Protozoan diseases

1. PROTOZOAN DISEASES
AMEBIASIS:
Etiology: 2 morphologically identical but genetically distinct sp:
1. E. dispar = more prevalent sp.
2. E. histolytica = pathogenic sp.
= symptomatic disease
♦Can be killed by heating to 550
C
♦Resistant to low temperature and chlorine

2. Epidemiology:
♦Prevalence of 5 – 81%
♦Humans – major reservoir
♦Means of infection: food and drink contaminated
with E. cyst in direct fecal – oral route

3. Pathogenesis:
Trophozoites
↓ Galactose – specific lectin receptor
Colonic mucosa
↓ Cysteine – rich proteinase
Tissue destruction
(flask-shaped ulcers)
♦Commonly invade:
-cecum
-transverse colon
-sigmoid colon

4. Clinical Manifestations:
Intestinal Amebiasis:
♦incubation period = 2 weeks
♦gradual onset, colicky abdominal pain, frequent bowel
movement
♦association with tenesmus
♦stools blood stained, fair amount of mucus, few
leukocytes
♦1/3 of pts with fever
♦amebic colitis = affects all age group
= increased incidence 1-5 y.o.

5. Hepatic Amebiasis:
♦< 1% infected
♦fever is hallmark
♦assoc. with abdominal pain, distention, enlargement and
tenderness of liver
♦lab findings: sl. Leukocytosis
moderate anemia
inc. ESR
inc. Alkaline phosphate
>50% (-) stool exam
♦computed tomography and MRI – localize and delineate
size of abscess cavity

6. Diagnosis:
♦Stool exam – 3X (90% sensitivity)
♦Sigmoidoscopy
♦Tissue biopsy
♦Aspirate of liver abscess
♦Antigen detection tests – differentiate E. dispar from E.
histolytica
Treatment: Luminal Amebicides
1. Iodoquinol
2. Paromomycin
3. Diloxonide furoate

7. Extraluminal Amebicides:
1. Metronidazole
2. Nitroimidazole
3. Chloroquine
4. Dehydroemetine
♦All individuals with E. histolytica trophozoites or cysts
in their stools, whether symptomatic or not,
should be treated

8. Iodoquinol - asymptomatic carriers
- 30-40 mg/k/24 hours in 3 divided doses orally
X 20 days
Paromomycin - non-absorbable aminoglycoside
- 25-35 mg/k/24 hours in 3 divided doses orally
X 7 days
Metronidazole- tissue amebicidal drug
- 30-50 mg/k/24 hours in 3 divided doses
(max. 500-750 mg/dose) orally X 10 days
- A. R. nausea, abdominal discomfort, metallic
taste
Dehydroemetine – Metronidazole – resistant to E. histolytica
- 1 mg/k/24 hours (IM, SQ)
Chloroquine - for amebic hepatic abscess
♦Stool exam should be repeated every 2 weeks until (-)

9. Prognosis:
= death occurs in 5% having extraintestinal infection
Prevention:
1. proper sanitary measures
2. avoiding fecal – oral contact
3. regular exam. of food handlers
♦No prophylactic drug or vaccine available

10. GARDIASIS:
♦ Giardia lamblia = flagellated protozoan infecting
duodenum and S. I.
= clinical manifestation from asymptomatic
to acute or chronic diarrhea and
malabsorption
= significant pathogen with malnutrition,
immunodeficiency and cystic fibrosis

11. Life Cycle:
♦Composed of 2 stages:
1. trophozoites
2. cysts
Ingested cyst (10-100 cysts)
↓
2 trophozoite in S. I
↓
Excystation
↓
Lumen of duodenum and proximal jejunum
↓
stools (2 mos.)
♦viability not affected by usual chlorine conc.

12. Epidemiology:
♦inc. in childhood and decreased in adolescents
♦water contaminated with G. cyst – major reservoir
♦foodborne transmission is documented
♦resistant to UV light irradiation
♦boiling effective for inactivating cysts
♦person-person spread in low hygiene, lack of toilet
training child care centers

13. Clinical Manifestation:
♦inc. period = 1-2 but may be longer
♦asymptomatic, excretion, acute infectious diarrhea,
chronic diarrhea
♦no extraintestinal spread but may migrate to bile and
pancreatic ducts
♦signs and symptoms: with or without fever, nausea,
anorexia, diarrhea and abdominal distention and
cramps
♦stools profuse and watery and later greasy and foul
smelling, no mucus, blood or fecal leukocytes

14. Diagnosis:
♦Definitive: cysts or trophozoites in stools or duodenal fluid
by DFS (within 1 hour)
♦Cyst – infectious form
♦Others: Aspiration or Biopsy of duodenum or upper jejunum
Enterotest
Polymerase Chain Reaction (PCR) for environment
monitoring
Gene probe-based detection system
♦DFS – 70% diagnosis single exam
85% 2nd
stool exam
>90% 3rd
stool exam
♦Medications can interfere presence of parasite in stool
♦Radiographic: irregular thickening of mucosal folds
♦NO
blood count: NO eosinophilia

15. Treatment:
♦Metronidazole – drug of choice
♦Paromomycin
♦Furazolidone – 92% cure rate
Prevention:
1. .Strict hand washing after contact with feces
2. .Adequate purification of water supply
3. .Travelers advice to avoid uncooked foods

16. BALANTIDIASIS:
♦Balantidium coli - ciliated protozoan
- largest protozoan
- close assoc. with pigs (host of org.)
- infects L. I.
♦Symptoms similar with Amebiasis
♦No extraintestinal spread
♦Diagnosis: Direct Saline Smear – trophozoites and cysts

17. ♦Treatment:
1. Metronidazole (35-50mg/k/24hrs) divided by doses
(max. dose 750mg/day) orally X 5 days
2. Tetracycline (40mg/k/24hrs) divided by 4 doses
(max. dose 500mg/dose) orally X 10 days in
> 8 years
3. Iodoquinol (40mg/k/24hrs) divided by 3 doses
(max. dose 650mg/dose) orally by 20 days
Prevention:
Prevent contamination of the environment by pig feces

18. SPORE – FORMING INTESTINAL PROTOZOA
1. Cryptosporidium
2. Isospora digestive tract
3. Cyclospora
4. Microsporidia – many organ systems
- broad spectrum of disease

19. I. CRYPTOSPORIDIUM:
♦Leading cause of diarrhea in children worldwide
♦Common cause of outbreaks in child care centers
Etiology:
♦Cryptosporidium parvum
♦Infection due to infectious oocyst
♦2 stages:
a)Asexual – autoinfection at luminal surface of
epithelium
b) Sexual – production of oocysts
♦Cysts immediately infectious

20. Epidemiology:
♦In developing countries and <2 years of age
♦Etiologic agent of persistent diarrhea
♦Transmission: - contact with infected animals
- person to person
- contaminated water
- zoonotic (cows)

21. Clinical Manifestation:
♦Incubation period – 2-14 days
♦Profuse, watery, non-bloody diarrhea, diffuse crampy
abdominal pain, nausea, vomiting and anorexia
♦Non-specific symptoms: myalgia, headache, weakness
fever – 30-50% cases
malabsorption, lactose intoerance
dehydration, weight loss, malnutrition–in severe cases
♦In immunocompromised hosts:
= assoc. with biliary tract disease
= fever ® upper quadrant pain, nausea, vomiting and
diarrhea
= detected in pancreatic duct of child with AIDS

22. Diagnosis:
♦Self-limited
♦Supportive care
♦Immunocompromised: Paromomycin (25-35mg/k/24hrs)
4 doses orally
Paromomycin (1g/day) and
Azithromycin (600mg daily) followed by
Paromomycin monotherapy X 8 weeks in adult patients
with AIDS

23. II. ISOSPORA:
♦Isospora belli
♦Diarrhea in intestinal outbreaks, travelers, contaminated
water and food
♦More common in tropical and subtropical climates
♦Not assoc. with animal contact
♦May infect 15% of AIDS patients
♦Life cycle same with Cryptosporidium except oocysts are
not immediately infectious and must undergo
maturation below 37O
C
♦Clinical manifestation: indistinguishable from
Cryptosporidiosis but fever is more common
♦Eosinophilia may be present

24. ♦Diagnosis: AFS of stool
Fecal leukocytes not detected
♦Treatment:
1. Trimethoprim – Sulfamethoxazole (TMP – SMZ)
(5mg TMP, 25mg SMZ/k/dose) max. 160mg TMP,
800mg SMZ/dose
orally 4 X/day X 10 days then 2 X a day X 3 weeks
2. Pyrimethamine alone or Folinic acid – in patients
intolerant of Sulfonamide drugs

25. III. CYCLOSPORA:
♦Cyclospora cayetanensis–AKA cyanobacterium– like body
♦Common in <18 months of age
♦Pathogenesis and path. findings similar to isosporiasis
♦Patients almost always have diarrhea
♦Linked to contaminated food and water
♦Clinical manif. similar to Crypto and Isosporiasis
♦Moderate illness: Median of 6 stools/day with median
duration of 10 day (range 3 – 35 days)

26. ♦Assoc. symptoms: fatigue, abdominal bloating or gas,
abdominal cramps, nausea, muscle joints and pains,
fever, chill and weight loss
♦Oocysts remain infectious for days to weeks
♦Diagnosis: Ident. of oocysts in stool
- modified AFS
- phenosafranin stain
- autofluorescence
Fecal leukocytes not present
♦Treatment: TMP – SMZ (5mg TMP, 25mg/k/dose SMZ)
2X/day; max. 160mg TMP, 800mg SMZ/dose orally
X 7 days

27. IV. MICROSPORIDIA:
♦Infect most animal groups including humans
♦Assoc. with GI disease:
a) Enterocytozoon beineusi
b) Septata intestinalis
♦Spores inject contents to host cells to cause infection
♦Spores detected in urine and resp. epithelium
♦Spores remain infectious up to 4 months
♦Almost exclusively reported in patients with AIDS
♦Diarrhea is intermittent, copious, watery and non-bloody
♦Biliary disease can occur

28. ♦Diagnosis: Hematoxylin – Eosin
Periodic acid – Schiff (PAS)
Giemsa and Gram stain
AFS
Electron Microscopy
♦Treatment: No proven therapy
Albendazole (adult dose: 400mg 2X/day X 4 weeks)
Atovaquone – dec. symptoms, no clinical trials

29. TRICHOMONIASIS
♦Trichomonas vaginalis
♦Sexually transmitted
♦>60% - female partners of infected men
♦30 – 80% male sexual partners of infected women
♦rare in menarche: if (+) in younger child – a possibility of
sexual abuse
♦can be transmitted to neonates thru infected birth canal
♦pathogenesis:
Vaginal secretions – 101
– 105
or more protozoa/ml
pear-shaped

30. ♦clinical manifestations:
-incubation period – 5 – 28 days
-10% - 50% asymptomatic female
-copious, malodorous yellow vaginal discharge
-vulvovaginal irritation
-dysuria, dyspareunia
-P.E: frothy discharge with vaginal erythema and
cervical hemorrhages (“strawberry cervix)
♦Most males are asymptomatic
♦5 – 15% of men with non-gonococcal urethritis
♦Symptomatic males: Dysuria
Scant urethral discharge – 36% resolve
spontaneously

31. ♦Diagnosis:
Demonstration of protozoan in genital secretions
Wet mount technique = 60-70% infected females
= 50-90% infected men
♦A (-) wet mount method does not rule out diagnosis of
trichomoniasis
♦Culture of the organism
= most sensitive
= >95% sensitive
= not routinely available

32. ♦Treatment:
1. Nitroimidazole
2. Metronidazole
3. Tinidazole
4. Ornidazole
Metronidazole = 2g orally single dose in adoles females
250mg 3X/day or 375mg 2X/day orally X
7days in infected
children – 15mg/k/24hrs / 3 doses orally X 7 days
♦All sexual partners should be treated
♦It is now recommended to treat trichomoniasis during
pregnancy – safe in last 2 trimesters

33. TOXOPLASMOSIS:
♦Toxoplasma gondii
♦Acquired perorally, transplacentally, rarely parenterally,
transfusion, transplacented organ
♦Organism persist for lifetime
♦Organism remain in tissues especially CNS, skeletal and
heart muscles oocysts excreted by infected cats
♦Cat excreted 105
– 107
oocysts/day
♦Acquired by oral route via uncooked or raw meat
containing cysts or by ingestion of oocysts
= pork – 5.35%
= lamb – 60%
= beef – 0-9%
♦Freezing meat – 200
C or heating 600
C – uninfectious

34. Pathogenesis:
Ingestion of Oocysts
↓
bradyzoites released from cyst
sporozoites from oocysts
↓
GIT
↓ lymphatics
disseminate throughout body
- pneumonitis
- myocarditis
- necrotizing encephalitis

35. Congenital Toxoplasmosis:
♦Mother acquires infection during gestation
♦Disseminate hemaatogenously to placenta
(transplacentally) or during vaginal delivery
♦1st
trimester – 17% infected
♦3rd
trimester – 65% infected
♦almost all infected fetuses manifest chorioretinitis
by adolescence

36. Clinical Manifestation:
Acquired Toxoplasmosis:
♦fever, stiff neck, arthralgia, maculopapular rash sparing
palms and soles, localized or gen. lymphadenopathy,
hepatomegaly, hepatitis, meningitis, brain abscess,
pneumonia, pericardial effusion, myocarditis
Ocular Toxoplasmosis:
♦blurred vision, photophobia, loss of central vision
♦strabismus, microophthalmia, microcornea, cataract,
nystagmus

37. Congenital Toxoplasmosis:
SKIN: rashes, petechiae, ecchymoses, large
hemorrhages 20
thrombocytopenia
Jaundice due to hepatic involvement
Systemic signs:
Endocrine: hypothalamic or pituitary involvement
myxedema, persistent hypernatremia,
D.I. without polyuria –
polydispsia, sexual precosity
CNS: hydrocephalus, seizures
EYES: chorioretinal lesions – 50% severe visual
impairment
EARS: Sensorineural hearing loss

38. Diagnosis:
1. Culture – isolation from blood or body fluids
- demo. of tachyzoites in tissues and body tissues
- cysts in placenta or tissues of fetus
2. Serologic testing:
a) Sabin-Feldman dye test – sensitive & specific
- measures IgG antibodies
b) IgG – indirect fluorescent – antibody (IgG – IFA)
- does not correlate severity of illness
c) Agglutination test – detect IgM antibodies
d) IgM – IFA – dx of acute infection in older children
e) Double Sandwich ELISA – more sensitive and specific
than IgM-IFA test
f) Immunosorbent agglutination assay (ISAGA)
g) Indirect hemaglutination (IHA) measures diff. T. gondii
antibodies

39. Treatment:
1. Pyrimethamine + Sulfadiazine or Trisulfapyrimidines
= act synergistically
= treat many forms of toxoplasmosis
2. Spiramycin – prevent transmission of infection to fetus
Acquired Toxoplasmosis:
Pyrimethamine – 2mg/k/24hrs (max. 50mg) 1st
2 days
1mg/k/24hrs (max. 25mg/24hrs)
Folinic Acid – 5-20mg 3X/week orally
Sulfadiazine – in >1year of age
- 75mg/k/24hrs LD then 50mg/k/24hrs

40. Ocular Toxoplasmosis:
Pyrimethamine
Sulfadiazine 1 week
Leukovorin
Congenital Toxoplasmosis: should be treated for 1
year
Oral Pyrimethamine – 1-2mg/k/24hrs X 2days then,
1mg/k/24hrs X 2 or 6months then,
1mg/k/24hrs M – W – F
Sulfadiazine – 100mg/k/24hrs LD
100mg/k/24hrs / 2 doses
Calcium leukovorin – 5 –10mg/k/24hrs M-W-F

41. Pregnant Women with Toxoplasmosis:
Spiramycin and Pyrimethamine + Sulfadiazine
= reduces infection in placenta and severity of
disease
Spiramycin – 1g every 8hrs. without food
Prognosis:
♦Early treatment for congenital infection cures
manifestations
♦Guarded – infected babies
Prevention:
1. Counseling women about methods of preventing
transmission of T. gondii during pregnancy
2. Eat well cooked meat
3. Avoid contact with oocysts excreted by cats

42. PNEUMOCYSTIS CARINII
♦Pneumocystis carinii pneumonia
(interstitial plasma cell pneumonitis)
♦Extracellular parasite of the lungs
Epidemiology:
♦Mostly affected - <4years of age
♦Immunocompromised patient - 40%
= infants and children
70% = adults with AIDS
12% = leukemia
10% = organ transplant

43. Pathogenesis:
2 types of histopathologic features of P. carinii pneumonia:
a) infantile interstitial plasma cell pneumonitis
= 3-6mos. of age
b) diffuse desquamative alveolar dis.
= immunocompromised children and adult
Clinical Manifestation:
♦Tachypnea without fever
♦intercostal, suprasternal and infrasternal retractions
♦nasal flaring
♦cyanosis
♦rales not detected
♦chest radiograph: bilateral diffuse alveolar disease with
granular pattern

44. Diagnosis:
♦demonstration of P. carinii in the lung
1) bronchoalveolar lavage
2) tracheal aspirate
3) transbronchial lung biopsy
4) bronchial brushings
5) percutaneous transthoracic needle aspiration
6) open lung biopsy – most reliable

45. Treatment:
TMP – SMZ – (15-20mg TMP, 75-100mg SMZ/k/24hrs)
4 doses
IV or orally = 3 weeks with AIDS
2 weeks in other patients
Pentamidine isethionate (4mg/k/24hrs)
SD IV – resistant to TMP – SMZ
Prednisone = inc. survival rate in mod. – severe infections
= >13 years old–80mg/24hrs/ 2 doses 1–5 days
40mg/24hrs 6 – 10th
days
20mg/24hrs 11 – 21st
days
= children – 2mg/kg/24hrs 1st
7 – 10 days
taper next 10-14 days

46. Prognosis:
♦without treatment – fatal
♦10 – 30% mortality rate
♦chemoprophylaxis - TMP – SMZ
Dapsone
Aerosolized pentamidine

47. MALARIA (PLASMODIUM)
♦acute and chronic protozoan illness charac. by
paroxysms of fever, chills, sweats, fatigue, anemia and
splenomegaly
Etiology:
♦Plasmodium protozoa
♦Transmitted to humans by female Anopheles mosquito
♦4 species:
1. P. falciparum
2. P. malariae
3. P. ovale
4. P. vivax
Life Cycle:
a) Asexual phase – in human host
b) Sexual phase – mosquito
♦Exoerythrocytic phase = cells in the liver

48. Exoerythrocytic phase:
Inoc. of sporozoites to blood stream by
Female Anopheles mosquito
↓
Hepatocytes (multiply asexually)
↓
Schizont (1-2 weeks)
↓
Rupture of hepatocytes
↓
Release of merozoites to circulation

49. Erythrocytic phase:
Merozoites from liver center erythrocytes
↓
Ring formation _____trophozoite
↓
Multiply to form erythrocytic merozoite
↓
bloodstream
↓
rbc membrane rupture (fever)
↓
ingested by mosquito
↓
male and female gametocyte fuse to form zygote
↓
sporozoites enter the salivary glands of mosquito

50. Epidemiology:
♦Transmitted through blood transfusion, use of
contaminated needles, pregnant woman to her fetus
Pathogenesis:
4 important pathologic process:
a) fever = when the rbc ruptures and merozoites are
released
b) anemia = hemolysis, sequestration of rbc’s in the spleen
and other organs, suppression of the rbc prod. in BM
c) immunopathologic events = formation of immune
complexes, immuno-suppresion, release of
cytokines
(TNF)
d) tissue anoxia = resulting from cytoadherence of infected
erythrocytes
= occur in P. falciparum malaria

51. • Clinical Manifestations:
Incubation period:
1. P. falciparum = 9-14 days
2. P. vivax = 12-17 days or as long as 6-12
months
3. P. ovale = 16-18 days
4. P. malariae = 18-40 days
Prodromal symptoms = 2-3 days
= headache, fatigue,
anorexia, myalgia, slight
fever, pain in chest,
abdominal and joint pains

52. • P. falciparum = most severe form
= infects both immature and
mature erythrocytes
P. ovale & vivax = infects immature rbc’s
P. malariae = infects mature erythrocytes
= mildest & most chronic
P. ovale = least common type
= in conjunction with P. falciparum

53. • Diagnosis of P. falciparum malaria constitute a
medical emergency
• Diagnosis:
Giemsa-stained peripheral smear
thick smear = scan large no. of rbc’s quickly
thin smear = identification of malaria species
& determine % of infected
erythrocytes

54. • A single negative blood smear does not rule out
malaria
• Other tests:
Monoclonal Antibody test = as sensitive as thick
smear
PCR

55. • Treatment:
1. Therapeutic
- Chloroquine phosphate = oral DOC
- Quinidine gluconate = IV DOC
2. Supportive
1. blood transfusion to maintain hematocrit
of >20%
2. exchange transfusion in P. falciparum
malaria with parasitemia of 15%
3. careful IV rehydration

56. 4. supplemental oxygen + ventilatory support
for pulmonary edema or cerebral malaria
5. IV glucose for hypoglycemia
6. anticonvulsants
7. dialysis for renal failure
Complications:
1. cerebral malaria = 20-40% fatality rate
2. renal failure
3. “Blackwater fever” = clinical syndrome that
consist of sevre hemolysis, hemoglobinuria
and renal failure

57. • Prevention:
1. reducing exposure to infected mosquitoes
2. travelers to endemic areas should remain in
well screened areas
3. using of mosquito repellants
4. use of chemoprophylaxis

58. SCHISTOSOMIASIS
Etiology:
♦Schistosoma sp:
1.S. haematobium
2.S. mansoni
3.S. japonicum
4.S. intercalatum
5.S. menkongi
♦Flukes or trematodes that parasitize bloodstream
♦Cercariae – infective stage

59. ♦Anatomic sites migrated by schistosoma
S. haematobium – perivesical and periureteral venous
plexus
S. mansoni – inferior mesenteric veins
S. japonicum – superior mesenteric veins
S. intercalatum and mekongi – mesenteric vessels
♦Charac. egg morphologic features:
S. mansoni – lateral spine
S. haematobium – terminal spine
S. japonicum – smaller size and short curved spine
♦Humans – only definitive host

60. Clinical Manifestations:
♦Papular pruritic rash (schistosomal dermatitis or
swimmer’s itch)
♦Katayama fever = serum sickness – like syndrome
- acute onset of fever, chills, sweating,
lymphadenopathy, hepatosplenomegaly,
eosinophilia
♦S. japonicum – may migrate to brain vasculature
Diagnosis:
♦Kato’s thick smear
Treatment:
Praziquantel

61. TRICHINOSIS
♦Etiology: Trichinella spiralis
♦Transmitted by ingestion of pork or other meat carrying
parasite
♦Larva penetrate gut wall, striated muscle, CNS, heart
♦Clinical manif: 1st
week = gastroenteritis
muscle = periorbital, facial edema, myalgia
= common in masseters, diaphragm, intercostals

62. ♦Diagnosis: - periorbital edema
- myalgia fever
- eosinophilia
- muscle biopsy
- bentonite flocculation test
- inc. creative kinase + lactose
dehydrogenase = 50%
♦Treatment:
Mebendazole – eliminate adult worm from gut

63. TRICHURIASIS
♦Etiology: Trichuris trichiura or whipworm
♦Final habitats: cecum and ascending colon
♦Clinical manif: abdominal pain, colic, distention
♦Adult worm suck 0.005ml of blood/worm/day
Anemia, blood diarrhea, rectal prolapse – massive
infantile trichuriasis
♦Associated with Shigellosis and protozoan infections of
GIT
♦Treatment: Mebendazole – 70 – 90% cure rate
- 90 – 99% reduce egg output
- 100mg bid X 3 days or
500mg once a day
Albendazole – alternative
- 400mg X 3 days

64. STRONGYLOIDIASIS
♦Etiology: Strongyloides stercoralis
♦Filariform larva
♦Capable of infecting same individual (autoinfection)
♦Pathogenesis: Dermatitis – repeated skin penetration
- larva currens
Loffler’s Syndrome
♦Clinical manif: Pruritus and popular erythematous rash
Abdominal pain, vomiting, diarrhea
♦Diagnosis: feces or duodenal fluid for larva
♦Treatment: Ivermectin – 200mg/k/24 hrs X 1-2 days
Thiabendazole – 50mg/k/24 hrs divided by
2 doses X 2 days

65. LYMPHATIC FILARIASIS
Etiology:
1. Brugia malayi (Malayan filariasis)
2. Wuchereria bancrofti (Bancroftian filariasis)
Characterized by: - lymphadenitis
- lymphangitis
- lymphatic obstruction and hydrocoele
- elephantiasis

66. Clinical manifestation:
-Fever
-Lymphangitis of extremity
-Lyphadenitis
-Headaches, myalgias
Diagnosis: Blood – microfilariae
Treatment:
1. Diethylcarbamazine – modifies course of acute
lymphangitis
2. Ivermectine

67. HELMINTHIC DISEASES
Ascariasis:
♦Ascaris lumbricoides
♦Common in pre-school and early school age
Etiology:
♦Mature larva containing egg – infective stage
♦Female – life span 1-2 years
200,000 eggs/24 hours
Epidemiology:
♦MOT– hand–mouth, fingers contaminated by soil contact
♦Foods - raw

68. Pathogenesis:
Ingested eggs
↓
larva
↓
intestinal wall
↓
pulmonary tissues
↓
alveolar spaces
↓
bronchial tree and trachea
↓
re-swallowed

69. Clinical Manifestation:
♦Pulmonary ascariasis: Cough blood-stained sputum +
Eosinophilia =
Loeffler’s – like Syndrome
♦GI : Abdominal pain and distention
Intestinal obstruction – 1-6 year old ,sudden,
severe, colicky abdominal pain
and vomiting (bile – stained)

70. Diagnosis:
♦DFS
♦Kato’s thick smear method
♦Pulmonary ascariasis or GI is based on clinical
symptoms and high index of suspension
Treatment:
1. Albendazole – 400mg PO SD
2. Mebendazole – 100mg BID X 3 days
500mg once
3. Pyrantel pamoate – 11mg/k once (max.1g) PO
4. Piperazine – 50-75mg/k X 2 days PO
- neuromuscular paralysis and expulsion of
parasite
Prevention:
1. Deworming every 3-6 months
2. Improve sanitary practices

71. HOOKWORMS
♦Ancylostoma
♦Necator americanus
Etiology:
1. Ancylostoma:
a) A. duodenale – classical hookworm infection
b) A. ceylanicum
c) A. caninum – eosinophilic enteritis syndrome
d) A. braziliense – cutaneous larva migrans
2. Necator americanus – anthropophilic hookworm
= infect humans thru skin penetration

72. Pathogenesis:
• adhere to mucosa & submucosa of S.I. (cutting plates) = causes
intestinal blood loss
•In moderate to severe infections: Anemia + IDA
Clinical Manifestations:
• “ground itch” = skin penetration
• Cough = Laryngotracheobronchitis; pharyngitis
• Chronic: Chlorosis – yellow green pallor
• Malnutrition

73. Diagnosis :
• DFS
• Colonoscopy
Treatment:
• !. Nutritional support
• 2. Albendazole
• 3. Mebendazole
• 4. Pyrantel pamoate

74. Prevention:
• 1. Sanitation
• 2. Health education
• 3. Avoidance of human feces as fertilizers

75. ENTEROBIASIS (Pinworm Infection)
• Enterobius vermicularis
• Embryonated egg in fingernails, clothing, beddings or house
dust
• Gravid female migrate by night to perianal region
• Humans = only natural host
• High in 5-14 years of age
Clinical Manifestations:
• nocturnal anal pruritus
• sleeplessness

76. Diagnosis:
• parasite eggs or worms in stools
• pressing adhesive cellophane tape technique
Treatment:
• 1. Albendazole
• 2. Mebendazole
• 3. Pyrantel pamoate
•Repeat treatment after 2 weeks

77. TOXOCARIASIS:
• Visceral larva migrans
= < 10 yrs of age
= fever, hepatomegaly, pulmonary disease & eosinophilia
= Toxocara cati – feline ascarid
= Toxocara canis – canine ascarid
Clinical manifestations:
• fever = 80%
• cough with wheezing = 60-80%
• seizures = 20-30%
• Hepatomegaly = 65-87%
• rales or rhonchi = 40-50%

78. • urticarial rash = 20%
• lymphadenopathy = 8%
• decreased visual acuity = 75% (ocular larva migrans)
Diagnosis: ELISA
Treatment:
• In pulmonary disease: Prednisone
• Ocular Larva Migrans : Diethylcarbamazine
Albendazole
Mebendazole
Prevention:
• Wash hands after playing with pets
• Periodic deworming of dogs & cats

79. TAPEWORM INFECTIONS
TAENIASIS:
1. Taenia saginata = beef tapeworm
2. Taenia solium = pork tapeworm
Difference:
T. saginata = 4 anterior suckers
= > 20 uterine branches
T. solium = scolex with double row of hooks
= < 10 uterine branches
Treatment: Preaziquantel

80. DIPHYLLOBOTHRIASIS:
• Diphyllobothrium latum = fish tapeworm
= longest human tapeworm
• Uses Vitamin B12 for production of segments
• Inhibits Vitamin B12 uptake by inactivating Vit. B12 intrinsic factor
• Megaloblastic anemia
• Treatment: Praziquantel = 5-10 mg/k P.O. single dose

81. HYMENOLEPIASIS:
• Hymenolepis nana = dwarf tapeworm
= in rodents, ticks, fleas
= poor hygienic conditions
Treatment:
•Praziquantel
•Niclosamide
DIPYLIDIASIS:
• Dipylidium caninum = tapeworm of domestic dogs & cats
Treatment: Praziquantel

82. CYSTICERCOSIS:
•Infection due to T. solium
•Common parasitic cause of CNS disease (Neurocysticercosis)
•Invade primarily the brain and muscle tissues
Clinical manifestations:
• seizures – primary finding
- 70% of cases
- 80% generalized
- initially simple or complex partial
•4th
ventricle = most common site of obstruction

83. Diagnosis:
• CT scan
•EITB (Enzyme Linked Immunotransfer Blot)
Treatment:
•Albendazole
•Corticosteroids

84. ECHINOCOCCOSIS:
•Hydatid disease of Hydatidosis
•Most serious human cestode infection
•Echinococcus species:
1. E. granulosus = unilocular or cystic hydatid disease
2. E. multiformis = alveolar hydatid disease
•Lungs = commonly affected
•Right lobe of the liver = 70% affected in adults
Treatment:
•Surgery = in alveolar hydatidosis
•Prophylactic Albendazole

85. MYCOTIC INFECTIONS
Neonatal Infections:
•Candida species = common cause
•Oral thrush & diaper dermatitis
•Isolated from GIT & vaginal flora
•10% term infants – GIT & respiratory tract
- 1st
5 days of life
•30% in <1,500 grams neonate
•Systemic infections in VLBW infants

86. Risk factors:
•Abdominal surgery
•Prolonged ventilatory support
•Prolonged IV catheterization
•Use of IV alimentation
•Administration of broad spectrum antibiotics
Clinical manifestations:
•Asymptomatic
•Associated with sepsis or shock in severe cases
•Disseminated candidiasis = mimics bacterial sepsis with respiratory
distress, apnea, bradycardia, temperature instability, glucose
intolerance, abdominal signs and symptoms

87. •Cutaneous: diffuse erythroderma or vesiculopustules
>50% renal involvement
•CNS – 1/3 of cases
- meninges, ventricles, cerebral cortex with abscess formation
•Endolphthalmitis = 20-50% of cases
•Candidal endocarditis = central venous catheters extending to atrium
•Pneumonia = 70% of cases
Diagnosis:
•Culture = body fluids
•Buffy coat smears = show yeast
= preliminary diagnosis
•Skin scrapings

88. Treatment:
1. Amphotericin B = Drug of choice
= 0.5-0.1 mg/k/24 hrs IV
= active against yeast & mycelial forms
= duration of therapy depends on the extent of
infection, clinical response, drug toxicity
= adverse reaction: Nephrotoxicity
2. Liposomal Amphotericin B = 5 mg/k/24 hr
= less renal toxicity
= in neonates with renal compromise
3, Flucytosine = 100-150 mg/k/24 hrs every 6 hrs P.O.
= CNS and parenchymal kidney infections

89. ORAL CANDIDIASIS:
•Oral thrush or oral pseumembranous candidiasis
•2-5% in newborns
•7-10 days of age
•Recurrent or persistent thrush = use of antibiotics during 1st
year of
life
•Removal of plaques causes bleeding = confirms the diagnosis
•Asymptomatic or with pain, causes decreased feeding
•No history of antibiotic intake = diabetes mellitus, HIV infection
Treatment:
•Mild = no therapy
•Severe = nystatin, Miconazole gel, Amphotericin B suspension,

90. DIAPER DERMATITIS:
•Complicates oral antibiotic treatment of otitis media
•Treatment: Nystatin cream, powder or ointment
1% Clotrimazole cream
2% Miconazole ointment
1% hydrocortisone = inflammation

91. VULVOVAGINITIS:
•Common in pubertal & post pubertal women
•Predisposing factors: pregnancy
oral contraceptive use
poor hygiene
use of oral antibiotics
Clinical manifestations:
•Pain or itching
•Dysuria
•Vulvar or vaginal erythema
•Cheesy exudate
•Thrush like mucosal palques

92. Treatment:
•Nystatin cream
•Clotrimazole
•Miconazole
•Fluconazole

93. CRYPTOCOCCOSIS:
•Cryptococcus neoformans =
•Soil contaminated with avian droppings, fruits & vegetables
carried by cockroaches
•60% in adults
•5-10% in HIV infected adults
•Acquired by inhalation of fungal spores
•Disseminate into the brain, meninges, skin, eyes, skeletal; system
•Pulmonary cryptococcosis = granuloma
= subpleural location
= contain yeast forms
•CNS = cystic cryptococcomas
= 20% non-HIV infected patients

94. Clinical Manifestations:
•Pneumonia = most common form
= fever, cough, pleuritic chest pain
= x-ray: poorly localized bronchopneumonia
•Disseminated infection = follows primary pulmonary disease
= in immunocompromised individuals
•Meningitis = sub acute or chronic
= headache as initial symptom – good outcome
= cryptococcal antigen titer < 1:32
= 15-30% mortality
= >50% relapse in HIV infection

95. •Skeletal infection = 5% of cases
= soft tissue swelling and tenderness
= arthritis ( effusion, erythema, pain on motion)
= vertebrae – common site
•Ocular infection = acute loss of visual acuity, eye pain, visual
floaters, photophobia
= >20% mortality rate
= 15% recover full vision
Diagnosis:
•Cuture
•Histology

96. Treatment:
•In immunocompromised host with asymptomatic or mild disease =
oral fluconazole (200-400 mg/24 hrs) for 3-6 months
•Immunocompetent with progressive pulmonary disease or non-HIV
infected = Amphotericin B (15mg/k/24 max. 1.5 g total dose)
•CNS and disseminated infections = combination of Amphotericin B
and Flucytosine
•Cutaneous infections = surgical biopsy for diagnosis and apply
appropriate topical antifungals
•Skeletal = surgical debridement & systemic antifungal
•Chorioretinitis = amphotericin B + Flucytosine of Fluconazole

97. HISTOPLASMOSIS:
• Histoplasma capsulatum = contaminated bird droppings or
decayed wood
• Often carried by wings of birds
• Resembles Ghon complex of TB
• 3 forms:
1. Acute pulmonary infection
2. Chronic pulmonary histoplasmosis
3. Progressive disseminated histoplasmosis

98. Acute Pulmonary Histoplasmosis:
•Follows initial or recurrent respiratory exposure to microconidia
•Flu-like symptoms: headache, fever, chest pain, cough
•Hepatosplenomegaly in children and infants
•In severe cases: respiratory distress, hypoxia – may require intubation,
ventilation, steroid therapy
Chronic Pulmonary Histoplasmosis:
•Opportunistic infection in adults with centrilobular emphysema
•Rare in children

99. Progressive Disseminated Histoplasmosis:
•Affects infants & immunosuppressed individuals
•Infants <1 year & follows primary pulmonary histoplasmosis
•Fever = most common
= last for weeks to months
•Hepatosplenomegaly, anemia, thrombocytopenia
Diagnosis:
•Culture of bronchoalveolar lavage fluid
•Culture of blood = >90% patients with progressive disseminated
histoplasmosis
Treatment:
•Amphotericin B = DOC
•Ketoconazole
•Itraconazole

100. MUCORMYCOSIS:
•Characterized by vascular invasion, thrombosis and necrosis
•Rhinocerebral and pulmonary infections – inhaled spores
•Occur in patients with leukemia, DM, Fanconi’s anemia
•Headache, retro orbital pain, fever, nasal discharge
•Nasal discharge = dark & bloody
•Nasal mucosa = black with necrotic areas
•Brain abscess may occur
•Pulmonary mucormycosis: fever, tachypnea, productive cough, pleuritic
chest pain, hemoptysis

101. Diagnosis:
•Culture
•Histology
Treatment:
•Amphotericin B (1-1.5mg/k/24 hrs to a total dose of 70 mg/kg)
•Extensive surgical debridement