Communicable Diseases

1. PCP 023
COMMON COMMUNICABLE
DISEASES
1

2. LEARNING OBJECTIVES
• Discuss the burden and impact of communicable
diseases
• Identify priority communicable diseases
• Explain basic principles of control and treatment of
communicable disease
2

3. EXPECTED OUTCOMES
• Recognize communicable diseases
• Effectively manage common communicable diseases
• Review and determine when to refer patients with
communicable disease
3

4. COURSE OUTLINE
• Definitions and prerequisites for treatment
• Treatment of HIV/AIDS
• Treatment of Malaria
• Treatment of Diarrhea
• Syndromic management of STIs
4

5. COMMUNICABLE DISEASES
Communicable diseases are those transmitted directly
or indirectly from person or animal to man, animal
to animal, or from the environment through air, water,
food or by discharges and infected objects including
blood, body fluids, bites and scratches.
5

6. PREREQUISITES
• Sufficient information should be obtained to enable an
appropriate assessment of the situation to be made.
• Information should include, who has the problem, what
are the symptoms, how long has a condition persisted, has
any action already been taken and which medicines, if
any, the person concerned is already taking.
• Establish whether the symptoms might be strongly
associated with a serious condition and in such
circumstances refer the individual for immediate medical
advice
6

7. CONSIDERATIONS BEFORE
REFERRAL BY PHARMACIST
• Whether symptoms have persisted over a considerable
period
• Whether a condition has recurred or worsened
• Whether there is severe pain
• Whether one or more medicines which appeared to be
appropriate for treatment of the symptoms have been
tried without success
• Whether there are suspected adverse reactions to
prescribed or non prescribed medicines
• Whether symptoms are recognised as being very
serious. 7

8. CONSIDERATIONS BEFORE REFERRAL
BY PHARMACIST (cont.d)
• In the case of symptoms which do not meet above
criteria in previous slide, a pharmacist should give
appropriate advice which may or may not include a
recommendation to use a particular medicinal
product.
• Advice should also be given that a prescriber should
be consulted should the symptoms persist beyond a
stated time.
8

9. Referral
• When a decision is made that a patient should seek
medical advice, it is important that the information
provided to the prescriber should be adequate and
accurate.
Confidentiality
• A pharmacist must respect the confidentiality of
information acquired in the course of professional
practice.
Prescriber/Pharmacist Co-operation
• Close co-operation between prescribers and
pharmacists is as important in order to achieve
treatment goals. 9

10. HIV/AIDS
10

11. 11

12. 1. Binding and Fusion: HIV begins its life cycle when
it binds to a CD4 receptor and one of two co-
receptors on the surface of a CD4+ T-lymphocyte.
The virus then fuses with the host cell. After fusion,
the virus releases RNA, its genetic material, into the
host cell.
Possible interventions: Fusion inhibitors
2. Reverse Transcription: An HIV enzyme called
reverse transcriptase converts the single-stranded
HIV RNA to double-stranded HIV DNA.
Possible interventions: NRTIs, nNRTIs
12

13. 3. Integration: The newly formed HIV DNA enters the
host cell's nucleus, where an HIV enzyme called
integrase "hides" the HIV DNA within the host cell's
own DNA. The integrated HIV DNA is called provirus.
The provirus may remain inactive for several years,
producing few or no new copies of HIV.
4. Transcription: When the host cell receives a signal to
become active, the provirus uses a host enzyme called
RNA polymerase to create copies of the HIV genomic
material, as well as shorter strands of RNA called
messenger RNA (mRNA). The mRNA is used as a
blueprint to make long chains of HIV proteins
Possible interventions: Integrase inhibitors
13

14. 5. Assembly: An HIV enzyme called protease cuts the
long chains of HIV proteins into smaller individual
proteins. As the smaller HIV proteins come together
with copies of HIV's RNA genetic material, a new
virus particle is assembled.
Possible interventions: Protease inhibitors
6. Budding: The newly assembled virus pushes out
("buds") from the host cell. During budding, the new
virus steals part of the cell's outer envelope. This
envelope, which acts as a covering, is studded with
protein/sugar combinations called HIV glycoproteins.
These HIV glycoproteins are necessary for the virus to
bind CD4 and coreceptors. The new copies of HIV can
now move on to infect other cells.
14

15. ARV CLASSIFICATION
• Non-nucleoside Reverse Transcriptase Inhibitors
(NNRTIs) such as nevirapine and efavirenz stop HIV
production by binding directly onto the reverse
transcriptase enzyme thus preventing the transcription
of viral RNA to DNA. A recent addition to this class is
etravirine.
• Nucleoside/Nucleotide Reverse Transcriptase
Inhibitors (NRTIs/NtRTIs) incorporate themselves
into the DNA of the virus, thereby stopping the
building process. The resulting DNA is incomplete
and cannot create a new virus.
15

16. ARV CLASSIFICATION (cont.d)
• Protease Inhibitors (PIs) work later in the virus
reproduction cycle. They prevent HIV from being
successfully assembled and released from the infected
CD4+ cell.
• The chemokine receptors antagonists which bind to
CCR5 or CXCR4 on the T cell surface and thereby
prevent viral attachment to these co-receptors. This class
includes Maraviroc
• Fusion inhibitors which bind to viral gp41 and prevent
the virus from penetrating the T-cell membrane such as
enfurvitide.
• Integrase Inhibitors prevent the integration of viral
DNA into the T-cell DNA and such as raltegravir. 16

17. Source: Vander Horst D ( 2016 ) HIV pharmacotherapy: back to basics 17

18. Source: Vander Horst D ( 2016 ) HIV pharmacotherapy: back to basics
18

19. STAGING OF HIV INFECTION
• Stage I: Asymptomatic, generalized lymphadenopathy,
Performance scale 1
• Stage II: Weight loss <10%, prurigo, fungal nail
infection, herpes zoster, recurrent URTIs
• Stage III: Weight loss > 10%, chronic diarrhea or
fever, oral candidiasis/hairy leukoplakia, pulmonary TB,
severe bacterial infections
• Stage IV: AIDS-defining illnesses: e.g HIV wasting
syndrome, PCP, brain toxoplasmosis, candida
oesophagitis, extra-pulmonary TB, CMV retinitis,
Kaposi’s sarcoma, non-Hodgkins lymphoma and/or
performance score 4: bedridden >50% of the day during
the last month 19

20. FIRST LINE DRUGS USED IN
NIGERIA
• Preferred first line regimens in Nigeria are:
– TDF+3TC (or FTC)+EFV
– TDF+3TC (or FTC)+NVP
– AZT+3TC+EFV
– AZT+3TC+NVP
• Current WHO preferred regimens are (Also preferred
first line regimens in the U.S.):
– EFV/TDF/FTC
– ATV/r + TDF/FTC
– DRV/r + TDF/FTC
– RAL + TDF/FTC 20

21. COMMENCING THERAPY
• All patients with HIV infection who have a CD4 count
< 350 cells/mm3 including pregnant women irrespective
of clinical symptom
• All patients with WHO clinical stage 3 or 4 irrespective
of CD4 count
• Start ART in HIV infected individuals with active
Tuberculosis (TB) irrespective of CD4 cell count.
• In all HIV patients where CD4 cells count > 350/mm3
start ART in the presence of ;
– High viral load (≥100 000 HIV RNA copies/mL)
– Chronic Hepatitis B or C virus co infections
– HIV-associated nephropathy. (Based on proteinuria
>1g/3+
21

22. COMMENCING THERAPY
- CrCl <60ml/min, and no alternative diagnoses)
• For pregnant women with a CD4 count > 350, ARV
should be provided for PMTCT
• Discordant relationships (Decrease transmission)
• Consider ART in patients with rapid decline in CD4
cell count (≥100 cells /year)
22

23. HARRT
– 3drugs from 2 classes
23

24. Source: Vander Horst D ( 2016 ) HIV pharmacotherapy: back to basics 24

25. SOME COMMON SIDE EFFECTS
• ZIDOVUDINE –Bone marrow suppression, anaemia,
neutropenia
• NEVIRAPINE-rash (20%) , hepatotoxicity
• ABACVIR- hypersensitivity ( HLA-B 5701 testing)
• Protease Inhibitors- Metabolic abnormalities,
dyslipidemia, Lipodystrphy
25

26. SOME COMMON SIDE EFFECTS
• NVP closely associated with Hepatotoxicity and
hypersensitivity especially where CD4>250 and more
frequently in women
• AZT closely associated with anaemia, lipodystrophy,
lactic acidosis
• D4T induced peripheral neuropathy, lipoatrophy;
hyperlactatemia, including symptomatic and life-
threatening lactic acidosis, hepatic steatosis, and
pancreatitis has resulted in withdrawal of the drug
from adult regimen but still a component of
paediatric regimens
26

27. SOME POINTS TO NOTE
• TDF. Creatinine clearance should be monitored and
dosage adjustments effected where necessary to
reduce risk of renal toxicity (Use Cockcroft’s
equation and serum Creatinine level). May have long
term effects on bone density.
• ATZ/r. Requires dose separation when co-
administered with H2 antagonists.
• Most guidelines recommend TDF backbone regimens
as first line option – superior virological suppression.
27

28. ADHERENCE
• Best outcomes require adherence rates over 95%
Reinforce the need for strict adherence
For every
10%
decrease in
adherence
1.17 times higher likelihood
of progression
to AIDS
and/or death
16% increase in
HIV-related mortality
28

29. PROMOTING ADHERENCE
• Providing education about the medications and
expectations of treatment
• Minimizing toxic effects- anticipating and effectively
managing adverse effects
• Simplifying treatment regimens – use co formulated
pills of
 Reduced pill burden- use fixed-dose combinations
 Decreasing drug costs-use generics
29

30. PMTCT
30

31. FACTORS AFFECTING
TRANSMISSION
• High maternal viral load
• Viral characteristics advanced disease
• Immune deficiency
• HIV infection acquired during pregnancy or
breastfeeding
• Sexually transmitted infections
• Mixed feeding
• Breast disease (abscess / mastitis / cracked nipples)
• Prolonged breastfeeding 31

32. FACTORS AFFECTING
TRANSMISSION (cont.d)
Malaria
Vaginal delivery
• Rupture of the membranes for more than 4 hours
• Prolonged labour
Prematurity infant
• First of multiple deliveries
M
32

33. WHO 2012 REVISED PMTCT
RECOMMENDATIONS
• In addition to the two pronged approach intervention
for PMTCT (2010)
– Life-long ART for HIV-infected pregnant women in
need of treatment
– Prophylaxis, or the short-term provision of ARVs, to
prevent HIV transmission from mother to child, for
women who don’t require treatment for their own
health
• WHO has recommended a third intervention which is
lifelong treatment for every pregnant woman for life –
Option B+ 33

34. WHO 2012 GUIDELINES FOR PMTCT
- PROPHYLAXIS
OPTION A OPTION B OPTION B+
MOTH
ER
Antepartum: AZT
starting as early as
14 weeks gestation
Intrapartum: at
onset of
labour, sdNVP and
first dose
of AZT/3TC
Postpartum: daily
AZT/3TC
through 7 days
postpartum
Triple ARVs starting
as early
as 14 weeks
gestation
and continued
intrapartum
and through
childbirth if
not breastfeeding
or until
1 week after
cessation of all
breastfeeding
Regardless of
CD4 count,
triple ARVs
starting as soon
as diagnosed,
continued for
life
35

35. WHO 2012 GUIDELINES FOR PMTCT
- PROPHYLAXIS
OPTION A OPTION B OPTION B+
BABY Daily NVP from
birth
through 1 week
beyond
complete cessation
of
breastfeeding; or, if
not
breastfeeding or if
mother
is on treatment,
through
age 4–6 weeks
Daily NVP or AZT
from
birth through age 4–
6
weeks regardless
Daily NVP or
AZT from
birth through
age 4–6
weeks
regardless
36

36. MALARIA
37

37. MALARIA
• Malaria is the world’s most devastating human
parasitic infection affecting nearly 500 million people
and causing some 2 million deaths annually
• Complications of untreated malaria may include,
renal failure, pulmonary edema, cerebral malaria,
coma and death. Another potential complication with
malaria infection The prognosis of cerebral malaria is
poor, and even with treatment, residual neurological
deficits are not ruled out.
38

38. AETIOLOGY AND
PATHOPHYSIOLOGY OF MALARIA
• Causative organism: Protozoan parasites of the genus
Plasmodium. Four species exists : P. falciparum, P.
vivax, P. ovale and P. malaria.
• P. falciparum is the most widespread and dangerous
of the four.
39

39. MANAGEMENT OF MALARIA
• Goals of Therapy
– The overall goal of therapy is to eradicate the parasite
on both its erythrocytic and exoerythrocytic forms.
Thus, there are 3 separate goals of therapy:
• Prophylaxis (suppression therapy)
• Treatment of an acute attack (clinical cure)
• Prevention of relapse (radical cure)
40

40. Source:Esperança Sevene, Raquel González & Clara Menéndez Current knowledge and challenges of
antimalarial drugs for treatment and prevention in pregnancy Expert Opin. Pharmacother. (2010) 11(8
11:8, 1277-1293
41

41. LIFE CYCLE
• Tissue schizonticides: Act against pre-erythrocitic
schizonts (e.g., primaquine, atovaquone--proguanil,
pyrimethamine).
• Blood schizonticides: Suppress infection symptoms
by elimination of erythrocytic forms; also called
‘clinicallycurative’ (e.g., atovaquone--proguanil,
sulfadoxine, sulfones, tetracyclines, halofantrine,
quinine, mefloquine and chloroquine).
42

42. LIFE CYCLE
• Gametocytocides: eliminate gametocytes forms in
the blood, preventing mosquito infection (e.g.,
primaquine has activity against all Plasmodium spp,
chloroquine and quinine against P. vivax and P.
malariae).
• Sporontocides: prevent the development of oocyst
and multiplication of parasites in the mosquito gut
when ingested with the blood of the human host (e.g.,
primaquine, chloroguanide, pyrimethamine).
43

43. LIFE CYCLE
• Since none of the drugs kills sporozoites, it is not
truly possible to prevent infection but only to prevent
the development of symptomatic malaria caused by
the asexual erythrocytic forms.
• None of the anti malaria is effective against all liver
and red cell stages of the life cycle that may co-exist
in the same patient. Complete cure therefore may
require more than one drug.
44

44. SUPPRESSION
• Suppressive therapy cannot prevent primary infection of
the liver because drug therapy does not affect sporozoites.
Suppressive therapy does prevent the erythrocytic
infection, which causes the symptoms of malaria.
However, once the liver has a primary infection, the
patient can have an acute attack when he or she is no
longer taking the suppressive drugs.
• Selection of suppressive drug therapy depends on which
region the patient intends to visit. In chloroquine-resistant
areas, mefloquine is the preferred suppressive agent.
• Alternative agents include hydroxychloroquine,
doxycycline and a pyrimethamine/sulfadoxine
combination.
45

45. TREATMENT OF ACUTE
ATTACK
• Drugs that eradicate plasmodia in the erythrocytic
stage of replication are used to treat an acute attack.
• Chloroquine
• Hydroxychloroquine
• Mefloquine
• Primaquine
• Pyrimethamine
• Quinine
46

46. PREVENTION OF RELAPSE
• A radical cure for malaria is necessary for strains of
P. vivax because the infection is harboured in the
liver. The radical cure is postponed until the patient
leaves the endemic malaria area because re-infection
with continued bites is almost a certainty. The drug
of choice for radical cure is Primaquine.
47

47. ARTEMISININ AND DERIVATIVES
• Natural- Arteminisin
• Semi synthetic derivatives- dihydroartemisinin,
artemether, artesunate
• 10 – 100 fold more potent than other anti-malarials
and fast-acting
• They have gametocytocidal activity but do not affect
either primary or latent liver stages.
• No clinical evidence of resistance.
• No cross-resistance to other drugs
• Avoid monotherapy 48

48. MALARIA IN PREGNANCY-
STRATEGIES
• Prompt and effective case management of malaria
• Intermittent preventive treatment (IPT) with at least
two treatment doses of SP
• Insecticide-treated nets (ITNs)
49

49. MALARIA IN PREGNANCY
Drugs that can be used in pregnancy
• Quinine
• Chloroquine
• Amodiaquine
• Mefloquin
• Sulfadoxine—pyrimethamine
• Proguanil
• Artemisinins
• Clindamycin
50

50. WHO POLICY
The WHO’s Policy
• 1ST TRIMESTER: Quinine (Drawback: long
duration, low tolerability), Clindamycin
(Drawback : High cost)
• 2ND & 3RD TRIMESTER: Artemisinin-based
combination therapies
Source: WHO. A strategic framework for malaria prevention and control during pregnancy
in the African region. World Health Organization, Geneva 2004, 2004: AFR/MAL
51

51. Source::Esperança Sevene, Raquel González & Clara Menéndez Current knowledge and
challenges of antimalarial drugs for treatment and prevention in pregnancy Expert Opin.
Pharmacother. (2010) 11(8 11:8, 1277-1293
52

52. DIARRHOEA
53

53. DIARRHOEA -DEFINITION
• An increase in frequency of loose, watery stools
(three or more daily) usually over a period from 24 to
48 hours.
• The overall weight and volume of the stool is
increased (>200g or mL/day) and the water content is
increased to 60 – 90%
54

54. PATHOPHYSIOLOGY OF
DIARRHOEA
• In general, diarrhoea results when some factor
impairs the ability of the intestine to absorb water
from the stool, which causes excess water in the
stool.
55

55. MANAGEMENT OF DIARRHEA:
GOALS OF THERAPY
• To reduce the symptoms of diarrhoea
• To make the patient as comfortable as possible
• To identify and eradicate causative factors if possible
• To replace lost fluid and electrolytes in order to avoid
serious complications from dehydration.
.
56

56. TREATMENT-NON-
PHARMACOLOGIC -ORT
Ongoing fluid replacement
Frequent feeding with appropriate food including
breastfeeding- feeding does not make the diarrhoea
worse and may actually improve the condition
57

57. TREATMENT- NON-
PHARMACOLOGIC- ORT
ORT has been described as “potentially the most
important medical advance of this century”. Reasons:
– ORT can be used alone to successfully rehydrate 90%
of patients with dehydration due to acute diarrhoea
who earlier received iv therapy.
– ORT reduces hospital case-mortality rates by 40 –
50%.
– ORT reduces diarrhoea disease hospital admission
rates by 50 – 60%, and the costs of treatment of
diarrhoea are reduced up to 80%.
58

58. TREATMENT- NON-
PHARMACOLOGIC- ORT
– ORT used at home in the early stages of the
diarrhoeal illness prevents dehydration.
– ORT is cheap and simple, and can be administered by
mothers and other family members.
59

59. ORS
– The most important part of treating acute diarrhoea is
the replacement of lost fluids and electrolytes.
– For mild to moderate fluid loss, fluid replacement can
be achieved with ORS.
– The ORS has no effect on the duration of the
diarrhoea. Not every patient needs ORS. For a child
without evidence of dehydration, administer 10ml/kg
or half 1 cup of ORS for each loose stool.
– If child is vomiting, administer smaller amounts (1 -2
teaspoonfuls) every 2 – 5 minutes as tolerated.
60

60. TREATMENT
• If severe (>10% loss of body weight) and/or severe
vomiting persists
IV Rehydration before oral maintenance fluids
61

61. PHARMACOLOGIC-ORAL ZINC
TABLETS
• Shown to reduce duration and severity of diarrheal
episodes
• Protective action may last for 2 to 3 months
DOSE:
• Child below 6 months : 10 mg daily
• Child above 6 months: 20 mg daily
62

62. PHARMACOLOGIC
TREATMENT- PROBIOTICS
• Probiotics are live microorganisms that when
ingested in adequate doses can potentially produce
health benefits. They include various strains of:
• Lactobaccilus spp
• Saccharomyces
• Bifidobacterium
• Streptoccocus
63

63. PHARMACOLOGIC
TREATMENT- PROBIOTICS
• They stimulate optimal mucosal immune response and
prevent GIT infections .they have been shown to
significantly reduce risk of diarrhea , stool frequency
and duration
• DOSE:
• Children: 5-10 billion colony forming units(CFU)
daily
• Adults: 10-20 billion colony forming units(CFU) daily
Use strains with proven efficacy and at appropriate dose
64

64. PHARMACOLOGIC-ROTAVIRUS
VACCINE
• A live vaccine that has been proven to positively have
protective value against diarrhea
• RotaTeq : Pentavalent vaccine , 3 dose regimen
• Rotarix : 2 dose in infants 6 to 24 weeks old
65

65. PHARMACOLOGIC-
ANTIMOTILITY AGENTS
Opioid Agonists
Diphenoxylate – 2.5 – 5mg qid; Loperamide – 4 – 16mg/d
in divided doses. Difenoxin – the active metabolite of
diphenoxylate is also used.
Caution:
• Antimotility effects may exacerbate infectious diarrhoea.
• Use cautiously in patients with fever, bloody stools or
faecal leukocytes.
• Do not use in children
66

66. PHARMACOLOGIC-
ANTISPASMODIC AGENTS
• Act by diminishing intestinal motility and associated
abdominal cramps Examples – propantheline bromide
(probanthine) and dicyclomine hydrochloride
(merbentyl)
Opiates
Reduce the propulsive movements of the colonic muscle
permitting the feaces to remain longer in the lumen, and
water is reabsorbed.
Examples: Paragoric (camphorated tincture of opium)
4ml; laudanum (tincture of opium) 0.3 – 0.6 ml;
Codeine sulphate 16 – 32 m 67

67. PHARMACOLOGIC- ADSORBENTS
AND ABSORBENTS
• Kaolin, pectin and attapulgite (kaopectate) – start 30
– 120ml of liquid or 2 tablets after each bowel
movement; range-up to 7 doses a day;
• Polycarbophil (Fiber-con)-1-6g/d. Usually given
after each bowel movement until diarrhoea is relieved
or maximum dose given.
68

68. RECOMMENDED ORDER OF
TREATMENT FOR DIARRHOEA
• First line: Loperamide: easy to use, tablet or liquid.
• Second line: Adsorbents or antisecretory agent;
selection based on drug-drug interactions or allergies
(eg. Aspirin sensitivity and Bismuth subsalicylate)
• Third line: Diphenoxylate; side-effect profile,
especially with atropine added, lowers its utility.
• ORT today is recognised as the first line treatment in
most cases of acute diarrhoea. Antibacterial agents
are required only in infectious diarrhoea where
pathogens have been positively identified. 69

69. STIs

70. MAJOR STIs -VIRUSES
• Human Papilloma virus Warts
• Herpes Simplex-- Herpes
• Hepatitis B Hepatitis
• HIV AIDS
71

71. MAJOR STIs -BACTERIA
• Chlamydia Chlamydia
• Neisseria gonorrheae Gonorrhea
• Treponema pallidum Syphilis
• Hemophilus ducreyi Chancroid
72

72. MAJOR STIs -OTHERS
Fungi
Candida albicans Candidiasis
Protozoa
• Trichomonas vaginalis Trichomoniasis
• Insects
• Sarcoptes scabii Scabies
73

73. STIs TREATMENT OPTIONS
AETIOLOGIC
– Lab isolation of the causative organism
CLINICALASSESSMENT
– “Aetiology” based on clinical appearance
SYNDROMIC
– Syndromes- clinical symptoms, signs, risk
assessment, rapid and cost-effective tests
MIXED
– All of the above; but which give immediate results
for “point of first contact” management
74

74. TREATMENT OF STIs
The Syndromic Approach
• Involves treating the signs or symptoms (syndrome) of a
group of diseases rather than treating a specific disease
• Identifies consistent groups of signs and symptoms
(syndromes)and treats accordingly
• Provides treatment for majority of serious organisms
responsible for producing a syndrome
• Overcomes lack of laboratory infrastructure, expensive
tests and special trained personnel.
75

75. TREATMENT OF STIs
The Syndromic Approach
• In addition initiate contact tracing, condom use,
HIV and risk reduction counseling, adherence
measures and maintain confidentiality, follow-up
after completion of treatment.
76

76. TREATMENT OF STIs
The Syndromic Approach
Requirements
• Adequate medical history
• Good sexual history
• Complete STI clinical examination
• Management guidelines
• Good supply of effective drugs
77

77. SYNDROME 1- Vaginal
Discharge/Pruritis
78

78. SIGNS
• Vaginal discharge
• Pruritus (itching) of the vulva or vagina
• Lower abdominal pain
• Spotting
• Pain with urination (dysuria)
• Pain with sexual intercourse (dyspareunia)
• Genital ulcers or warts
• Inflammation
79

79. VAGINAL
DISCHARGE/PRURITIS
• Inflammation is the most common pathological
condition of the cervix and vagina. Usually caused by
an infection
• Discharge can be due to cervicitis (inflammation of
the cervix) or vaginitis(inflammation of the vagina)
80

80. VAGINAL
DISCHARGE/PRURITIS (cont.d)
Most common causes
• Trichomonas vaginalis
• Bacterial vaginosis
• Candida albicans
• Gonoccal/Chlamydial cervicitis (Rarely)
81

81. Discharg
e
Itchin
g
Inflamation Odor
Candida White,
curd-like
Yes Yes No
Trich Yellowish
,
frothy
Yes Yes Yes
Bacteria
Vaginitis
Greyish,
white
No No Yes
82

82. VAGINAL
DISCHARGE/PRURITIS (cont.d)
• All women presenting with vaginal discharge should
receive treatment for vaginitis and cervicitis.
83

83. VAGINAL DISCHARGE/PRURITIS-
Syndromic Treatment
• Trichomoniasis or Bacterial vaginosis
–Metronidazole (Flagyl) 2g PO,once stat
– Metronidazole (Flagyl) 400-500mg BID x 7
• Candidiasis
– Fluconazole 150-200mg PO, once stat
– Clotrimazole 500mg intravag, once stat
– Miconazole or clotrimazole 200mg intravag,
daily x 3
– Nystatin pessary daily x 5
84

84. 85

85. VAGINAL DISCHARGE/PRURITIS-
Syndromic Treatment
• Chlamydia
– Azithromycin 1g PO, once stat
– Doxycycline 100mg PO BID x14 d
– Erythromycin 500mg PO QID x 7 d
• Gonorrhea
– Ciprofloxacin 500mg PO, once stat
– Ceftriaxone 125mg IM Stat
86

86. SYNDROME 2-
Vaginal Discharge
+Lower Abdominal Pain

87. VAGINAL DISCHARGE +LOWER
ABDOMINAL PAIN
Signs
• Vaginal discharge
• Lower abdominal tenderness on palpation
• Temperature > 38C
Symptoms
• Lower abdominal pain
• Dyspareunia
88

88. VAGINAL DISCHARGE +LOWER
ABDOMINAL PAIN
Most common causes
• Gonococcus
• Chlamydia
• Mixed anaerobes
89

89. VAGINAL DISCHARGE +LOWER
ABDOMINAL PAIN
Syndromic Treatment
• Chlamydia
– Azithromycin 1g PO stat
– Doxycycline 100mg PO BID x14 d
– Erythromycin 500mg PO QID x14 d
• Gonorrhea
– Ciprofloxacin 500mg PO Stat
– Ceftriaxone 125mg IM Stat
• Mixed Anaerobes
– Metronidazole (Flagyl) 400-500mg BID x14 d
90

90. VAGINAL DISCHARGE +LOWER
ABDOMINAL PAIN
Reasons for referral
• Rebound tenderness
• Guarding
• Last menstrual period overdue
• Recent abortion or delivery
• Menorrhagia—profuse or prolonged menses
• Metrorrhagia—irregular bleeding
91

91. 92

92. SYDROME 3-
Cervicitis

93. CERVICITIS
Symptoms
• Unusual vaginal discharge
• Dysuria (pain on urination)
• Dyspareunia (pain on intercourse)
• Abnormal bleeding
Signs
• Swollen, reddened, and ―beefy‖ cervix
• Cervix bleeds easily when touched
• Mucopurulent or copious discharge from os
94

94. CERVICITIS
Cause
• Gonococcus (?)
• Chlamydia(?)
95

95. CERVICITIS
Treatment
Syndromic Treatment
• Chlamydia
– Azithromycin 1g PO stat
– Doxycycline 100mg PO BID x 7
– Erythromycin 500mg PO QID x 7
• Gonorrhea
– Ciprofloxacin 500mg PO Stat
– Azithromycin 2g PO Stat
– Ceftriaxone 125mg IM Stat
96

96. SYNDROME 4-
Genital Ulcer Disease

97. GENITAL ULCER DISEASE
Most common causes
• Genital herpes
• Chancroid
• Syphillis
• Associated with an increased risk of HIV
infection
98

98. GENITAL HERPES
• Characterized by multiple, painful vesicles grouped
together
• First episode- Bilateral
• Recurrences- Unilateral
99

99. CHANCROID
• Cause: Haemophilus ducreyi
• Single or multiple ulcers on the labia,
vagina, or anus with or without swollen
inguinal lymph nodes and cervicitis.
• May be co-infected with HIV, herpes, or
Treponema pallidum (syphilis)
• Refer
100

100. SYPHILIS
• Cause: Treponema pallidum
• Characterized by painless ulcer or chancre on the
vulva, vagina, or cervix
• Co-infection with HIV is common
• Refer
101

101. 102

102. KEY LEARNING POINTS
• Communicable diseases are those that can be passed
to humans from infected humans, animals , body
fluids or other objects
• Pharmacists should distinguish between minor illness
which can be managed and major symptoms which
should be referred for expert management
• Common communicable diseases include HIV,
Malaria, Diarrhea and STIs
• Pharmacists should have a clear understanding and be
skillful in the management of these conditions
following appropriate protocols and guidelines
103

103. REFERENCES
• Oral rehydration therapy/Oral rehydration salt
Fact Sheet , Seattle PATH,2008.
• Zinc treatment for diarrhea
http//www.pathorg/files/immm_EDD-zinc.fs.pdf
• DEPT of HEALTH, Republic of south Africa
Sexually Transmitted Infections Management
Guidelines 2015Adapted from: Standard Treatment
Guidelines and Essential Drugs List PHC
• CCPP Training module- Syndromic management of
STIs
104

104. REFERENCES
• WHO. A strategic framework for malaria prevention
and control during pregnancy in the African region.
World Health Organization, Geneva 2004, 2004:
AFR/MAL
• Esperança Sevene, Raquel González & Clara
Menéndez Current knowledge and challenges of
antimalarial drugs for treatment and prevention in
pregnancy Expert Opin. Pharmacother. (2010) 11(8
11:8, 1277-1293
• Key facts about Rotavirus disease and vaccination
available at
http//wwwrotavirusvaccine.org/documents/keyfacts.pdf
105