

hrs

Artemether 3.2 mg/kg IM (loading dose) followed by 1.6

mg/kg IM daily for 6 days

58
 Relative Contraindications: IM Artemether should

only be used during the first trimester of pregnancy

when IV/IM artesunate (preferred) and IV/IM quinine
are both unavailable.

59
 Malaria in Pregnancy
Maternal effect
High level parasitemia
Common complications: Fetal effects
Anemia Fetal distress
Prone to severe infection Premature labor
Hypoglycemia and
Still birth
Acute pulmonary edema
LBW
Congenital malaria
in new born

60
 Prevention and control

1.Early Dx and Rx of cases

2.Vector control
 Avoiding mosquito breeding sites

 Residual DDT spray or other chemicals

 Personal protection against mosquito bite (use of bed

nets, etc.)

61
 Prevention....
3.Chemical control - insecticide
-larvicide
4.Biological control- larvivorish fish
-biological larvicide
-toxin producing bacteria
5. Environmental management
covering /discarding man made container
clearing vegetation
filling pools, springs, land depressions
intermittent irrigation
drainage for swampy or marshy areas
62
 6. Chemoprophylaxis
1wk before departure and for 4wks after leaving the

endemic area. Drug options:

- Mefloquine 228mg of base (250mg of salt) po/week

- Doxycycline 100mg once a day

- Chloroquine 300mg of base orally, once\wk

- Proguanil 200mg orally, once \day, in combination with

weekly chloroquine
63
 3.Relapsing fever
 An acute, infectious, bacterial disease, characterized by

alternating febrile periods (recurrent pyrexia attacks).

Infectious agent
 Borrelia recurrentis- cause of louse borne relapsing fever.

 Borrelia duttoni-cause of tick borne relapsing fever.

Borreliae are gram negative bacteria that belong to the

family spirochetaciae and are distinguished by

64
remarkable antigenic variability.
 Epidemiology
It affects the homeless men crowded together in

unhygienic circumstances especially during the cool

rainy season.
It is principally a disease seen in the developing world

Common in the highland.

The over all case fatality rate is 2-10%.

Reservoir- Humans for Borrelia recurrentis.

for tick borne relapsing fever, wild rodents and soft ticks .
65
 Con...

MOT: vector borne, acquired by crushing of

infective louse so that it contaminates the bite wound

or an abrasion of the skin.
IP: 5-10 days usually 8 days.

POC: Louse becomes infective 4-5 days after

ingestion of blood from an infected person and

remains so far for life (20-40 days).

66
 Clinical manifestation

Sudden onset of illness with chills, fever/ irregular

mostly >40˚c and prostration, headache, mayalgia and

arthralgia.
It is characterized by recurrent episodes of fever, which

accompanies spirochetemia. The disease relapses are

due to antigenic variation by the spirochetes

Nausea, vomiting, jaundice and Hepatomegally .
67
 c/m...
Scattered petechiae develop on the trunk, extremities and

mucus membranes in one-third or more of patients with

LBRF & in fewer pts with TBRF.
Epistaxis and blood tinged sputum, intracranial hemorrhage

After 4-5 days the temperature comes down, the patient

stays free for 8-12 days and then a relapse follows with the
same signs but less intense.
In untreated cases there may be up to ten relapses.

68
 Diagnosis
 Clinical and epidemiological grounds.

 Giemsa or Wright stain (blood film).

 Dark field microscopy of fresh blood.

 Detection of spirochetes in blood ,Bone marrow aspirate.

 Culture.

69
 Treatment
Admit the patient

Open iv-line before administering penicillin.

Administer 400,000-600,000 IU procaine penicillin IM

stat.
Tetracycline during discharge for 3 days.

CAF in infants and children can be used in place of

tetracycline 3-5 days.

70
 Prevention and control

 Control of vectors (louse)

 Personal hygiene

 Health education about hygiene and modes of disease

transmission.
 Delousing of patient’s clothes and his/her family

 Chemotherapy of cases and chemoprophylaxis for

contacts.
71
 4. Typhus
Typhus is an acute febrile illness caused by Rickettsia

bacteria.
Is a disease caused by bacteria (mainly Rickettsia typhi

or R. prowazekii).
There are two major types of typhus:

o Epidemic typhus.
o Endemic (or murine typhus)

72
 Rickettsiae
Group disease Bacterium vector Reservoir

Spotted fever

Rocky R. Rickettsii Ticks Dogs, rodents, ticks

mountain

Rickettsial pox R. akari Mites Mice

Typus group

Epidemic R. Prowazekii Human Humans

louse

Endemic R. Typhi Fleas Rodents

73
Scrub Orientia tsutsugamushi Mites Rodents
 Epidemic typhus (Louse-Borne Diseases )
 An acute rickettsial disease often with sudden onset.
 Infectious agent- Rickettsia Prowazeki

 Occurrence- In colder areas where people may live

under unhygienic conditions and are louse infected.

 Occurs sporadically or in major epidemics for example

during wars, famine when personal hygiene deteriorates

and body lice flourish.

Reservoir- Humans
74
 Con...
Mode of transmission-
 The body louse and head louse is infected by feeding on

the blood of a patient with acute typhus fever.

 Infected lice excrete rickettsiae in their feces and usually

defecate at the time of feeding.

 People are infected by rubbing feces or crushed lice in to

the bite or into superficial abrasions (Scratch

inoculation).
75
 IP: From 1 to 2 weeks, commonly 12 days.
 Con...
o POC: patients are infective for lice during febrile illness

and possibly for 2-3 days after the temperature returns to

normal.
o Infected lice pass rickettsiae in their feces with in 2-6

days after the blood meal; it is infective earlier if crushed.

o The louse die with in 2 weeks after infection.

o Rickettsiae may remain viable in the dead louse for

weeks.
76
 Clinical manifestation
 Early symptoms of fever, headache, mayalgia, macular

eruption appear on the body.

 Patient may have pneumonia, renal or CNS involvement,

GI disease, skin rash singly or in combination.

 Disease usually terminates by rapid lysis after 2 weeks of

fever.

77
 Diagnosis
Based on clinical and epidemiologic grounds.

Serologic test (weil-felix agglutination test)

Treatment
 Doxycycline 100mg PO BID for at least five days.

 CAF 50mg/kg maximum 2 g PO QID for five days for

pregnant mothers.

78
 Prevention and control
Delousing of clothes by insecticides or deeping in to

boiling water.
Public education on personal hygiene.

Treatment of cases.

Chemoprophylaxis for contacts.

79
 5. Filaria
- a roundworm
•Adult filaria live in body cavities, lymphatics, and
subcutaneous tissues
- adults 2 cm – 120 cm
•embryos (microfilaria) live in blood or dermis
-all require an insect or crustaean vector
 Lymphatic Filariasis… elephantiasis

It is a disease caused by the reaction of the body to the

presence of worms in the lymphatic system.

Infectious agent
Wucheriria bancrofti (vectors are culex, Anopheles and

Aedes species).
Brugia malayi (vector is mansonia species) and

Brugia timori (vector is Anopheles).

81
Loa Onchocerca

Wuchereria
Epidemiology

Found in Gambella region (west Ethiopia).

Reservoir- Humans are definitive hosts

MOT: by bite of mosquito harboring infective larvae.

IP: one month , but allergic inflammatory

manifestations may appear .

83
POC: Humans may infect mosquitoes when
microfilaria are present in the peripheral blood.
Microfilaremia may persists for 5-10 years or longer.

The mosquito becomes infective about 12-14 days after

an infective blood meal.

Susceptibility and resistance- Universal Susceptibility

84
85
 Clinical manifestation
 The presence of worms in the lymph vessels gives rise to

a foreign-body reaction.

Three phases may be distinguished:

a. Acute phase
 Starts within a few months after infection.

Lymphadenopathy

Fever

86
 Con...
Eosinophilia

In this stage microfilariae are not demonstrable in

the peripheral blood because the worms are not yet

mature.
The acute phase is mainly due to a

hypersensitivity reaction.

87
 b. Sub acute phase
 This occurs after one year following acute phases.

 Worms have matured and micro filariae are present in the

peripheral blood.
 Reactions to the adult worms cause attacks of fever with

lymphangitis, Epididymitis; recurrent attacks will sooner

or later lead to hydrocele.
 Lesions caused by microfilariae are less common and are

associated with hypereosinophilia and lung symptoms

88 (tropical pulmonary eosinophilia syndrome).
 c. Chronic phase
 After many years of repeated attacks, lymph glands and

lymph vessels become obstructed as a result of lymph

edema develops.
 Lymph edema commonly seen in the legs or scrotum

(elephantiasis) but may also be present in vulva, breasts,

or arms.
 Since the adult worms have usually died, microfilariae are

not seen in the blood.

89
90
 Diagnosis
 Clinical and epidemiological grounds.

 Obstructive signs with history and travel to and residence

in endemic areas.
 Best established by identifying microfilariae in the

peripheral blood (blood film).

-direct examination (thick or thin smear)

91
 Diagnosis.....
Before taking blood sample microfilariae appear in the

peripheral blood during the night (nocturnal).

Single dose of Diethylcarbamazin (DEC) causes the

sequestered microfilariae to emerge to blood 45-60

minutes later.
This test is said to be mazoti test used in nocturnal

periodicity.

92
 Treatment
 Diethyl carbamazin (DEC) 6mg/kg for 12 days results in

rapid disappearance of most microfilariae from blood.

 Because of this, we need to repeat DEC annually for

some years.
 Refer the patient for surgical treatment of hydrocele.

93
 Prevention and control

 Reducing the vector population

 Mass and selective treatment

 Personal protection against mosquito bite

94
 Unit 7
Prevention and control of food borne diseases

terms applied to illnesses acquired by

consumption of contaminated food
food borne infections
food poisoning- heavy metals and organic
compounds
food borne intoxications
95
 1. Staphylococcal food poisoning (intoxication)

 An intoxication (not infection) of abrupt and sometimes

violent onset.

Infectious agent (Toxic agent)

Several enterotoxins(A-E) of staphylococcus aureus

stable at boiling temperature.

Staphylococci multiply in food and produce the toxins.

 Occurrence- Wide spread and relatively frequent

 Reservoir- Humans in most instance; occasionally cows

96
  Mode of transmission

- By ingestion of a food product containing staphylococcal

enterotoxin.
- Foods involved are particularly those that come in contact

with food handlers’ hands, either with out subsequent

cooking or with inadequate heating or refrigeration,
e.g. salad, sandwiches, sliced meat and meat products,

pastries, etc.

97
 When these foods remain at room temperature for several

hours before being eaten, toxin producing staphylococci

multiply and elaborate the heat-stable toxin.
The organisms may be of human origin from purulent

discharges of an infected finger or eye, abscesses and

nasopharynyeal secretions.

Incubation period- 30 minutes to 8 hours, usually 2-4 hours.

Period of communicability- not applicable

Susceptibility and resistance- most people are susceptible.

98
 Clinical manifestation

Sudden onset of vomiting and watery diarrhea

Fever and abdominal cramp

The intensity of illness may require hospitalization.

99
 Diagnosis
Group of cases with characteristic acute predominantly

upper gastrointestinal symptoms and the short interval

between eating a common food item and the onset of
symptoms.
Culture –staphylococcal recovery (≥105organisms per gram

of food) or detection of enterotoxin from an

epidemiological implicated food item will confirms the
diagnosis.

100
 Treatment
Fluid and electrolyte replacement if fluid loss is

significant ,particularly in sever cases.

Prevention and Control

Educate food handlers in strict food hygiene, sanitation

and cleanliness of kitchens, proper temperature control,

hand washing, cleaning of finger nails, need to cover
wounds on the skim, etc.

101
 Prevention and Control..

Reduce food-handling time (initial preparation to

service) to an absolute minimum, with no more

than 4 hours at ambient temperature.
Keep perishable food hot (>60c0) or cold (below

10c0).
Temporarily exclude people with boils, abscesses

and other purulent lesions of hands, face or nose

102 from food handling.
 2. Botulism
A paralytic disease that begins with cranial nerve
involvement and progresses caudally to involve the
extremities.
a rare but potentially life-threatening neuroparalytic
syndrome
Infectious agent (Toxic agent)
 Toxin produced by Clostridium botulinum

103
 Epidemiology

Occurrence- Worldwide occurrence.

Home canned foods, particularly vegetables, fruits and
less commonly with meat and fish.
Out breaks have occurred from contamination through
cans damaged after processing.
Commercial products occasionally cause out breaks but
some of these out breaks have resulted from improper
handling after purchase.
Food born botulism can occur when a food to be
preserved is contaminated with spores.

104
 Reservoir- The bacteria is found in the soil and
in the intestine of animals
Mode of transmission- Food ingestion in which
preformed toxin is found
Incubation period- Neurologic symptoms of
food borne botulism usually appear with in 12-36
hours, some times several days, after eating
contaminated food.
Period of communicability- not communicable
Susceptibility and resistance- Susceptibility is
general
105
 Clinical manifestations
Illness varies from a mild condition to very severe
disease that can result in death with in 24 hours.
Symmetrical descending paralysis is characteristic
and can lead to respiratory failure and death
Cranial nerve involvement, marks the onset of
symptoms usually produces diplopia, dysphagia,
weakness progresses, often rapidly, from the head to
involve the neck, arms thorax and legs
the weakness is occasionally asymmetrical.
Nausea, Vomiting, abdominal pain may proceed or
follow the onset of paralysis
106
 Clinical manifestations..
Dizziness, blurred vision, dry mouth, and
occasionally sore throat are common.
No fever
Ptosis is frequent
Papillary reflexes may be depressed, fixed or
dilated pupils are noted in half of patients
The gag reflex may be suppressed
deep tendon reflexes may be normal or decreased.
Paralytic illus, sever constipation and urinary
retention are common
107
 Diagnosis

Appropriate History.
Clinical- Afebrile, mentally intact patients who
have symmetric descending paralysis without
sensory findings.
Demonstration of organisms or its toxin in
vomitus, gastric fluid or stool is strongly
suggestive of the diagnosis
Wound culture

108
 Treatment
Hospitalize the patient and monitor closely
Respiratory failure is the primary cause of
death in these patients.
Prompt intubation with mechanical ventilation
will dramatically decrease the risk of mortality.
Antitoxin administration after hypersensitivity
test to horse serum
Emesis and lavage if short time after ingestion
of food to decrease the toxin.

109
 Prevention and control
• Ensure effective control of processing and
preparation of commercially canned and
preserved foods.
• Education about home canning and other food
preservation techniques regarding the proper time
pressure and temperature required to destroy
spores, the need for adequate refrigeration,
storage, boiling with stirring home canned
vegetables for at least 10 minutes to destroy
botulinal toxin.
• Canned foods in bulging containers should not be
110
used or eaten or tasted
There are many types of Salmonella, including those that
3. Salmonellosis
cause typhoid fever and those that cause gastroenteritis
 A bacterial disease commonly manifested by an acute
enterocolitis.
enteric infection with nontyphoidal Salmonellae may be
clinically mild or even asymptomatic
Infectious agent
Salmonella typhimurium and
 Salmonella enteritidis are the two most commonly
reported.
Occurrence- World wide
Salmonella is the leading cause of foodborne illness in the
111
United States.
 Reservoir: Domestic and wild animals including
poultry, swine, cattle, rodents ,dogs, cats and
humans
Mode of transmission:
- ingestion of organisms in food derived from
infected food animals or contaminated by feces of
an infected animal or person.
- Raw and under cooked eggs and egg products
- raw milk and its products, contaminated water,
meat and its products, poultry and its products.
- Consumption of raw fruits and vegetables
112 contaminated during slicing
  Incubation period –from 6–72 hours, usually
about 12-36 hours
 Period of communicability- extremely
variable through the course of infection usually
several days to several weeks.
 Susceptibility and resistance- Susceptibility is
general and increased by achlorhydria, antacid
therapy, gastro intestinal surgery, prior or current
broad spectrum antibiotic treatment, neoplastic
disease, immunosuppressive treatment and
malnutrition
113
 Clinical manifestation
Self limited fever and diarrhea (bloody or
dysenteric when colon is involved)
Nausea, vomiting and abdominal cramp
Microscopic leukocytosis.
Highest Morbidity and Mortality among:-
Elderly/Infants, HIV infected individuals
Diagnosis
• Blood culture initially
• Stool culture
114
 Treatment
 Nontyphoidal Salmonella gastroenteritis is
usually self-limited.
Fever generally resolves within 48 to 72 hours,
and diarrhea within 4 to 10 days .
Diarrhea persisting more than 10 days should
lead to consideration of other diagnoses.

 Symptomatic
Antibiotic is indicated for metastatic infections
and immune suppressed patients
115
 Prevention and control
Improved animal rearing and animal
marketing
Quality testing of the known and commonly
contaminated food
Avoid consuming raw eggs or partially cooked
Wearing gowns and gloves when handling
stool and urine and hand washing after patient
contact.

116
 Unit 8: zoonotic diseases
Infectious diseases transmitted under natural
conditions between vertebrate animals and man
for most of these diseases man is a dead end of
the transmission cycle.
This means under normal conditions man will
not infect other human beings .

117
 Food of animals

1. Taeniasis
 Taeniasis is an intestinal infection with the
adult stage of large tapeworms.
Cysticercosis is a tissue infection with the
larval stage
Infectious agent
Taenia saginata (beef tapeworm)
Taenia solium (pork tape worm)

118
T. solium pork T. saginata beef
 Occurrence- World wide; frequent where
beef or pork is eaten raw or insufficiently
cooked and
- where sanitary conditions permit pigs and cattle
to have access to human feces.
- Prevalent in Latin America, Africa, South East
Asia and Eastern Europe.
 Reservoir- Humans are definitive host of both
species of Taenia; cattle are the intermediate
hosts for Taenia saginata and pigs for Taenia
solium.
120
  Mode of transmission- Eggs of Taenia
saginata passed in stool of an infected person
are infectious only to cattle in the flesh of which
the parasites develop in to “cysticercus bovis”
the larva stage of Taenia saginata.
 In humans-infection follows after ingestion
of raw or under cooked beef containing
cysticerci; the adult worm develops in the
intestine.

121
 Mode of transmission –
- Taenia Solium eggs to mouth of oneself or to
another person or ingestion of food or water
infected with eggs embryos escape from the
shells-penetrate the intestinal wall lymphatics or
blood vessels and are carried to the various tissues
where they develop to produce the human disease
of cysticercosis.
 Incubation period- 8-14 weeks, eggs appear in
stool in both species

122
 Period of communicability- T. saginata- not
directly transmitted from person to person but T.
solium may be.
- Eggs of both species are disseminated in to the
environment as long as the worm remains in the
intestine, some times more than 30 years;
- eggs may remain viable in the environment for
months.
 Susceptibility and resistance- Susceptibility is
general. No apparent resistance follows infection
but more than one tapeworm in a person has rarely
123
been reported.
 Clinical manifestation (for both species)
Symptoms of cysticercosis may appear from
days and stay for 10 years after infection
Passage of proglottidis (segmented adult
worms) in the feces and perianal discomfort
when proglottidis are discharged.
Minimal or mild abdominal pain,discomfort,
nausea, change in appetite, weakness and weight
loss.
Usually asymptomatic
Epigastric discomfort, nausea, a sensation of

124
hunger, weight loss, nervousness, and anorexia.
 Taenia solium (cysticercosis)

clinical

1. intracerebral space occupying (1.5 cm)

lesion (headaches, seizures, focal neurological
defects)

2. C.S.F flow obstruction (hydrocephalus)

3. basalar meningitis (cranial nerve palsies,

hydrocephalus)
 Diagnosis
Identification of proglottidis (segments)
eggs in feces or anal swab
cysticercus – palpable subcutaneous
cysticercus and microscopic examination of an
excised cysticercus confirms the diagnosis
intracerebral and other tissues- CT scan, MRI
or by x-ray when the cysticerci are calcified.

126
 Treatment
Single dose of praziqantel is highly effective,
15 mg/kg/ day in 3 doses
Albendazole 400 mg bid x 21 days
Niclosamide or
Mebendazole

127
 Treatment
T. Solium
Treatment is the same as to T. saginata but
praziqantel can evoke an inflammatory
response in the CNS if cryptic cysticercosis is
present.
Cysticercosis management .Chemotherapy,
Surgery and supportive medical treatment
For symptomatic patients with
neurocysticercosis admission is required.
Combination of Praziquantel and Albendazole
can be used.
128 high dose of glucocorticoids can be used to
 Prevention and control
Educate the public to:
Prevent fecal contamination of soil, water, human
& animal foods
Cook beef and pork thoroughly
Use latrine
Identification and immediate treatment of cases.
Freezing of pork/beef below –5c o for more than 4
days kills the cystraci effectively or cooking to a
temperature of 56co for 5 minutes distroys cystcerci
Deny swine access to latrines and human feces.
129
 2. Brucellosis
 A systemic bacterial disease with acute or
insidious onset transmitted to humans from
infected animals.
Infectious agent
 These are small aerobic gram-negative bacilli,
intracellular parasites.
Potential biowarfare agent
Brucella melitensis (most common cause world
wide) and acquired primarily from goats, sheep
and camels.
B. abortus from cattle
130
 Occurrence- World wide.
Predominantly an occupational disease of those
working with infected animals or their tissues
especially
- farm workers, veterinarians and
- abattoir workers which is more frequent among
males.
- Out breaks among consumers of raw milk and
milk products especially unpasteurized soft
cheese from cows, sheep and goats
Reservoir- cattle, swine, goats and sheep, pet
131 dogs.
 Mode of transmission- by contact with
tissues, blood, urine, vaginal discharges, aborted
fetuses and especially placentas (through breaks
in the skin).
Most commonly through ingestion of raw milk
and dairy products from infected animals (raw
meat or bone marrow).
Air borne infection occurs to humans in
laboratories and abattoirs
 Incubation period- may last about 1-3 weeks
but may be as long as several months
132
  Period of communicability- no evidence of
communicability from person to person
 Susceptibility and resistance- severity and
duration of clinical illness are subject to wide
variation. Duration of acquired immunity is
uncertain.

133
 Clinical manifestation

Abrupt onset of symptoms

Most common symptoms are: Fever, chills,
diaphoresis, headaches, myalgia, futigue,
anorexia, joint and low back pain, weight loss,
constipation, sore throat, and dry cough.

134
 Physical examination reveals
Often no abnormalities and patient looks
well
Some are acutely ill, with pallor,
lymphadenopathy, hepatosplenomegally,
arthritis, spinal tenderness, skin rash,
meningitis, cardiac murmurs, or pneumonia
Reactive asymmetric polyartaritis (knees,
hips, shoulders, sacroiliac and
sternoclavicular joints)

135
 Diagnosis
Exposure and consistent clinical features
Serology- raised levels of B. agglutinin
Blood or bone marrow culture on biphasic media (Ruiz-
Castaneda)
Treatments
Regimen A — Doxycycline 100 mg PO BID for six weeks plus
streptomycin 1 gram IM daily for the first 14 to 21 days.
Gentamicin can be substituted for streptomycin.
Regimen B — Doxycycline 100 mg PO twice daily plus
Rifampin 600 to 900 mg PO (15 mg/kg) once daily for six weeks.
Both regimens have comparable out come and high rate of
relapse.
Fluroquinolons and ceftriaxone also have effect against brucella,
136 but less effective.
 Prevention and Control

Control depends on elimination of the disease

among domestic animals
Educate people not to drink untreated milk or eat
products made form untreated milk.
Educate farmers and slaughter house workers
and those in meat processing plants and butchers
shop as to the nature of the disease and the risk
in the handling of carcasses and products of
potentially infected animals

137
 Prevention and Control…..

Educate hunters to use barrier precaution

(gloves and clothing)
Eliminate infected animals
Pasteurize milk, cook meat, and bone well.
Proper disposal of placental, discharges or
fetus from an aborted animal.
Disinfect contaminated areas.

138
3. Toxoplasmosis
Toxoplasmosis is a systemic protozal disease that
could be either acute or chronic type with intra
cellular parasite.
Infectious agent -Toxoplasma gondii
 Occurrence- World wide in mammals and birds.
- In united states and most European countries, the
prevalence of seroconversion increases with age
and exposure.
- In Central America, France, Turkey and Brazil
seroprevalence is much higher approaching 90%
139 by age of 40.
Epidemiology
Seropositivity
IgG /past or previous infection
IgM/early infection
IgA ~ 85% (in Ethiopia, general population)
Serology tests can help to exclude the
diagnosis when negative (in high
prevalence setting)

CNS disease increased in the era of HIV

TOXOPLASMOSIS

Cat - only host with sexual stage – sheds from

intestinal tract
Reservoir - cyst (bradyzoite) in many animals and
birds
Mode of transmission:
Ingestion of cysts in raw or under cooked meat
Ingestion of oocysts in food, drink or hand
contaminated with faces of an infected cat.
Trans placental /congenital
Blood transfusion
Organ transplantation
 Vertical transmission to fetus
Toxoplasmosis infection in mother
Trimester

before
pregnancy I II III

% of fetuses 0% 15 % 30 % 60 %
infected

severity of 0 +++ ++ +
sequelae
There are five main developmental forms
in the life cycle, but only trophozoites and
cyst stage are found in human but all stages
occur in the felines (cats)
Toxoplasma has two forms
Tachyzoite- occur in the early acute stage of
infection
Bradyzoites- occurs in the chronic stage of
infection develops slowly and multiplies in the
tissue to form a true cyst.
143
Definitive host
Incubation period- from 10-23 days. One
common source out break from ingestion of under
cooked meat is possible.
Period of communicability- Not directly
transmitted from person to person, except in
utero.
Oocysts shed by cats sporulats and become
infective 1-5 days later and may remain infective
in water or moist soil for about a year.
 Cysts in the flesh of an infected animals remain
infective as long as the meat is edible and
145
uncooked.
  Susceptibility and resistance- general, but
immunity is readily acquired and most
infections are asymptomatic.
Duration and degree of Immunity are unknown,
but assumed to be long-lasting or permanent.
Antibodies persist for a year probably for life.
Patient undergoing cytotoxic or
immunosuppressive therapy or patient with
AIDS are at risk of developing the disease.

146
 Clinical manifestation

General symptoms:. The acute form of this

disease is characterized by
fatigue, lymphodenitis,
chills, fever, headache and myalgia.
In addition to chronic disease patient may
develop maculopapular rash, encephalomyelitis
and hepatitis, retinochoriditis with subsequent
blindness has been known to occur on rare
occasions.

147
 Clinical manifestation..
Congenital Toxoplasmosis: The typical
symptoms, an infected child experience includes
hydrocephaly,
microcephaly, choreoretinitis,
convulsion and psychomotor disturbance.
Most of these infections ultimately result in
mental retardation, sever visual impairment or
blindness.

148
 Diagnosis

Clinical sign and symptom

Serological test
Demonstration of the agent in body fluid or
tissue biopsy
cell culture

149
 Treatment
Treatment is not routinely indicated for a
healthy immunocompetent host, except in an
initial infection during pregnancy or the
presence of active choreoretinitis and
myocarditis or other organ involvement.
For pregnant women, Spirmycin is commonly
used to prevent placental infection.
If ultrasound or other studies indicate that fetal
infection has occurred, Pyrimethamine and
sulfadiazine should be considered.
150
 Treatment

Pyrimethamine 2 mg/kg once daily for two

days; then 1 mg/kg once daily for six months;
then 1 mg/kg every other day to complete one
year of therapy, plus
Sulfadiazine 100 mg/kg per day divided in two
doses every day for one year, plus
Folinic acid ( leucovorin ) 10 mg three times
per week for 4week

151
 Prevention and control..
The cause of primary infection with Toxoplasma can
be reduced by avoiding eating under cooked or raw
meat and avoiding cyst contaminated materials (i.e
cat’s lifter box)
Meat should be heated to 600c or frozen to kill cysts.
Hands should be washed thoroughly after work in the
garden and all fruits and vegetables should be washed.
Discourage cats from hunting
Dispose cats feces daily.
Control stray cats and prevent them from gaining
access to sand boxes and sand piles.
152
 Prevention and control..
Educating pregnant women
To avoid cleaning lifter pans or contact with
cats.
To wear glove during gardening.
Blood intended for transfusion in to Toxoplasma
seronegative immuno compromised individuals
should be screened for antibody to toxoplasma
gondii.
Patients with HIV/AIDS who have severe
symptomatic toxoplasmosis should receive
treatment (Prymethamine, sulfadizine, folinic acid)
153
 Animal bite diseases
1. Rabies
 It is a fatal disease resulting in acute vial
encephalomyelitis (attacking brain and meanings)
Infectious agent
Rabies virus
Epidemiology
 Occurrence- world wide in wildlife particularly in
developing countries.
It is primarily a disease of animals (zoonotic).
It is primarily an infection of carnivours transmitted
through bite.
154
  Reservoir- Dog is common in urban areas, in the
wild life wild carnivors and bats.
 Mode of transmission- Transmitted with saliva of
rabid animal introduced by a bite or scratch.
Transmission from man to man is dead ended
 Incubation period- average 1-2months
 Period of communicability -is usually 3-7 days
before the onset of the disease and through out the
course of the disease
 Susceptibility and resistance- all mammals are
susceptible to varying degrees. Humans are more
resistant to infection than several animal species
155
 Clinical Manifestation
 The clinical manifestation which is the same
in all species including humans has 2 phases.
Prodromal phase
Encephalitic phase
I. Prodromal phase: lasts for about a week
sense of anxiety, head ache, fever and nausea
abnormal sensations referred to the site of
inoculation (bite) is most significant
paraesthesia, tingling sensations at the bite site

156
 Clinical Manifestation….
II. Encephalitic phase – lasts for about a week.
excessive motor activities, excitation, agitation,
confusion, hallucinations,
bizarre thoughts, muscle spasm, meningismus
seizure, paralysis.
Excessive sensitivity to bright light, loud noise,
touch.
They will have high grade fever (eg 40.60C)
Two third of patients have hydrophobia or
aerophobia
157
 Diagnosis
History of bite by known rabid animal and the
bitten person shows typical symptoms leading to
clinical diagnosis
Treatment
1. Wound Care
Wash the wound with soap and water thoroughly to
decrease the viral load
If there is bleeding cover the wound
Never suture the wound as this will spread the
virus
There is no proven effective antiviral therapy
158
 Prevention and control

Immunize all dogs and cats

Detain and clinically observe for 10 days any
healthy appearing dog or cat known to have
bitten a person.
Post exposure prophylaxis - Rabies immune
globulin
Treatment of bite wounds
Keep dogs and cats at home
Destroy stray animals where rabies is endemic.

159
 Rabies pre-exposure prophylaxis

Human diploid cell vaccine (HDCV) or purified

chick embryo cell vaccine (PCECV); 1 mL (deltoid
area), one each on days 0, 7, and 21 or 28
Post exposure prophylaxis
– Whenever there is animal bite wound should be
thoroughly cleaned, TAT and antibiotic given.
– Known domestic animal (dog, Cat) –can be observed
for 10 days, and if healthy, there is no need for PEP.
Rabies postexposure prophylaxis should begin as
soon as possible after the presumed exposure.

160
 Unit 9: Other infectious diseases

Tetanus
Clostridium tetani ,Gram positive spore forming
anaerobic rod
Reservoir – soil
Transmission – puncture wounds, trauma, human bites
Pathogenesis
– Spores germinate in tissues and produce tetanus
toxins
– Tetanospasmin – neurotoxic
– Tetanolysin –hemolytic , tissue lysis
161
 Forms
generalized, localized, cephalic, neonatal

Definition of terms:
– IP – time gap b/n injury and first symptom (trismus)
– Onset time – time between trismus and first spasm
– Risus sardonicus – recession of the lips backward
and a grinning like grimace
– Opisthotonus – backward arched posture
– Trismus (lockjaw) 20 to masseter muscle
hypertonicity
162
 Generalized tetanus
Most common presentation of tetanus
Trismus (lockjaw) 20 to masseter muscle
hypertonicity
Neck, shoulder and back muscle stiffness and
pain
Rigid abdomen and stiff proximal limb muscles
 Risus sardonicus, Arched back (Opisthotonus)
generalized muscle spasm, apnea /Cyanosis
/laryngospasm
 Hyperpyrexia with clear mentation
163
 Severity of generalized tetanus

Mild tetanus Moderate tetanus • Severe tetanus

IP > 14 days IP= 7 -14 days - IP <7 days
Onset time >7days Period of onset - Period of onset <
Mild trismus 3-6 days 3days
- frequent explosive
Localized spasm and Marked trismus
spasms
rigidity Mild dysphagia
- spontaneous
No autonomic dysfn Rigidity and spasm
spasm - asphyxia
No autonomic - Autonomic
dysfn dysfunction

164
 Complications
Aspiration pneumonia
Vertebral fracture
Muscle rupture
Decubitus ulcer
Rhabdomyolysis (pigment-induced nephropathy)
Autonomic dysfunction - Labile or sustained HTN,
Tachycardia, Hyperpyrexia, Profuse sweating,
Bradycardia and hypotension episodes, Sudden
cardiac arrest
165
 Neonatal tetanus
Generalized form of tetanus
Develops in neonates born in unimmunized mothers after
unsterile treatment of the umbilical cord stump
Occurs within 2 weeks of neonatal life
Manifests with poor feeding, rigidity and spasm
High rate of mortality

Local tetanus
Uncommon form of tetanus
Manifests with localized muscle contraction near the wound
good prognosis

166
 Cephalic tetanus
Rare form of local tetanus
Follows head injury or ear infection
Manifests with trismus and CN palsy (often VII
CN)
High mortality

Diagnosis
Entirely on clinical findings
Spatula test – gag stimulation causes masseter
muscle spasm
167
 General measures
Admit in a quiet ICU with a possibility for continuous
monitoring
Hydration ,Nutritional support (IV/PO)
Physiotherapy to prevent contracture
psychological support, analgesia
Treatment of superimposed infection eg aspiration
pneumonia
Treatment of source infection
Antibiotic therapy to eradicate vegetative C.Tetani;
choice are: Metronidazole, Penicillin, Clindamycin,
Erythromycin
wound debridement
168
Control of muscle spasm
Benzodiazepines (Diazepam, midazolam), Barbiturates,
chlorpromazine
Respiratory care
Intubation / Tracheostomy + mechanical ventilation for
adequate oxygenation
Vaccine - Tetanus toxiod
Indicators of poor outcome
• Neonates /elderly
• Short IP (< 3 days)
• Short period of onset (< 48 hrs)
• Presence of autonomic dysfunction
169
Unit 10

Sexually Transmitted Infections

170
 Learning objectives

At the end of this chapter, the student will be able to:

 List the common sexually transmitted diseases

 Identify the diagnostic symptoms of sexually transmitted

diseases.
 Apply the management of sexually transmitted diseases

 State the preventive and control measures for sexually

transmitted diseases

171
 Introduction

STI – Infections acquired through sexual intercourse (may

be symptomatic or asymptomatic)
STD – Symptomatic disease acquired through sexual

intercourse
STI is most commonly used because it applies to both

symptomatic and asymptomatic infections

172
 Introduction….
The diseases belonging to this group are usually

transmitted during sexual intercourse.

During sexual intercourse there is close body contact,

which is an ideal situation for transmission.

 STDS are very common in adults.

 Single young men are a high – risk group for STDS, as

they satisfy their sexual needs with women who have

many sexual partners.
173
 Distribution of STIs

 Prevalence is higher in urban than rural

 Higher in unmarried & young adults

 More frequent among females than males between the

ages of 14-19.

in people with untreated STIs, the complications

and sequel can be devastating.

174
 STI statistics are underestimated
Due to:

People with asymptomatic STIs do not seek treatment.

Poor access: health facilities offering treatment for

STIs may be too far away for many people.

Missed opportunity: people seeking other health care

such as antenatal services may not be routinely

screened for STIs.

175
 Underestimation.......
Stigma: many patients perceive a stigma in attending

modern STIs services.

Non-reporting facilities: large number of people visit

private and traditional care providers that are not

reporting.
Cost of services etc…

176
 Factors Affecting Transmission
 Socio-economic
 Behavioral Factors
-Poverty
-Many partner
-Religious Restrictions
-Change of partners
-Not using condoms - Women’s position
 Cultural
- Casual sex

- Sex with CSW & partner -Harmful traditional practices

- Alcohol & substance use  Biological & clinical

- Asymptomatic STIs
 Personal factors
- Age
- Delay in getting Rx
- Stigma being ashamed - Sex

177 - - Vulnerability, immunity

Noncompliance to Rx
 Causes of STIs

1. Bacteria -Neisseria gonorrhea (gonorrhea)

-Treponemia palladium (syphilis)

-Chlamydia trachomatis (Chlamydia)

-Haemophilus ducryi (Chancroid)

178
 Causes.....
2. Viral - herpes simplex type 1 and 2

- human papilloma virus (genital warts)

- hepatitis B virus

- Cytomegalo virus and

-HIV virus

3. Protozoal- Trichomoniasis (tricomonas vaginalis)

4. Fungal –Candidia albicans(Vaginal candidiasis)

5. parasitic –sacroptos scabis (scabis)

179
 1. Gonorrhea

 It’s a sexually transmitted infection of epithelium and

commonly manifests as cervicitis, urethrits, Proctitis&

conjunctivitis.
 N.gonorrhea: are gram negative diplococci, nonmotile,

nonspore forming.
 Highest incidence occurs in developing countries.

 Transmition from males to females is more efficient than

in the opposite direction.

180
 Clinical features
Males:- acute urethritis is the most common clinical
feature.
IP is 2 to 7 days.

Urethral discharge & dysuria, usually without urinary

frequency and urgency, are the major symptoms.

The discharge is initially scanty & mucoid but becomes

profuse and purulent within a day or two.

181
 Females
Gonococcal cervicitis
 ed vaginal discharge and dysuria (often with frequency

and urgency ) are the most common symptoms.

IP is about 10 days

P\E reveals a mucopurulent discharge from the cervical

os.

Complications include dyspareunia, lower

abdominal or back pain, endometritis, PID,

183
infertility.
www.afraidtoask.com
 Con....

 Gonococcal vaginitis:

 Red & edematous vaginal mucosa with abundant vaginal

discharge.
 Anorectal gonorrhea

 Pharyngeal gonorrhea

 Disseminated gonococcal infection (DGI) :- results from

gonococcal bacteremia.

- It has two stages:- a bacteremic stage & a joint localized stage

185 with suppurative arthritis.
Gonococcal Infections in
Women & Men

 Urethritis
 Proctitis
 Pharyngeal infections
 Conjunctivitis
 Disseminated Gonococcal
Infection
 Disseminated Gonococcal Infection

Gonococcal bacteremia

Sources of infection include symptomatic and

asymptomatic infections of pharynx, urethra, cervix

Occurs in < 5% of GC-infected patients

More common in females

 DGI Clinical Manifestations
“Dermatitis-arthritis syndrome” Arthritis: 90%
- Characterized by fever, chills, skin lesions, arthralgias
Less commonly, hepatitis, myocarditis, endocarditis,

meningitis
Rash characterized as macular or papular, pustular,

hemorrhagic or necrotic, mostly on distal extremities

DGI Skin Lesion
 Necrotic,
grayish
central lesion
on
erythematous
base

STD Atlas, 1997

Gonococcal Complications in Pregnancy

 Gestational bleeding
 Preterm labor and delivery
 Premature rupture of membranes
 Septic abortions
 Postpartum endometritis
 Post-abortal PID
Vertical Transmission and Neonatal Complications on
Gonorrhea

Overall vertical transmission rate ~30%

Neonatal complications include:

Ophthalmia neonatorum

Disseminated gonococcal infection

(sepsis, arthritis, meningitis)

Vaginal and rectal infections

Pharyngeal infections
 Laboratory diagnosis
Gram’s staining of urethral exudates

culture of urethral discharge - Thayer- Martin media

PCR DNA detection

Blood cultures in DGI

Synovial fluid culture

192
 Treatment

1. Uncomplicated gonococcal infection

 Ceftriaxone 125 mg IM stat

Alternatives - Spectinomycin 2gm IM stat

Cefotaxime 500 mg IM stat

2. Disseminated Gonococcal Infection

Higher dosage and longer duration of Rx

193
 2. Chlamydia
 Caused by Chlamydia Trachomatis

 Reservoir – human genital tract and eyes

 Transmission - sexual, at birth, hand to eye contact

 Pathogenesis - Granuloma formation and damage of

infected mucosal cells by Chlamydial Trachomatis

194
 C. trachomatis......
STDs – by serotypes D-K

- manifested by: urethral discharge, dysuria and urethral

itching.

P\E:- meatal erythema and tenderness and urethral exudate.

195
 Con...
Epididymitis

CF - unilateral scrotal pain, fever and epididymal

tenderness or swelling on P\E.
Reiters syndrome: - consists of conjunctivitis, Urethritis

(or cervicitis in females), arthritis and characteristic

mucocutaneous lesions.

196
 Con...
Proctitis - mild rectal pain, mucosal discharge, tenesmus

and bleeding.
PID - tubal scarring  infertility; ectopic pregnancy

Inclusion conjunctivitis and pneumonia in neonates.

197
 Lymphogranuloma venereum

LGV - sexually transmitted infection caused by C.

trachomatis strains of the L1, L2 and L3 serovars.

C/F

Primary genital lesion develops 3 days to 3 weeks after

exposure & heals in a few days without scarring.

The inguinal syndrome (commonest presentation) is

characterized by painful inguinal LAP in 2 to 6 weeks

after presumed exposure.
198
 Con...

The nodes are initially discrete  then matted mass of

nodes fluctuant & suppurative multiple draining

fistulas
Spontaneous healing occurs after several months 

inguinal scars\granulomatous masses.

constitutional symptoms are common during the stage of

regional LAP
late Cxns: genital elephantiasis, strictures and fistulas of

199 the penis, urethra and rectum.

200
201
 Diagnosis
 Direct microscopy of tissue for inclusion bodies

 Cell culture isolation

 antigen or nucleic acid detection.

 antibody detection in serum or in local secretions

202
 Treatment
Uncomplicated infections - Azithromycin 1 gm PO stat
OR Doxycycline 100 mg po bid for 7 days/,
Tetracycline 500 mg po qid for 7 days/.
 Complicated infections (e.g.PID, epididymitis) - 2 weeks

course antibiotics.
 Lymphogranuloma venereum- 3 week course.

doxycycline 100 mg PO twice daily for 21 days

erythromycin 500 mg four times daily as a

203
second-line choice
 3. Chancroid
Etiologic agent: Haemophilus ducreyi, a highly fastidious

gram-negative coccobacilli
IP - 4 to 7 days

The initial lesion is a papule with surrounding erythema &

in 2 to 3 days  pustule  spontaneously ruptures 

ulcers which are painful and bleed easily
Half of the patients develop enlarged, tender inguinal LNs,

which frequently become fluctuant and spontaneously

204
rupture.
Clinical Features (contd.)
 Dx
 Gram’s staining - gram negative coccobacilli.

 Culture - accurate diagnosis from the lesion; aspiration of

suppurative lymph nodes.

Treatment
o Ceftriaxone 250mg IM stat

o Azithromycin 1gm po stat

o Erythromycin 500mg po QID for 7 days

o Ciprofloxacin 500mg po BID for 3 days

206
 4. Genital Warts (Condylomata Acuminate)

Soft, skin-colored, fleshy warts occurring on ano-genital

or oral mucosa or skin.

Caused by infection with a mucosal type of human

papillomaviru (HPV).

in adults is commonly caused by HPV 6 and 11

207
 Con....
 Transmitted sexually and nonsexually.

 softening and , breaks of the skin is an important

predisposing factor
 Oral lesions have also been detected.

 They vary in size and can form large, exophytic

(“cauliflower-like”) masses.

208
209
210
 Diagnosis
o Visual and Colposcope may be needed.

o Papanicolaou’s smear

o PCR

Treatment
Cryosurgery

Podophyllin 0.5 % solution

Trichloroacetic Acid 80 % to 90 %.

Electrodesiccation/Electrocautery
211
Intralesional Interferon
 5. Herpes Genitalis
o The most common viral STDs.

Etiology

HSV I Oral (genital) cold sores.

HSV II Genital Herpes

o HSV is ubiquitous.

o Most individuals show evidence of infection due to HSV

212
Herpesviridae
1. HSV I Oral (genital) coldsores
2. HSV II Genital Herpes
3. VZV
4. CMV
5. EBV
6. HHV 6
7. HHV 7
8. HHV 8
Transmission is usually sexual and skin-to -skin

contact
Aerosol or fomitic spread unlikely

 primary infection at inoculation site,

-HSV ascends peripheral sensory nerves and

enters sensory or autonomic nerve root ganglia,

where latency is established
IP 2 to 20 days (Average 6).
 Clinical Features
50 % to 70 % of HSV-2–infected individuals are

asymptomatic
Primary Genital Herpes: An erythematous plaque

followed soon by grouped vesicles.

- Severe illness with aseptic meningitis may occur.

Recurrent Genital Herpes: Lesions similar to primary

infection but on a reduced scale. Heals spontaneously

with in 1 to 2 weeks. Meningitis may occur.
 Clinical Features
characterized by multiple, shallow, tender ulcers that

may be vesicular; a history of recurrent disease may

be elicited
Reactive painful nodes common
217
 diagnosis

Clinical

Wright’s, Giemsa’s or papanicolaou’s stain

Best confirmation:- isolation of virus in tissue

culture
demonstration of HSV antigens or DNA in

scrapings from lesions.

218
 Treatment

Acyclovir 200 mg PO five times a day for 7 to

10 days.
Best benefit if started with in 2 days of

symptoms.
Genital herpes may be recurrent and has no

cure
 6. Syphilis

o Etiology:- Treponema pallidum.

o gram-negative rods.

o A member of a family Spirochaeteceae.

o Because of inability to grow in culture, the diagnosis of

syphilis depends upon

- the sexual exposure history

- recognition of variable clinical signs and symptoms, and

- interpretation of diagnostic testing.

220
 Transmission

Almost always sexual, rarely – vertical, blood

transfusion, organ transplantation

Penetrate intact mucus membrane and micro abraded

skin.
500-1000 organisms for naturally acquired infections.

Median IP = 3 weeks

221
Clinical Features
 Clinical forms

A. Primary syphilis:
Hard chancre: Clean based, non tender, indurated single

genital ulcer with bilateral non tender inguinal LAP.

o Multiple 10 lesions in men with HIV infection.

o Atypical l 0 lesion is common: depends on inoculums'

dose and host immunity.

Eg. Papules only with small inoculums dose.
o Persist for 4-6 weeks and then heals spontaneously.

223
 B. Secondary Syphilis
Constitutional, mucocutaneous and parenchymal

manifestations after 6- 8 wks of 10 lesion healing.

Mucocutaneous lesions with generalized LAP.

Macules, Papules, papulosquamous lesion over the

trunk, proximal extremities, and palm and sole.

Constitutional symptoms (as many as 30%).

224
Rash (contd.)
Lymphadenopathy
Condyloma lata
Large, raised, gray to white lesions, involving warm,

moist areas such as mucous membranes in the mouth

and perineum,
which occur before or soon after the rash and are

highly infectious
Condylomata lata
 C. Latent syphilis

 Patients are symptom free and diagnosis is by serologic test

but infectious.
Early latent syphilis - Occurs within 1 yr of developing 10

syphilis.
Late latent syphilis - Occurs after 1 yr of infection or

unknown duration.
 70% of untreated cases do not develop clinical late syphilis

(late latent and 30 syphilis) but spontaneous cure is doubtful.

229
 D. Tertiary syphilis
The result of a chronic, progressive

inflammatory process that eventually produces

clinical symptoms years to decades after the
initial infection.
This stage is characterized by destructive,

non-infectious lesions of the skin, bones,

viscera, and mucosal surfaces.
Tertiary syphilis
Most common neuro syphilis

Decrease peripheral reflex due to CNS involvement

General paresis

change in personality

Sensation change

Ocular abnormality like pupil are small and irregular not

reactive to light
Affects the heart (aortits, aortic incompetence, stenosis)

affect CNS( neuro-syphilis, dementia....)

Cardiovascular Syphilis 10-40yr

1) Aortitis
2) Aortic aneurysm,
3) Aortic insufficiency;
4) Coronary ostial stenosis
 Symptomatic neurosyphilis

Categories Onset of symptoms after

infection
Meningeal neurosyphilis <1 yr
Meningovascular syphilis 5-10 yrs
General Paresis 10-20 yrs
Tabes dorsalis 25-30 yrs

Usually present with mixed, subtle or incomplete

syndromes

233
Cutaneous Gummata
Tabes Dorsalis- is z final complcn
 Diagnosis
Serological test (VDRL) – will be positive 6 to 8 weeks

after infection.
 Dark field microscopy of smears from primary lesion

(hard chancre) or from skin lesions in the early

secondary stage will show the spirochaetes.

236
Table 162-2 Recommendations for the Treatment of Syphilis a

Stage of Syphilis Patients without Penicillin Allergy Patients with Confirmed Penicillin
Allergy
Primary, Penicillin G benzathine (single dose Tetracycline hydrochloride (500 mg PO
secondary, or early of 2.4 mU IM) qid) or doxycycline (100 mg PO bid) for
latent 2 weeks
Late latent (or Lumbar puncture Lumbar puncture
latent of uncertain CSF normal: Penicillin G CSF normal and patient not infected
duration), benzathine (2.4 mU IM weekly for 3 with HIV: Tetracycline hydrochloride
cardiovascular, or weeks) (500 mg PO qid) or doxycycline (100 mg
benign tertiary CSF abnormal: Treat as PO bid) for 4 weeks
neurosyphilis CSF normal and patient infected with
HIV: Desensitization and treatment with
penicillin if compliance cannot be
ensured
CSF abnormal: Treat as neurosyphilis
Neurosyphilis Aqueous penicillin G (18–24 mU/d Desensitization and treatment with
(asymptomatic or IV, given as 3–4 mU q4h or penicillin
symptomatic) continuous infusion) for 10–14 days
or
Aqueous penicillin G procaine (2.4
mU/d IM) plus oral probenecid (500
mg qid), both for 10–14 days
 The link between STI and HIV/AIDS
Certain STIs facilitate the spread of HIV. In
fact, the interrelationship between STI and HIV
is more complex, in that:
- Certain STIs facilitate the transmission of HIV
- The presence of HIV can make people more
susceptible to the acquisition of STIs
- The presence of HIV increases the severity of
some STIs and their resistance to treatment

238
 Approaches to STI diagnosis
 Classical approaches

Etiologic diagnosis – using lab to identify the causative agent

Clinical diagnosis –using clinical experience to identify

causative agent
Syndromic: identifying & treating the Syndrome

- a group of symptoms patient complains & clinical signs you

observe during examination

- Different organisms that cause STIs give rise to limited

239 number of syndromes.

 Etiologic diagnosis

Advantages:-

Avoids over treatment

Satisfies patients who feel not properly attended too.

Can be extended as screening for the asymptomatics.

240
 Disadvantages of etiologic approach

 Requires skilled personnel & consistent supplies

 Treatment does not begin until results are available

 It is time consuming & expensive

 Testing facilities are not available at primary level

 Some bacteria are fastidious & difficult to culture (H.ducrey,

C.trachomatis)
 Lab results often not reliable.

 Miss-treated/untreated infections can lead to complications and

241
continued transmission.
 Principles of Syndromic Approach
STI sign and symptoms are rarely specific to a particular

causative agent.
Laboratories are either non-existent or non functional

due to lack of resources.

Dual infections are quite common and both clinician and

laboratory may miss one of them.

Waiting time for lab results may discourage some

patients.
242
 Advantages of Syndromic management
 Problem oriented (responds to patient’s symptoms )

 Highly sensitive & does not miss mixed infections.

 Treats the patient at first visit.

 Can be implemented at primary health care level.

 Use flow charts with logical steps.

 Provides opportunity & time for education & counseling.

 Saves time for patients

 Reduces laboratory expenses

243
 Limitations of Syndromic management

Risk of over treatment .

Misses sub-clinical infection.

Needs validation study.

- Require prior research to determine the common causes

of particular syndrome and its treatment.

Asymptomatic infections are missed.

Needs training
244
 Treat the seven syndromes

245
 1. Urethral Discharge
Etiologic agents:

 N.gonnorhea

 C. Trachomitis

Treatment
Ceftriaxone 250mg IM stat
Plus
Azithromycin 1gm po stat

246
 Flow chart for UD

247
 Management of Recurrent/Persistent Urethritis

Look for objective signs of urethritis

Possible causes for recurrence/reappearance

non-compliant or i.e. inadequately treated or

re-infected - Re-treat with initial regimen

T. Vaginalis- Treat with Metronidazole 2 gm p.o. Stat

Drug resistance

248
 2. Genital Ulcers

249
 Etiologies
Vesicular
HSV2: Genital Herps
Non-Vesicular
T. Pallidum: Syphilis
H. Ducreyi: Chancroid
LGV(rare)

250
 Treatment
Acyclovir 400mg po tid for seven days plus

Bezanthine Peniciline 2.4 mIU IM stat or

Doxicycline 100mg po bid for 14 days (for

Penicillin allergy) Plus
Ciprofloxacillin 500mg po bid for 3 days

251
 Vaginal discharge syndrome
Etiologies:

Sexually transmitted

Neisseria gonorrhoeae

Chlamydia trachomatis

Trichomonas vaginalis

Endogenous infection

Candida albicans1

252
 Initial evaluation of patients with vaginal
discharge include
Risk assessment

o Age less than 25 years

o Having multiple sexual partner in the last three months

o Having new partner in the last three months

o Having ever traded for sex

o Clinical speculum examination to determine site of

infection.
253
 Flow chart

254
 Recommended treatment

255
 Lower Abdominal Pain(PID)

Infection of pelvis not related to pregnancy or surgery

Ascending infection of the uterus , fallopian tubes,

ovaries and or adjacent structures

Sexually transmitted: N.gonorrhea, C.trachomatis

May or may not be sexual: Anaerobes i.e. (poly

microbial)
Bacteroids, Streptococcus, E. Coli, H. Influenza.

256
 treatment
The preferred regimen is Ceftriaxone 250mg IM
stat plus Azithromycin 1gm po stat plus
Metronidazole 500 mg bid for 14 days

Scrotal Swelling
N.gonnorhea
C.trachomatis
The preferred regimen is Ceftriaxone 250mg IM
stat plus Azithromycin 1gm po stat
257
 Inguinal bubo
H.ducreyi
C. Trachomatis Serovars
L1-L3: LGV
K.Granulomatis
Treponema pallidum

Treatment
Ciprofloxacin 500mg bid orally for 3 days Plus
Doxycycline 100 mg bid orally for 14 days /
If patient have genital ulcer, add Acyclovir 400mg tid
orally for 10 days
258
 HIV/AIDS
AIDS was first recognized in the United States in 1981,

unexplained occurrence of Pneumocystis jiroveci (formerly P.

carinii) pneumonia in five previously healthy homosexual men
in Los Angeles and of Kaposi's sarcoma (KS).
In 1983, human immunodeficiency virus (HIV) was isolated

from a patient with lymphadenopathy

by 1984 it was demonstrated clearly to be the causative agent of

AIDS.
259
In Ethiopia, the first confirmed cases of HIV were

detected in 1984 and the first hospitalized AIDS

patients were reported in 1986
The Ethiopian free ART program was launched in 2005

Currently, 98.5 % of the patients are on first line

regimens.
 HIV
HIV stands for human immune deficiency virus.
Viruses are simple in structure and cannot replicate alone
and thus they require the components of other cells to
replicate
Viruses need a receptor on the cell surface in order to
attach themselves and get inside.
In order for a cell to be infected by HIV, there must be
CD4 receptor molecules present. These receptors occur
on Tcells and other cells in the monocyte-macrophage
cell lines.
Thus HIV infects these cells and uses them for its

261
multiplications.
 Transmission
Sexual transmission

Blood transfusion

Mother to infant

Accidental occupational exposure

262
 Typical Risk of Unprotected Exposures

Estimated Average Per Contact Transmission Risk (%)

Receptive anal sex 1%

Shared Needles 0.7%
Occupational Needle stick 0.3 %
Male to female, vaginal sex 0.2%
Female to male, vaginal sex 0.1%
Insertive anal sex 0.1%
Receptive oral sex with male 0.03%
 HIV can be transmitted through:
Transfusion of infected blood or contaminated
products made from infected blood.
Needles and syringes with infected blood (even
small quantities).
Perforating or cutting instruments contaminated
with infected blood.
Transplantation of organ donated by HIV
infected person

264
 vertical transmission or perinatal transmission

100 infants born to HIV-infected women who

breastfeed;
55–80 infants will not be HIV infected, 20–45
infants will be HIV-infected
5–10 infants infected during pregnancy
10–15 infants infected during labour and delivery
5–20 infants infected during breastfeeding

265
 risk factors influence MTCT of HIV

Maternal factors:
High viral load
Low CD4 count with advanced disease
Prolonged rupture of membrane
HIV infection during pregnancy/ breast
feeding
Mixed feeding
Crackled nipples and breast abscess

266
 risk factors influence MTCT of HIV

Infant factor:
Prematurity
Oral thrush and ulcer
Birth order (first twin) in twin pregnancies
Invasive fetal monitoring during labor and
delivery
Instrumental delivery

267
 The clinical course of HIV infection has three
stages.
i. Primary HIV infection
ii. Asymptomatic stage/latent infection
iii. AIDS

268
 Primary HIV Infection
The period immediately after infection characterized by

high level of viremia (>1 million) for a duration of a few

weeks
Associated with a transient fall in CD4

Patients develop non-specific ‘flu-like’ symptoms, which

do not lead directly to the diagnosis of HIV infection

because the symptoms are nonspecific. These symptoms
include;
Fever, Fatigue, Pharyngitis, Lymphadenopathy, Rash etc
269
 Primary HIV infection: Significance
Primary infection resolves as body mounts HIV-specific

adaptive immune response

Difficult to diagnose (window period)

Very high viral load; most infectious phase. It may

account for 40% of all transmissions

Massive depletion of CD4 lymphocytes mostly in the GIT
 AIDS
After several years, the person’s immune
system will be very weak;
they are vulnerable to diseases that they could
normally fight off.
These diseases are called opportunistic
infections (OIs) because they take advantage of
a weakened immune system to cause disease.

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 Patterns of HIV Disease Progression varies
Typical progressors account for 90% of
individuals who can stay for 8-10 years before
developing symptoms. The viral set point is
medium in this group.
2. 5% of individuals are called rapid progressors
because they develop AIDS within 3years. Often
this group of patients has high viral set point.
Up to 10% individuals will have stable CD4
count for more than 8 years and are called long
term non-progressors. This group has
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remarkably low viral set point.
 WHO clinical staging
Clinical stage 1

- asymptomatic

- Persistent generalized lymphadenopathy (non-tender,

enlarged lymphnodes of greater than 1cm in 2 or more
non-contiguous sites (excluding inguinal) and persisting
for ≥3 months

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Clinical stage 2
 Moderate unexplained weight loss (>5 and <10% of presumed or

measured body weight)

 Recurrent upper respiratory tract infections (sinusitis, tonsillitis,

otitis media, pharyngitis)

 Herpes zoster

 Angular cheilitis

 Recurrent oral ulceration

 Papular pruritic eruption

 Fungal nail infections

 Seborrhoeic dermatitis
Clinical stage 3
Unexplained severe weight loss (>10% of presumed or measured
body weight)
Unexplained chronic diarrhoea for longer than 1 month
Unexplained persistent fever (intermittent or constant for longer
than 1 month)
Persistent oral candidiasis
Oral hairy leukoplakia
Pulmonary tuberculosis
Severe bacterial infections (such as pneumonia, empyema,
pyomyositis ,bone or joint infection, meningitis, bacteraemia)
Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis
Unexplained anaemia (<8 g/dl),
neutropaenia (<0.5 x 109/l) and/or
chronic thrombocytopaenia (<50 x 109/L)
Stage 4
 HIV wasting syndrome
 Pneumocystis (jirovecii) pneumonia
 Recurrent severe bacterial pneumonia
 Chronic herpes simplex infection (orolabial, genital or anorectal of more
than 1 month’s duration or visceral at any site)
 Oesophageal candidiasis (or candidiasis of trachea, bronchi or lungs)
 Extrapulmonary tuberculosis
 Kaposi sarcoma
 Cytomegalovirus infection (retinitis or infection of other organs)
 Central nervous system toxoplasmosis
 HIV encephalopathy
 Extrapulmonary cryptococcosis, including meningitis
 Disseminated non-tuberculous mycobacterial infection
 Progressive multifocal leukoencephalopathy
 Chronic cryptosporidiosis
 Chronic isosporiasis
Disseminated mycosis (extra-pulmonary

histoplasmosis, coccidioidomycosis)
Lymphoma (cerebral or B-cell non-Hodgkin)

Symptomatic HIV-associated nephropathy or

cardiomyopathy
Recurrent septicaemia (including Non-typhoidal

Salmonella)
Invasive cervical carcinoma

Atypical disseminated leishmaniasis

 Mechanisms of CD4 Depletion and Dysfunction

Direct
Elimination of HIV-infected cells by virus-specific immune

responses
Loss of plasma membrane integrity because of viral budding

Interference with cellular RNA processing

Indirect
Syncytium formation

Apoptosis

Autoimmunity
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 Laboratory Markers of HIV Infection
 Rapid tests

= 1st One tie,2nd Unigold,3rd vikia

HIV virologic test- DNA PCR

Viral load

Marker of HIV replication rate

Number of HIV RNA copies/mm3 plasma

CD4 count

Marker of immunologic damage

279 Number of CD4 T-lymphocytes cells/mm3 plasma

 One- tie

280
281
282
HAART= It is the use of three or more anti-retroviral
drugs for the treatment of HIV infection
 The goal of ART is to reduce the number of virus in the blood and
increase the number of CD4 as much as possible

Nucleoside RTIs
Abacavir (ABC) 300 mg twice daily
Lamivudine (3TC) 150 mg twice daily or 300 mg
once daily
Zidovudine (ZDV) 300 mg twice daily.
Nucleotide RTI
Tenofovir (TDF) 300 mg once daily
Efavirenz (EFV) 600 mg once daily
Nevirapine (NVP) 200 mg daily for the first 14
days, then 200 mg twice
daily
Protease inhibitors
Lopinavir/ ritonavir 400 mg/ 100 mg twice daily
(LPV/r)
Atazanavir 300mg/100 once daily
/ritonavir(ATV/r)
 Drug class/ drug Adult Dose a,b
1. Nucleoside RTIs
 Abacavir (ABC) 300 mg twice daily
 Lamivudine (3TC) 150 mg twice daily or 300 mg once daily
 Zidovudine (ZDV) 300 mg twice daily.
2. Nucleotide RTI
 Tenofovir (TDF) 300 mg once daily
3. Non-nucleoside RTIs
 Efavirenz (EFV) 600 mg once daily
 Nevirapine (NVP) 200 mg daily for the first 14 days, then 200 mg twice daily
4. Protease inhibitors
 Lopinavir/ ritonavir (LPV/r) 400 mg/ 100 mg twice daily
 Atazanavir /ritonavir(ATV/r) 300mg/100 once daily
 Danuravir/ ritonavir (DRV/r) 600 mg/ 100 mg twice daily or 800…daily
5. Integrase strand transfer Inhibitors (INSTIs)
 Dolutegravir (DTG) 50 mg once daily
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 Raltegravir (RAL) 400mg twice daily
 Benefits of HAART
 Significantly decreases morbidity and mortality
 Improves quality of life
Decreased number of orphans
Reduces mother-to-child transmission of HIV
Increased number of people who accept HIV testing
and counselling test
Decreased stigma surrounding HIV infection
Less money spent to treat opportunistic infections and
provide palliative care
Treatment for prevention

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 TDF/3TC/EFV ----- first line
adults, adolescents and children older than ten years

pregnant and breastfeeding women

adults with TB co-infection

co-infected with HBV

Alternative First Line regimens

AZT + 3TC + EFV
AZT + 3TC + NVP
TDF + 3TC + NVP

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 For Children 3 years to less than 10 years
and adolescents <35 kg,Preferred first
Line regimens
ABC+ 3TC + EFV
AZT + 3TC + EFV

Alternative First Line regimens

ABC + 3TC + NVP
AZT + 3TC + NVP
TDF + 3TC + EFV
TDF + 3TC + NVP

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 Children <3 years , kg,Preferred first
Line regimens
ABC + 3TC + LPV/r
AZT + 3TC + LPV/r

Alternative First Line regimens

ABC + 3TC + NVP
AZT + 3TC + NVP

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 Prevention and control
There is no single magic bullet for HIV prevention.

Abstinence from sexual relations is the only absolute way

to prevent sexual transmission of HIV infection. w /h is not

feasible for most individuals
There are a number of relatively safe practices that can

markedly decrease the chances of transmission of HIV

infection.
 Core Programmatic Components

 Combination approach to prevent includes three types

of mutually reinforcing interventions:-

1. Biomedical interventions

2. Behavioral interventions

3. Structural interventions
1.Biomedical interventions

-Male and female condoms(F>M)

-treatment of sexually transmitted infections-use of
antiretroviral medications by HIV-infected person
-Prevention of the transmission of HIV after sexual
assault (PEP)
-Voluntary medical male circumcision ,reduces
acquisition of infection and the risk of acquisition for men
by up to 66% and offers a significant lifelong protection.
2. Behavioral interventions
-reduce behaviors that increase risk of transmission (e.g. mass
media)
Peer education

Strengthen workplace HIV prevention interventions

Strengthen community based HIV prevention

interventions to address the general population

• Condom distribution

• Risk reduction Counseling

• knowledge of sero-status,
3. Structural interventions - address the critical social, legal,
political, and environmental enablers that contribute to the spread of

HIV including:-

 Access to health services

 Address socio-cultural factors

- harmful traditional practices that fuel HIV/AIDS.

 Address stigma and discrimination

 Reduce economic vulnerability

 Promote gender equality and prevention of gender-based violence

 Four prongs to eliminate MTCT
Prong 1: Primary prevention of HIV infection - focuses on
keeping parents-to-be HIV negative.
Prong 2: Prevention of unintended pregnancies among
women infected with HIV.
Prong 3: Prevention of HIV transmission from women
infected with HIV to their infants –addresses care for
infants born to HIV-positive women and their mothers
during pregnancy, labor and childbirth, and the postpartum
period.
Prong 4: Provision of treatment, care, and support for
women infected with HIV, their infants, and their families.
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 Thank you

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 Assignment(10%)
SARS
Ebola
Trypanosomiasis
Anthrax
Schistosomiasis
Leprosy
Scabies
Definition, causative agents, disease distribution at global, national and
local level (epidemiology), Reservoir, MOT, Clinical manifestation ,
diagnostic methods treatment, prevention and control methods, IP,
susceptibility.

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