Giardiasis and trichomoniasis are intestinal protozoal infections caused by Giardia intestinalis and Trichomonas vaginalis respectively. Giardiasis causes diarrhea and is transmitted through ingestion of cysts from contaminated food or water. Trichomoniasis primarily causes vaginitis in women and is sexually transmitted. Both infections are generally treated with metronidazole or tinidazole and prevention involves handwashing and water purification. Malaria is a protozoal disease transmitted by mosquitoes that infects red blood cells and causes symptoms like fever. It is a major global health problem with Plasmodium falciparum being the most severe form.

1. 5.2 GIARDIASIS&TRICHOMONAS
1

2. GIARDIASIS…
5.2 Giardiasis
 Giardiasis
 Giardia intestinalis (also known as G. lamblia or G. duodenalis) is
a cosmopolitan protozoal parasite that inhabits the small intestines of
humans and other mammals. Giardiasis is one of the most common
parasitic diseases in both developed and developing countries
worldwide, causing both endemic and epidemic intestinal disease and
diarrhea.
 the most common intestinal parasite
 Life Cycle and Epidemiology
Infection follows the ingestion cysts 2

3. LIFE CYCLE
 is composed of 2 stages: trophozoites and cysts. Giardia infects
humans after ingestion of as few as 10-100 cysts (which measure 8-
10 mm in diameter). Each ingested cyst produces 2 trophozoites in
the duodenum.
 After excystation, trophozoites colonize the lumen of the duodenum
and proximal jejunum, where they attach to the brush border of the
intestinal epithelial cells and multiply by binary fission
3

4.  Pathogenesei
-villi atrophy
-crypt hyperplasia
4

5. GIARDIASIS…
CLINICAL MANIFESTATIONS
THE INCUBATION PERIOD OF GIARDIA INFECTION USUALLY IS
1-2 WK BUT MAY BE LONGER
SYMPTOM FREQUENCY (%)
Diarrhea 64-100
Malaise, weakness 72-97
Abdominal distention 42-97
Flatulence 35-97
Abdominal cramps 44-81
Nausea 14-79
Foul-smelling, greasy stools 15-79
Anorexia 41-73
Weight loss 53-73
Vomiting 14-35
Fever 0-28
Constipation 0-27
5

6. GIARDIASIS…
 Diagnosis
Stool microscopy-characterstic trophozoit or cyst
trophozoits
trophozoits
6

7. GIARDIASIS…
 Treatment
Tinidazole 2 g once
Metronidazole 250 mg tid for 5-7 days
ALTERNATIVE
Albendazole 400 mg once a day for 5 days
7

8. GIARDIASIS…
 Prevention
-practice strict handwashing after any contact with feces
-Methods to purify public water supplies adequately include chlorination,
sedimentation, and filtration
-boiling of water for at least 1 min.
-Treatment of water with chlorine or iodine is less effective but may be
used as an alternate method when boiling or filtration is not possible.
8

9. TRICHOMONIASIS
 Trichomoniasis (Trichomonas vaginalis)
 Trichomoniasis, caused by the protozoan parasite Trichomonas
vaginalis, is the most common nonviral sexually transmitted disease
worldwide.
It primarily causes vulvovaginitis in women but has been implicated in
pelvic inflammatory disease, adverse outcomes in pregnancy, chronic
prostatitis, and an increased risk of transmission of HIV.
9

10. TRICHOMONIASIS
 Epidemiology
 Over 170 million new cases of trichomoniasis occur yearly, the majority in resource-limited settings.
 Prevalence and incidence rates are likely underestimated, as most men and up to 30% of women
are asymptomatic. Diagnostic accuracy using wet mount microscopy, the mainstay of diagnosis, is
less sensitive than previously assumed. While the disease is easily treated, sequelae of untreated
infection remain a significant cause of morbidity due to high reinfection rates from untreated
partners,
 underrecognition of asymptomatic cases, and insensitive diagnostics.
 From 5 to 8 million cases of trichomoniasis occur each year in the USA. A population-based study
conducted in 2005 showed a prevalence of 2.8% in women, 1.7% in men, and an overall
prevalence of 2.3%. The incidence of trichomoniasis is highest among females with multiple sexual
partners and in groups with the highest rates of other sexually transmitted infections. T. vaginalis is
recovered from >60% of female partners of infected men and 70% of male sexual partners of
infected women. Vaginal trichomoniasis is rare until menarche. Its presence in a younger child
should raise the possibility of sexual abuse.
 Trichomoniasis may be transmitted to neonates during passage through an infected birth canal.
Infection in this setting is usually self-limited, but rare cases of neonatal vaginitis and respiratory
infection have been reported.
10

11. Pathogenesis
T. vaginalis is an anaerobic, flagellated protozoan parasite.
Infected vaginal secretions contain 101 to 105 or more protozoa/mL.
T. vaginalis is pear shaped and exhibits characteristic twitching motility in wet mount .
Reproduction is by binary fission. It exists only as vegetative cells; cyst forms have not been described.
T. vaginalis damages host cells and tissues by a number of mechanisms.
Adhesion molecules allow attachment of T. vaginalis to host cells, and hydrolases, proteases,
and cytotoxic molecules act to destroy or impair the integrity of host cells. Parasite-specific antibodies and
lymphocyte priming occur in response to infection, but durable protective immunity does not occur.
11

12. TRICHOMONIASIS
 Clinical Manifestations
 The incubation period in females is 5-28 days. Symptoms may begin or
exacerbate with menses. Most infected women eventually develop symptoms,
although up to one third remain asymptomatic. Common signs and symptoms
include a copious malodorous gray, frothy vaginal discharge, vulvovaginal irritation,
dysuria, and dyspareunia. Physical examination may reveal a frothy discharge with
vaginal erythema and cervical hemorrhages (“strawberry cervix”). The discharge
usually has a pH of >4.5. Abdominal discomfort is unusual and should prompt
evaluation for pelvic inflammatory disease (Chapter 114).
 Most infections in males are asymptomatic. Symptomatic males usually have
dysuria and scant urethral discharge. Trichomonads occasionally cause epididymitis,
prostatic involvement, and superficial penile ulceration. Infection is often self-limited,
spontaneously resolving in 36% of men. Trichomonas has been implicated as a
cause of recurrent or relapsing urethritis and can be isolated in 3-20% of men with
nongonococcal urethritis. Treatment failures with standard therapy for gonorrhea
and Chlamydia are frequently treated with antitrichomonal therapy.
12

13. TRICHOMONIASIS
 Trichomonads may be recognized in vaginal secretions by using the
wet mount technique. This technique has been estimated to have a
sensitivity of 60-70%
 Patients with T. vaginalis should be screened for other sexually
transmitted infections, including Chlamydia and gonorrhea.
13

14. TRICHOMONIASIS
 Complications
 Untreated trichomoniasis has been associated with pelvic
inflammatory disease, premature delivery, low birthweight, tubal
infertility, and vaginal cuff cellulitis. T. vaginalis infection increases the
risk of acquisition and transmission of HIV. Trichomonas-induced
inflammation of the genital mucosa recruits greater numbers of CD4+
cells in the epithelium and provides more direct access to the
bloodstream for HIV. In HIV-infected individuals, trichomoniasis is
associated with a higher viral load in cervical secretions and semen as
well as higher levels of infected lymphocytes in urogenital fluids. HIV-1
shedding in vaginal fluids is decreased by treatment of trichomoniasis
14

15. TRICHOMONIASIS
 Treatment
- metronidazole and tinidazole are used
-treat couples
15

16. TRICHOMONIASIS
 Prevention
 Prevention of T. vaginalis infection is best accomplished by treatment
of all sexual partners of an infected person and by programs aimed at
prevention of all sexually transmitted infections (Chapter 114).
 No vaccine is available
 Drug prophylaxis is not recommended.
16

17. MALARIA
17

18. MALARIA….
 a protozoan disease transmitted by the bite of infected female
Anopheles mosquitoes, which occurs mainly between dusk & dawn.
 The most important of the parasitic diseases of humans.
 causes approximately 2000 deaths each day.
 More than 80% of deaths occur in SSA.
18

19. MALARIA…
 Endemicity traditionally has been defined in terms of parasitemia rates
or palpable-spleen rates in children 2–9 years of age and classified
as;
-hypoendemic (<10%),
-mesoendemic (11–50%),
- hyperendemic (51–75%), and
- holoendemic(>75%).
19

20. MALARIA………
Stable vs Unstable transmission
Stable transmission
-year round infection
-protective immunity
-less chance of epidemicity
Unstable transmission
- low, erratic, or focal transmission
- full protective immunity is not acquired,
- symptomatic disease may occur at all ages.
- usually exists in hypo endemic areas
-high chance of endemicity
20

21. MALARIA…
 The entomologic inoculation rate[EIR] (i.e., the number of sporozoite
positive mosquito bites per person per year) is the most common
measure of malaria transmission intensity.
EIR<10/year-low transmission
EIR10-49/year-intermediate transmission
EIR>=50/year-high transmission
21

22. MALARIA…
 The principal determinants of the epidemiology of malaria are the
 number (density),
 human-biting habits, and
 longevity of the anopheline mosquito vectors.
 More than 100 of the >400 anopheline species can transmit malaria,
but the ~40 species that do so commonly vary considerably in their
efficiency as malaria vectors
22

23. MALARIA…
ETIOLOGY AND PATHOGENESIS
 Six species of the genus Plasmodium cause nearly all malarial
infections in humans.
- P. falciparum,
- P. vivax,
-two morphologically identical sympatric species of P. ovale
- P. malariae, and -P. knowlesi- the monkey malaria parasite in
Southeast Asia.
 While almost all deaths are caused by falciparum malaria, P. knowlesi
and occasionally P. vivax also can cause severe illness
23

24. MALARIA…
LIFE CYCLE 1 2
24

25. MALARIA…
 Life cycle
 Infected female anopheline mosquito inoculates plasmodial sporozoites from its
salivary gland during a blood meal [motile form]
intrahepatic or preerythrocytic schizogony or merogony swollen infected liver
cells eventually burst, discharging motile merozoites into the bloodstream.
 These merozoites then invade the red blood cells (RBCs) and multiply ->trophozoit-
>schizont->merozoit.But at some point some of the merozoites deferenciate to male
and female gametes[sexual forms]
After being ingested in the blood meal of a biting female anopheline mosquito, the
male and female gametocytes form a zygote in the insect’s midgut. This zygote
matures into an ookinete, which penetrates and encysts in the mosquito’s gut wall. The
resulting oocyst expands by asexual division until it bursts to liberate myriad motile
sporozoites, which then migrate in the hemolymph to the salivary gland of the mosquito
to await inoculation into another human at the next feeding. 25

26. MALARIA…
ERYTHROCYTE CHANGES IN MALARIA
 the growing malarial parasite progressively consumes and degrades
intracellular proteins, principally hemoglobin releasing hem which is
potentially toxic to malaria;but the parasite detoxifies to
hemozoin[malaria pigment]
 The RBC becomes more irregular in shape,more antigenic, and less
deformable, exprese parasite derived proteins[knobs] on their surface
, release inflammatory mediators such as TNF on their destruction&
anaerobic glycolysis enhanced to result in lactic acidosis.
Q. What could result from these RBC changes???
26

27. MALARIA…
 Answer;
 Anemia
 Hypoglycemia
 Lactic acidosis
 Cytoadherence
 Rosette sequestration only in P.falciparum!!!!!!
 agglutination
27

28. MALARIA…
HOST RESPONSE[factors]
Fever
P.vivax-Duffy negative RBC
P.falciparum
sickle cell disease,
hemoglobins C , E and F
hereditary ovalocytosis,
thalassemias, and
glucose-6-phosphatedehydrogenase(G6PD)
deficiency 28

29. MALARIA…
CLINICAL FEATURES
 The first symptoms of malaria are nonspecific; the lack of a sense of
wellbeing,headache, fatigue, abdominal discomfort, and muscle aches
followed by fever
 Nausea, vomiting, and orthostatic hypotension are common
29

30. MALARIA…
 The classic malarial paroxysms, in which fever spikes, chills, and
rigors occur at regular intervals, are relatively unusual and suggest
infection with P. vivax or P. ovale.
 Febrile convulsion may occur with any malarias ,but generalized
seizures[cerebral malaria] is for severe malaria
 For severe malaria see the table on the next slides
30

31. SEVERE FALCIPARUM MALARIA
Major Signs Manifestations
Unarousable coma/
cerebral malaria
Failure to localize or respond appropriately to noxious stimuli; coma persisting for >30
min
after generalized convulsion
Acidemia/acidosis Arterial pH of <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,
normocytic anemia
Hematocrit of <15% or hemoglobin level of <50 g/L (<5 g/dL) with parasitemia
<10,000/μL
Renal failure Serum or plasma creatinine level of >265 μmol/L (>3 mg/dL); urine output (24 h) of
<400 mL in adults or <12 mL/kg in children; no improvement with rehydration
Pulmonary
edema/adult
respiratory distress
syndrome
Noncardiogenic pulmonary edema, often aggravated by overhydration
Hypoglycemia Plasma glucose level of <2.2 mmol/L (<40 mg/dL)
31

32. SEVERE FALCIPARUM MALARIA
Hemoglobinuriaa Macroscopic black, brown, or red urine; not
associated with effects of oxidant drugs and
red blood cell enzyme defects (such as G6PD
deficiency)
Extreme
weakness
Parasitemia level of >5% in nonimmune patients
(>10% in any patient)
Hyperparasitemia Serum bilirubin level of >50 mmol/L (>3 mg/dL)
if combined with a parasite density of 100,000/μL
or other evidence of vital-organ dysfunction
Jaundice Serum bilirubin level of >50 mmol/L (>3 mg/dL)
if combined with a parasite density of 100,000/μL
or other evidence of vital-organ dysfunction
32

33. MALARIA…
Discussion
MALARIA IN PREGNANCY
MALARIA IN HIV/AIDS and malnutrition
MALARIA IN CHILDREN
TRANSFUSION MALARIA
33

34. MALARIA…
CHRONIC COMPLICATIONS OF MALARIA
1. TROPICAL SPLENOMEGALY (HYPERREACTIVE MALARIAL
SPLENOMEGALY
2. QUARTAN MALARIAL NEPHROPATHY
3. BURKITT’S LYMPHOMA AND EPSTEIN-BARR VIRUS INFECTION
34

35. MALARIA…
DIAGNOSIS
-DEMONSTRATION OF THE PARASITE
.Thick and thin bloodfilm-microscopy
.RDT[Rapid Diagnostic Test]->serology
Q.Discuss merit and demerit of the above tests
35

36. MALARIA…
P.FALCIPARUM GAMETOCYTES
Female gametocytes. Male gametocytes
36

37. MALARIA…
 TREATMENT of Malaria
 UNCOMPLICATED MALARIA
P.falciparum----Coartum/Quinine
P.vivax or other species---Chloroquine/Coartum
 Radical cure
-Primaquine-eradicates hepatic forms of P. vivax and P. ovale;
kills all stages of gametocyte development of P. falciparum
37

38. MALARIA…
 TREATMENT of Malaria
Severe Falciparum Malaria
 Artesunate (2.4 mg/kg stat IV followed by 2.4 mg/kg at 12 and 24 h and
then daily if necessary)h
or, if unavailable,
 Artemether (3.2 mg/kg stat IM followed by 1.6 mg/kg qd)
or, if unavailable,
 Quinine dihydrochloride (20 mg of salt/kgi infused over 4 h, followed by 10
mg of salt/kg infused over 2–8 h q8hj)
or, if unavailable,
 Quinidine (10 mg of base/kgi infused over 1–2 h, followed by 1.2 mg of
base/kg per hourj with electrocardiographic monitoring) 38

39. MALARIA…
 PREVENTION
Distribution of insecticide-treated bed-nets (ITNs)
PERSONAL PROTECTION AGAINST MALARIA
CHEMOPROPHYLAXIS-Chloroquine, Mefloquine, Doxycycline,
Primaquine
Other measures???
39

40. LEISHMANIASIS
KALA AZAR[VL]
40

41. LEISHMANIASIS…
DEFINITION
 a complex group of disorders of vector-born disease,sandfly.
 leishmaniasis is caused by more than 20 species of unicellular eukaryotic
obligatory intracellular protozoa of the genus Leishmania
 primarily affects the host’s reticuloendothelial system
41

42. LEISHMANIASIS…
 clinical syndromes ranging from self-healing cutaneous ulcers to fatal
visceral disease.
 syndromes fall into three broad categories:
1. visceral leishmaniasis (VL),
2.cutaneous leishmaniasis (CL), and
3. mucosal leishmaniasis (ML]
42

43. LEISHMANIASIS…
1. visceral leishmaniasis (VL),
 VL (also known as kala-azar, a Hindi term meaning “black fever”)
 is caused by the Leishmania donovani complex, which includes
 L. donovani and Leishmania infantum (the latter designated
Leishmania chagasi in the New World); these species are responsible
for anthroponotic and zoonotic transmission, respectively
 Leishmaniasis occurs mainly in tropical and temperate regionsIndia
and neighboring Bangladesh, Sudan, South Sudan, Ethiopia, and
Brazil are the four largest foci of VL and account for 90% of the
world’s VL burden, with India being the worst affected.
43

44. LEISHMANIASIS…
LIFE CYCLE
 sandflies of the genus Phlebotomus in the “Old World” (Asia, Africa,
and Europe) and the genus Lutzomyia in the “New World” (the
Americas). Transmission may be anthroponotic (i.e., the vector
transmits the infection from infected humans to healthy humans) or
zoonotic (i.e., the vector transmits the infection from an animal
reservoir to humans)
 Promastigotes are introduced through the proboscis of the female
sandfly into the skin of the vertebrate host.
 Neutrophils predominate among the host cells that first encounter
and take up promastigotes at the site of parasite delivery.
44

45. LEISHMANIASIS…
 The infected neutrophils may undergo apoptosis and release viable
parasites that are taken up by macrophages, or the apoptotic cells
may themselves be taken up by macrophages and dendritic cells. The
parasites multiply as amastigotes inside macrophages, causing cell
rupture with subsequent invasion of other macrophages.
 While feeding on infected hosts, sandflies pick up amastigotes, which
transform into the flagellate form in the flies’ posterior midgut and
multiply by binary fission; the promastigotes then migrate to the
anterior midgut and can infect a new host when flies take another
blood meal.
45

46. LEISHMANIASIS…
Immunopathogenesis
 The majority of individuals infected by L. donovani or L. infantum
mount a successful immune response and control the infection, never
developing symptomatic disease. Fortyeight hours after intradermal
injection of killed promastigotes, these individuals exhibit delayed-type
hypersensitivity (DTH) to leishmanial antigens in the leishmanin skin
test (also called the Montenegro skin test).
46

47. LEISHMANIASIS…
 proinflammatory cytokines and chemokines by the T helper1 (TH1) subset of
T lymphocyte and antigen presenting cells[IL-12,TNF..] which are important
for the development of acquired resistance to leishmanial infection are
overwhelmed by IL-10!!!
 IL-10-
-condition host macrophages for enhanced survival and growth of the
parasite
-render macrophages unresponsive to activation signals and inhibit
killing of amastigotes by downregulating the production of TNF-α
and nitric oxide.
- Multiple antigen-presentation functions of dendritic cells and
macrophages are also suppressed by IL-10
 Patients with such suppression do not have positive leishmanin skin test 47

48.  Organs of the reticuloendothelial system are predominantly affected,
with remarkable enlargement of the spleen, liver, and lymph
 nodes in some regions. The tonsils and intestinal submucosa are also
heavily infiltrated with parasites. Bone marrow dysfunction results in
pancytopenia.
48

49. LEISHMANIASIS…
Clinical Features
 The incubation period is usually 2-6months but can range from a few weeks to
several years.
 The most common presentation of VL is an abrupt onset of moderate- to high-grade
fever associated with rigor and chills.
 Fever may continue for several weeks with decreasing intensity, and
the patient may become afebrile for a short period before experiencing another bout of
fever.
 The spleen may be palpable by the second week of illness and, depending on the
duration of illness, may become hugely enlarged.
 Hepatomegaly (usually moderate in degree) soon follows.
 Lymphadenopathy is common in most endemic regions of the world except the
Indian subcontinent, where it is rare.
49

50. LEISHMANIASIS…
 Patients lose weight and feel weak, and the skin gradually develops dark discoloration due to
hyperpigmentation that is most easily seen in brown-skinned individuals
 Secondary infections such as measles, pneumonia,tuberculosis, bacillary or amebic dysentery, and
gastroenteritis are common. Herpes zoster, chickenpox, boils in the skin, and scabies may also occur.
 In advanced illness, hypoalbuminemia may manifest as pedal edema and ascites
 Untreated, the disease is fatal in most patients, including 100% of those with HIV co-infection.
 Leukopenia and anemia occur early and are followed by thrombocytopenia.
===Pancytopenia
Discussion
Q.Discuss effects of pancytopenia
50

51. LEISHMANIASIS…
 marked polyclonal increase in serum immunoglobulins.
 Serum levels of hepatic aminotransferases are raised in a
significant proportion of patients,
 serum bilirubin levels are elevated occasionally.
 Renal dysfunction is uncommon
 Spontaneous recovery is rare
 Sever anemia and frank jaundice are associated with poor
prognosis!!!
51

52. LEISHMANIASIS…
Laboratory Diagnosis
 Demonstration of amastigotes in smears of tissue aspirates is the gold
standard for the diagnosis of VL
 sensitivity of
-splenic smears is >95%,
-smears of bone marrow(60–85%) and
- lymph node aspirates (50%).
 Culture of tissue aspirates increases sensitivity. Splenic aspiration is
invasive and may be dangerous in untrained hands.
 Several serologic techniques are currently used to detect antibodies to
Leishmania
 PCR????
 CBC 52

53. LEISHMANIASIS…
 rK39-sensitivity of rK39 rapid diagnostic test (RDT) in
immunocompetent individuals is ~98% and its specificity is 90%.
 Q. Discuss the contraindications of splenic aspiration
53

54. LEISHMANIASIS…
Differential Diagnosis
 Malaria
 typhoid fever, tuberculosis, brucellosis,
 schistosomiasis, and histoplasmosis.
 Splenomegaly due to portal hypertension,
 chronic myeloid leukemia[CML]
 tropical splenomegaly syndrome[HMS]
54

55. LEISHMANIASIS…TREATMENT of Visceral Leishmaniasis
GENERAL CONSIDERATIONS
 Severe anemia should be corrected by blood transfusion, and other comorbid
conditions should be managed promptly
 Treatment of VL is complex because the optimal drug, dosage, and duration
vary with the endemic region.
 some patients experience relapse (most often within 6 months]
 A pentavalent antimonial is the drug of choice in most endemic regions of the
world, but there is widespread resistance to antimony in the India, where
either amphotericin B (AmB) deoxycholate or miltefosine is preferred.
 liposomal AmB is the drug of choice[deoxycholate and lipid formulations]
55

56. LEISHMANIASIS…
PENTAVALENT ANTIMONIAL COMPOUNDS
 Two pentavalent antimonial (SbV) preparations are available: sodium stibogluconate
(100 mg of SbV/mL) and meglumine antimoniate(85 mg of SbV/mL).
 The daily dose is 20 mg/kg by IV infusion or IM injection, and therapy continues for
28–30 days
 Adverse reactions to SbV treatment are common and include arthralgia, myalgia, and
 elevated serum levels of aminotransferases.
 Electrocardiographic changes are common. prolongation of QT to >0.5 s may herald
ventricular arrhythmia and sudden death. Chemical pancreatitis is common but
usually does not require discontinuation of treatment; severe clinical pancreatitis
occurs in immunosuppressed patients.
56

57. LEISHMANIASIS… AMPHOTERICIN B
 Conventional AmB deoxycholate is administered in doses of 0.75–1.0
mg/kg on alternate days for a total of 15 infusions.
 Fever with chills is an almost universal adverse reaction to AmB
infusions.
 Nausea and vomiting are also common, as is thrombophlebitis in the
infused veins.
 Acute toxicities can be minimized by administration of antihistamines
like chlorpheniramine and antipyretic agents like acetaminophen before
each infusion.
 AmB can cause renal dysfunction and hypokalemia
57

58. LEISHMANIASIS…
AMPHOTERICIN B
 The several lipid formulations of AmB developed to replace the deoxycholate
formulation are preferentially taken up by reticuloendothelial tissues.
 Because very little free drug is available to cause toxicity, a large amount of drug can be
delivered over a short period.
 Liposomal AmB has been used extensively to treat VL in all parts of the world. With a
terminal half-life of ~150 h,
 liposomal AmB can be detected in the liver and spleen of animals for several weeks
after a single dose.
 the regimen is 3 mg/kg daily on days 1–5, 14, and 21 (total dose, 21 mg/kg),but varies
among regions
 Side Effects-usually mild and include infusion reactions, backache, and occasional
reversible nephrotoxicity
 Other agents-PAROMOMYCIN, MILTEFOSINE[an alkylphosphocholine, is the first oral
compound approved for the treatment of leishmaniasis].
58

59. LEISHMANIASIS
Prevention
-indoor insecticide residual spray
-ITNs
-treating the index case
-wear appropriate clothes during the night times&repellents
-Others
59

60. HELMINTHIC INFECTIONS
60

61. HELMINTHIC INFECTIONS….
 helminth is derived from the Greek helmins (“parasiticworm”).
 Helminthic parasites of humans belong to two phyla:
1.Nemathelminthes, which includes nematodes (roundworms), and
2.Platyhelminthes, which includes cestodes (tapeworms) and
trematodes(flukes)
Roundworm infections
Ascariasis-A. lumbricoides is the largest intestinal nematode
parasite of humans,reaching up to 40 cm in length.
 Clinical disease arises from larval migration in the lungs or effects of
the adult worms in theintestines.
 Life cycle---Heart-lung migration 61

62. ROUND WORM
HOOKWORM
 Two hookworm species (A. duodenale and N. americanus) are responsible
for human infections
 Life Cycle
Adult hookworms, which are ~1 cm long, use buccal teeth
(Ancylostoma) or cutting plates (Necator) to attach to the smallbowel mucosa
and suck blood (0.2 mL/d per Ancylostoma adult) and interstitial fluid
 Infective larvae penetrate the skin and reach the lungs by way of the
bloodstream. There they invade alveoli and ascend the airways before being
swallowed and reaching the small intestine
62

63.  STRONGYLOIDIASIS
S. stercoralis is distinguished by its ability—unique among helminths(except
for Capillaria; see below)—to replicate in the human host. This capacity
permits ongoing cycles of autoinfection as infective larvae are internally
produced. Strongyloidiasis can thus persist for decadeswithout further
exposure of the host to exogenous infective larvae. In immunocompromised
hosts, large numbers of invasive Strongyloides larvae can disseminate widely
and can be fatal.
63

64. FLAT WORMS
 Cestode -Taeniasis
 Flukes-Schistosomisis
64

65. 7.BACTERIAL INFECTIOUS DISEASES…
 Out line
7.1-Salmonellosis
7.2-Spirochetal Diseases
7.3-Gonococal Infections
7.4-Rickettsial Diseases
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66. 7.1-SALMONELLOSIS (TYPHOID FEVER)
 genus Salmonella are highly adapted for growth in both humans and animals.
 gram-negative bacilli, non-spore-forming, facultatively anaerobic bacill , within the
family Enterobacteriaceae.
 The growth of serotypes Salmonella typhi and Salmonella paratyphi is restricted
to human hosts, in whom these organisms cause enteric (typhoid) fever.
 The remaining serotypes ->nontyphoidal Salmonella, or NTS
 Serotyping is based on the somatic O antigen (lipopolysaccharide cell wall
components), the surface Vi antigen (restricted to S. typhi and S. paratyphi C),
and the flagellar H antigen,
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67. 7.1-SALMONELLOSIS
 PATHOGENESIS
 - All Salmonella infections begin with ingestion of organisms, most commonly in
contaminated food or water.
 The infectious dose ranges from 200 colony-forming units (CFU) to 106 CFU.
 the ingested dose is an important determinant of incubation period,attack rate and
disease severity.
 Conditions that decrease either stomach acidity, intestinal integrity, or alteration of
the intestinal flora by antibiotic administration or immunosuppressive illnesses such
as AIDS increase susceptibility to Salmonella infection.
 Once S. typhi and S. paratyphi reach the small intestine, they penetrate the mucus
layer of the gut and traverse the intestinal layer through phagocytic microfold (M)
cells that reside within Peyer’s patches
 S.typhi proliferate in the submucosa, leading to hypertrophy of payer’s patches via
recruitment of monnuclear cells and lymphocytes->necrosis->RES spread
67

68. 7.1-SALMONELLOSIS…
CLINICAL COURSE
 The incubation period for S. typhi averages 10–14 days but ranges from 5 to 21 days,
Prolonged Fever[stepladder fever]
Abdominal pain,anorexia,nausea,vomiting,alternative diarrhea and constipation
 Headach, chills, cough, sweating, myalgias, malaise, and arthralgia
Dicussion:
chronic carriage???
DIAGNOSIS
Culture-blood>urine>stool in 1st ,2nd and 3rd weeks=“BUS”
Serology-Widal test mainly using O and H antigens.What is the difference between
these two antigens? 68

69. 7.1-SALMONELLOSIS…
TREATMENT
 Empirical Treatment- Ceftriaxonea 2 g/d (IV) 10–14 or Azithromycinb 1 g/d
(PO) 5
 Fully Susceptible-Ciprofloxacinc 500 mg bid (PO) or 400 mg q12h (IV) 5–7
 Multidrug-Resistant-Optimal treatment
Ceftriaxonea 2 g/d (IV) 10–14 or
Azithromycin 1 g/d (PO) 5
Alternative treatment
Ciprofloxacin 500 mg bid (PO) or 400 mg q12h (IV) 5–14
Note: Treat any complication if any
PREVENTION AND CONTROL???
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70. 7.2-SPIROCHETAL DISEASES
 7.2.1. Syphilis
 7.2.2. Relapsing fever
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71. 7.2.1. SYPHILIS
 Syphilis, a chronic systemic infection caused by Treponema pallidum subspecies
pallidum,
 usually sexually transmitted and is characterized by episodes of active disease interrupted
by periods of latency.
 After an incubation period averaging 2–6 weeks, a primary lesion appears—often
associated with regional lymphadenopathy—that resolves without treatment.
 secondary stage, associated with generalized mucocutaneous lesions and generalized
lymphadenopathy, is followed by a latent period of subclinical infection lasting years or
decades. Central nervous system (CNS) involvement may occur early in infection and may
be symptomatic or asymptomatic.
 In the preantibiotic era, about one-third of patients with untreated cases developed the
tertiary stage, characterized by progressive destructive mucocutaneous, musculoskeletal,
or parenchymal lesions; aortitis; or late CNS manifestations
ETIOLOGY
 Treponema species include T. pallidum subspecies pallidum-causes venereal syphilis;
 T. pallidum subspecies pertenue,-causes yaws;
 T. pallidum subspecies endemicum-causes endemic syphilis or bejel; and
 T. carateum-causes pinta
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72. CLINICAL MANIFESTATIONS
Primary Syphilis
-typical primary chancre usually begins as a single painless papule that rapidly becomes
eroded and usually becomes indurated, with a characteristic cartilaginous consistency on
palpation of the edge and base of the ulcer.
- Multiple primary lesions are seen in a minority of patients. In men the chancre is usually
located on the penis
-In women, common primary sites are the cervix and labia.
Secondary Syphilis
 -mucocutaneous lesions[condylomata lata]and generalized nontender
lymphadenopathy. 72

73. SYPHILIS…
 Constitutional signs and symptoms that may accompany or precede
secondary syphilis include;
- sore throat, fever, weight loss, malaise, anorexia, headache, and
meningismus
-Acute meningitis occurs in only 1–2% of cases, but CSF cell and protein
concentrations are increased in up to 40% of cases
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74. SYPHILIS…
Latent Syphilis
 Positive serologic tests for syphilis, together with a normal CSF examination
and the absence of clinical manifestations of syphilis,
 Early latent syphilis is limited to the first year after infection, whereas late
latent syphilis is defined as that of ≥1 year’s duration (or of
unknown duration).
Tertiary disease
-Gummas are usually solitary lesions ranging from microscopic to several
centimeters in diameter
-neurosyphilis –Tabes dorsalis
-cardiovascular syphilis-10–40 years after infection
endarteritis aortitis,aortic regurgitation, saccular aneurysm (usually of the
ascending aorta), or coronary ostial stenosis.
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75. SYPHILIS…
Dicussion
Congenital Syphilis
LABORATORY EXAMINATIONS
-Microscopy-darkfield microscope
-Serology
Nonspecific-VDRL and RPR tests---screenig
Specific treponomal tests- TPPA or FTA-ABS----confirmatory
-PCR
75

76. SYPHILIS…
 Penicillin G is the drug of choice for all stages of syphilis
 Primary, secondary, or early latent CSF normal or not examined: Penicillin G benzathine
(single dose of 2.4 mU IM] CSF abnormal: Treat as neurosyphilis
 Late latent (or latent of uncertain duration),cardiovascular, or benign tertiaryCSF normal or not
examined: Penicillin G benzathine
(2.4 mU IM weekly for 3 weeks)
 CSF abnormal: Treat as neurosyphilis
 Neurosyphilis (asymptomatic orsymptomatic) Aqueous crystalline penicillin G (18–24 mU/d
IV,given as 3–4 mU q4h or continuous infusion) for 10–14 daysm or Aqueous procaine
penicillin G (2.4 mU/d IM) plus oral probenecid (500 mg qid), both for 10–14 days
 Syphilis in pregnancy According to stage-Penicillin is the only recommended agent for the
treatment of syphilis in pregnancy. If the patient has a documented penicillin
allergy, desensitization and penicillin therapy should be undertaken
Treated women whose antibody titers rise by fourfold or whose titers do not decrease by
fourfold over a 3-month period should be re-treated. 76

77. 7.2.2 RELAPSING FEVER
 Relapsing fever is caused by infection with any of several species of Borrelia
spirochetes
 Antigenic variation of the spirochetes’ surface proteins accounts for the
infection’s relapsing course
 Treatment with antibiotics results in rapid cure but at the risk of a moderate to
severe Jarisch-Herxheimer reaction
77

78. RELAPSING FEVER
 Relapsing fever is caused by infection with any of several speciesof
Borrelia spirochetes
 Borrelia recurrentis, which is also the only species transmitted by the
louse. Louse-borne relapsing fever (LBRF) is usually acquired from a
body louse (Pediculus humanus corporis).Transmission???
 All other known species of relapsing fever agents are tick-borne(TBRF)—
in most cases, by soft ticks of the genus Ornithodoros
 Borrelia duttonii in sub-Saharan Africa, is largely maintained by tick
transmission between human host
78

79. RELAPSING FEVER
PATHOGENESIS AND IMMUNITY
 Unlike LBRF spirochetes[transmited by inoculation of bacteria in feces during
scratching, TBRF spirochetes enter the body in the tick’s saliva with the onset of
feeding
 spirochetes proliferate in the blood, doubling every 6 h to numbers of 106–107/mL or
more.
 Borrelia species are extracellular pathogens
 Binding of the spirochetes to erythrocytes leads to aggregation of red blood cells, their
sequestration in the spleen and liver,and hepatosplenomegaly and anemia.
 A bleeding disorder is probably the consequence of thrombocytopenia, impaired
hepatic production of clotting factors, and/or blockage of small vessels by aggregates
of spirochetes, erythrocytes, and platelets
79

80. RELAPSING FEVER
 IgM antibodies specific for the serotype-defining surface lipoprotein appear after a few
days of infection and soon reach a concentration that causes lysis of bacteria
CLINICAL MANIFESTATIONS
 sudden onset of fever.
 Febrile periods are punctuated by intervening afebrile periods of a few days; this
pattern occurs at least twice.
 The patient’s temperature is ≥39°C and may be as high as 43°C
 The symptoms that accompany the fevers are usually nonspecific.
-Headache, neck stiffness, arthralgia, myalgia, and nausea may accompany the first and
subsequent febrile episodes. An enlarging spleen and liver cause abdominal pain.
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81. RELAPSING FEVER…
 A nonproductive cough is common during LBRF and—in combination with
fever and myalgias—may suggest influenza.
 Acute respiratory distress syndrome may occurduring TBRF.
Physical examination???
-delirious or apathetic
-lice in the patient’s clothes or signs of insect bites
 -Epistaxis, petechiae, and ecchymoses are common during LBRF but not in
TBRF
 Splenomegaly or spleen tenderness is common in both forms of relapsing
feve 81

82. RELAPSING FEVER
DIAGNOSIS
-Polymerase chain reaction (PCR
-Blood film
-Culture of blood or CSF in Barbour-Stoenner-Kelly broth medium
82

83. RELAPSING FEVER
83

84. RELAPSING FEVER
 Penicillins and tetracyclines have been the antibiotics of choice for
 relapsing fever for several decades. Erythromycin has been a
longstanding second choice
 A single dose of antibiotic is usually sufficient for the treatment of
LBRF
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