I am giving the old names for these malarias in parentheses to give some historical perspective in case you see these terms again. I will also explain how these old terms relate to the pathogenesis of these respective diseases and the associated fever patterns.
Hemoglobinuria digest the blood it provide amino acid source
The life cycle of all species that infect humans is basically the same. There is an exogenous asexual phase in the mosquito called sporogony during which the parasite multiplies. There is also an endogenous asexual phase that takes place in the vertebrate or human host that is called schizogeny. This phase includes the parasite development that takes place in the red blood cell, called the erythrocytic cycle and the phase tthat takes place in the parencymal cells in the liver, called the exo-erythrocytic phase. The exo-erthrocytic phase is also called the tissue phase. The schizogeny that takes place here can occur without delay during the primary infection or can be delayed in the case of relapses of malaria. I will focus on the development of the parasite in the human host.
Infectious mononucleosis- viral disease, Discoid –skin, Systemic , Used to indicate reactions that occurs in leprosy patients
Nocturnal leg cramps - night
Thrombophelbitis- inflammation of vein in conjunction with thrombus water fever-
Parasitic protophorphrin IV – catalyses breakdown of endoperoxides (-0-0-) bridges of artemesin molecules generation high free radicals.
• Parasitic, endemic disease
• Malaria is a single cell protozoan
• It is caused by sporozoa of plasmodium
• Transmitted to human by bite of feMALe
AnopheLes mosquito .
• Symptoms become apparent only 7-10days
Pain in joints
Severe convulsions, coma
Classification of Malaria
• Uncomplicated Malaria
• Cold stage (sensation of cold, shivering)
• Hot stage (fever, headaches, vomiting; seizures
in young children)
• Sweating stage (sweats, return to normal
Classification of Malaria
• Severe Malaria
– Cerebral malaria (seizures, coma)
– Severe anemia
– Abnormalities in blood coagulation
– Cardiovascular collapse and shock (“rosettes”) P.F
Malaria Life Cycle
Liver- Tissue schizonts
RBC- Blood schizoints
Male & Female
(for P. vivax
and P. ovale)
Types of Infections
– All merozoites are not completely eradicated
– Surviving merozoites enter erythrocytic phase again (P.f.,
– Reactivation of hypnozoites forms of parasite in liver(P.v&
• Recurrence or reinfection
– exo-erythrocytic forms infect erythrocytes
Classification of antimalarials:
Based on clinical use (Based on stage of parasite they affect)
• True causal prophylactics:
• Causal prophylactics: Primaquine (3Ps)
– Maturation of sporozoites Schizonts in liver
• Supressives prophylactics :Quinine (MCQ-P)
– Destroy the merozoites so errythrocytic stage is prevented.
• Clinical cure: Chlorquinine, Pyrimethamine, Sulfadoxine (CPS)
– Blood schizonticides
• CQ resistance: Qunine, Mefloquinine , Artesunate
• Radical curatives: Primaquine (P.v& P.o)
4 aminoquinolines :Chloroquine
• Synthetic available as chloroquine phosphate
• Rapidly and completely absorbed oral/IM/IV slow.
Peak conc. 2-3 hrs after oral dose.
Highly conc. in liver, spleen ,lung, kidney.
Drug persist for longer period after discont.
t½ 3-4days but terminal t½1-2months
Metabolised to 4hydroxychloroquine.
Actions & Clinical use
• Potent blood schizonticidal
• Gametocidal P.Vivax, P.Ovale
• Relapse common so therapy followed by
primaquine 15mg OD for 15days
• P.falciparum is resistance
Uses & Dose
2.Ameobiasis - Hepatic
3.Acute manifestations of Lepra reaction.
6. Autoimmune disorder- Discoid lupus erythematous
Tab. Chloroquine 250 mg4tab stat
2tab after 6hrs
2tab daily for 2days
2 tab once a week
Others Hydroxychloroquine & Amidoquine
• Spectrum and clinical use are same
• A/E: Agranulocytosis
• Respond to chloroquine resistance P.falciparum
• Obtained from cinchona bark -1820
• P.K: Orally/slow IV for severe P.falciparum
• Wide distribution
• t½- 10-11hrs
meChAnism of ACtion:
• Being a protoplasmic poison to parasite
• Hampers the supply of aminoacids and
• Erythrocytic state
• Gametocidal activity in P.Vivax, P.Ovale
• Main drug for treating chloroquine resistant
• Loading dose.
• Require IV slow infusion in severe conditions
• Patient condition improve shifted to oral
• Present indication-cerebral malaria
• Nocturnal leg cramps
• GIT: Quinine inc. gastric acid secretion by
• CVS: Depress myocardium and cause hypotension
• Sk. Muscle : neuromuscular blockade
• CNS: In therapeutic dose – Hearing and vision
• IV it cause thrombophelbitis
• Stimulation of insulin Hypoglycaemia
• Black water fever – Rare characterized by
haemolysis, Haemoglobinemia, Haemoglobinuria
Quinoline methanol : Mefloquine
4 aminoquiniline derivative, haem poly. inhibitor
Highly effective against erythrocytic cycle
Orally. No parental Local irritation
High protein binding
It is used as Prophylaxis or clinical cure
Avoided during pregnancy
Should not be co-administered with quninie
Reserve drug for prophylaxis and R
chloroquinine resistant malaria
• Slow acting blood schizonticide
• Resistance rapid so combination with
• Sulfadoxine500mg+ Pyrimethamine25mg
combination adjunct with quinine to treat
chloroquinine resistance P.falciparum malaria
• At high dose it inhibits mammalian folate
• CNS stimulation causes seizures
• Large dose of Pyrimethamine+ Dapsone
combination cause anaemia, agranulocytosis
Same mech of action folate synthesis inhibitor
Produrg liver cycloguanil
Half life 16hrs
Alone resistance combination with Chloroquine
Prevents maturation of fertilized gametes
1.Git:stomatitis, mouth ulcers
DOSE:100 mg tab.
For causal prophylaxis
for multi drug resistance malaria.
Dose-4 tab od for 3 days
• 8- Aminoquinoline derivative
• Oral t½ 3-6hrs
• Mech: Inhibits respiratory process of parasite
in its erythrocytic state
• Use in radical cure and prevent relapse for P.
vivax & ovale
• CI : In pregnancy . foetus G6PD Risk of
• Dose:15 mg daily x 14 days for radical cure of p. vivax.
• artemisinin isolated from the verb Artemisia annua
• Parasitic protophorphrin IV – catalyses breakdown of
endoperoxides (-0-0-) bridges of artemesin
molecules generation high free radicals.
• Killing of malaria parasite is mediated by production
• Inhibit hemoglobin digestion by malaria parasites
Artemisinin induce rapid killing of parasites
Fast clearance rate
Very few side effects
Artemsinin-resistant parasites have not been
• Should be used in combination with other
• Clinical cure of severe malaria, chloroquine
• ADR:• Very few adverse reactions
• Common side effects include
• Safe for pregnant women
• In patients who can take drugs orally
Chloroquine 250mg 4 tab stat (600mg base)
300mg after 12hrs
300mg OD for 2nd and 3rd day
Note: chloroquine phosphate 250mg =150mg base
Quinine salts- 600mg tab TDS for 7days
In patients who cannot take drugs orally
Chloroquine IM 2.5mg/kg every 4 hrly
Chloroquine IV 10mg/kg over 4 hrs
5mg/kg over every 12 hrly
Chloroquine resistant malaria
1.Quinine 600mg TDS for 7 days along with
Pyrimethamine 75mg+sulfadoxine 1500mg
2. Quinine 600mg TDS + Teracycline 250mg qid -7 days.
3.Mefloquine 750mg stat followed by 500mg 12hr later.
4. Artesunate 100mgBD on 1stday followed by 100mg OD -5 days
5.Artesunate iv/im 120mg on 1st day followed by 60mg daily-4 days
6.Artemether (im)-80mg BD 1st day followed then OD -4 days.
7.Arteether (im)-150mg od -3 days.
• Serious disease-P.falciparum with strongly marked CNS
symptoms, impaires consciousness
-IV Quinine 600mg in 500ml of 5% dextrose slowly over 4 hrs
repeated every 8 hrs till patient is conscious
followed by oral treatment to complete 7 day course.
-Antipyretic for fever
-If fatal hypoglycemia -5%iv dextrose cont. infusion.
-correction of fluid and electrolyte balance, treatment of acidosis
Rapid iv can cause
• fall in BP
• Cardiac arrythmias.