{"id":6658,"date":"2024-11-19T11:50:10","date_gmt":"2024-11-19T11:50:10","guid":{"rendered":"https:\/\/workhouse.sweetdishy.com\/?p=6658"},"modified":"2024-11-19T11:50:10","modified_gmt":"2024-11-19T11:50:10","slug":"treatment-of-protozoal-infections","status":"publish","type":"post","link":"https:\/\/workhouse.sweetdishy.com\/index.php\/2024\/11\/19\/treatment-of-protozoal-infections\/","title":{"rendered":"TREATMENT OF PROTOZOAL INFECTIONS"},"content":{"rendered":"\n
    \n
  1. Treatment of Malaria<\/strong>
    Four species of Plasmodium are responsible for human malaria: P. vivax, P. malariae, P. ovale,
    and P. falciparum. Although all may cause severe illness, P falciparum causes most of the
    serious complications and deaths. The effectiveness of antimalarial agents varies between
    parasite species and between stages in their life cycles.
    1.1. Parasite Life Cycle<\/strong>
    The mosquito becomes infected by taking human blood that contains parasites in the sexual
    form. The sporozoites that develop in the mosquito are then inoculated into humans at its next
    feeding. In the exoerythrocytic stage, the sporozoites multiply in the liver to form tissue
    schizonts. Then, parasites escape from the liver into the bloodstream as merozoites. The
    merozoites invade red blood cells, multiply in them to form blood schizonts, and finally rupture
    the cells, releasing a new crop of merozoites. This cycle may be repeated many times. The
    gametocytes (the sexual stage) form and are released into the circulation, where they may be
    taken in by another mosquito. P falciparum and P malariae have only one cycle of liver cell
    invasion and multiplication, and liver infection ceases spontaneously in less than 4 weeks.
    Then, multiplication is confined to the red blood cells. So, treatment that eliminates these
    species from the red blood cells four or more weeks after inoculation of the sporozoites will cure
    these infections. In P vivax and P ovale infections, sporozoites also induce in hepatic cells the
    dormant stage (the hypnozoite) that causes subsequent recurrences (relapses) of the infection.
    Therefore, treatment that eradicates parasites from both the red cells and the liver is required to
    cure these infections.
    1.2. Drug Classification<\/strong>
    The antimalarial drugs are classified by their selective actions on the parasite’s life cycle.
    1) Tissue schizonticides: drugs that eliminate tissue schizonts or hypnozoites in the liver
    (eg, primaquine).
    2) Blood schizonticides: drugs that act on blood schizonts (eg, chloroquine, amodiaquine,
    proguanil, pyrimethamine, mefloquine, quinine) .
    3) Gametocides are drugs that prevent infection in mosquitoes by destroying gametocytes
    in the blood (eg, primaquine for P falciparum and chloroquine for P vivax, P malariae,
    and P ovale.).
    179
    4) Sporonticidal agents are drugs that render gametocytes noninfective in the mosquito
    (eg, pyrimethamine, proguanil).
    None of these drugs prevent infection except for pyrimethamine and proguanil which prevent
    maturation of P falciparum hepatic schizonts. Blood schizonticides do destroy circulating
    plasmodia. Primaquine destroys the persisting liver hypnozoites of P vivax and P ovale.
    1.3. Individual antimalarial drugs<\/strong>
    1.3.1. Chloroquine<\/em><\/strong>
    Pharmacokinetics:<\/strong> Chloroquine is a synthetic 4-aminoquinoline. It is rapidly and almost
    completely absorbed from the gastrointestinal tract, and is rapidly distributed to the tissues.
    From these sites it is slowly released and metabolized. The drug readily crosses the placenta.
    Renal excretion is increased by acidification of the urine.
    Antimalarial Action:<\/strong> Chloroquine is a highly effective blood schizonticide and is most widely
    used in chemoprophylaxis and in treatment of attacks of vivax, ovale, malariae, or sensitive
    falciparum malaria. It is moderately effective against gametocytes of P. vivax, P. ovale, and P.
    malariae, but not against those of P falciparum. Chloroquine is not active against the
    preerythrocytic plasmodium and does not effect radical cure.
    The exact mechanism of action has not been known. Selective toxicity for malarial parasites
    depends on a chloroquine-concentrating mechanism in parasitized cells. Chloroquine’s
    concentration in normal erythrocytes is 10-20 times that in plasma; in parasitized erythrocytes,
    its concentration is about 25 times that in normal erythrocytes.
    Clinical uses:<\/strong> Acute Malaria Attacks (it clears the parasitemia of acute attacks of P vivax, P
    ovale, and P malariae and of malaria due to nonresistant strains of P falciparum), and
    chemoprophylaxis (It is the preferred drug for prophylaxis against all forms of malaria except in
    regions where P falciparum is resistant to 4-aminoquinolines).
    Adverse Effects:<\/strong> Gastrointestinal symptoms, mild headache, pruritus, anorexia, malaise,
    blurring of vision, and urticaria are uncommon. A total cumulative dose of 100 g (base) may,
    contribute to the development of irreversible retinopathy, ototoxicity, and myopathy.
    Contraindications<\/strong>: It is contraindicated in patients with a history of liver damage, alcoholism,
    or neurologic or hematologic disorders, psoriasis or porphyria, in whom it may precipitate acute
    attacks of these diseases.
    1.3.2. Primaquine<\/strong>
    Primaquine phosphate is a synthetic 8-aminoquinoline derivative. After oral administration, the
    drug is usually well absorbed, completely metabolized, and excreted in the urine.
    Primaquine is active against the late hepatic stages (hypnozoites and schizonts) of P vivax and
    P ovale and thus effects radical cure of these infections. Primaquine is also highly active
    against the primary exoerythrocytic stages of P falciparum. When used in prophylaxis with
    chloroquine, it protects against P vivax and P ovale. Primaquine is highly gametocidal against
    the four malaria species.
    Clinical Uses<\/li>\n\n\n\n
  2. Terminal prophylaxis of vivax and ovale malaria.<\/li>\n\n\n\n
  3. Radical cure of acute vivax and ovale malaria.<\/li>\n\n\n\n
  4. Gametocidal action.<\/li>\n\n\n\n
  5. Pneumocystis carinii pneumonia
    Adverse Effects: Primaquine is generally well tolerated. It infrequently causes nausea,
    epigastric pain, abdominal cramps, and headache. Serious adverse effects like leukopenia and
    agranulocytosis are rare.
    1.3.3. Quinine<\/strong>
    Quinine is rapidly absorbed, reaches peak plasma levels in 1-3 hours, and is widely distributed
    in body tissues. The elimination half-life of quinine is 7-12 hours in normal persons but 8-21
    hours in malaria-infected persons in proportion to the severity of the disease. Bulk of the drug is
    metabolized in the liver and excreted for the most part in the urine. Excretion is accelerated in
    acid urine.
    Quinine is a rapidly acting, highly effective blood schizonticide against the four malaria
    parasites. The drug is gametocidal for P vivax and P ovale but not very effective against P
    falciparum gametocytes. The drug’s molecular mechanism is unclear.
    Clinical Uses<\/strong><\/li>\n\n\n\n
  6. Parenteral Treatment of Severe Falciparum Malaria<\/li>\n\n\n\n
  7. Oral Treatment of Falciparum Malaria Resistant to Chloroquine<\/li>\n\n\n\n
  8. Prophylaxis
    181<\/li>\n\n\n\n
  9. Other Uses: Quinine sulfate sometimes relieves night time leg cramps.
    Adverse Effects: Quinine often causes nausea, vomiting, hypoglycemia. Cinchonism; a less
    common effect and manifested by headache, nausea, slight visual disturbances, dizziness, and
    mild tinnitus and may subside as treatment continues. Severe toxicity like fever, skin eruptions,
    gastrointestinal symptoms, deafness, visual abnormalities, central nervous system effects
    (syncope, confusion), and quinidine-like effects occurs rarely.
    1.3.4. Proguanil and \u001fPyrimethamine<\/strong>
    Pyrimethamine and proguanil are dihydrofolate reductase inhibitors. They are slowly but
    adequately absorbed from the gastrointestinal tract.
    Pyrimethamine and proguanil are slow acting blood schizonticides against susceptible strains
    of all four malarial species. Proguanil (but not pyrimethamine) has a marked effect on the
    primary tissue stages of susceptible P falciparum and therefore may have causal prophylactic
    action.
    Resistance to pyrimethamine and proguanil is found worldwide for P falciparum and somewhat
    less ubiquitously for P vivax.
    Clinical uses<\/strong><\/li>\n\n\n\n
  10. Chemoprophylaxis<\/li>\n\n\n\n
  11. Treatment of Chloroquine-Resistant Falciparum Malaria<\/li>\n\n\n\n
  12. Toxoplasmosis treatment
    Adverse Effects: In malaria treatment, pyrimethamine and proguanil are well tolerated. In the
    high doses pyrimethamine causes megaloblastic anemia, agranulocytosis and
    thrombocytopenia (leucovorin calcium is given concurrently).
    1.3.5. Sulfones\u001f and Sulfonamides<\/strong>
    Sulfonamides and sulfones have blood schizonticidal action against P falciparum by inhibition of
    dihydrofolic acid synthesis. But, the drugs have weak effects against the blood schizonts of P
    vivax, and they are not active against the gametocytes or liver stages of P falciparum or P
    vivax. When a sulfonamide or sulfone is combined with an antifol, synergistic blockade of folic
    acid synthesis occurs in susceptible plasmodia. Sulfadoxine with pyrimethamine (Fansidar) and
    dapsone with pyrimethamine (Maloprim) are the most used combination.
    1.3.6. Pyrimethamine-Sulfadoxine (Fansid<\/strong>ar)
    Pyrimethamine-Sulfadoxine (Fansidar) is well absorbed. Its components display peak plasma
    levels within 2-8 hours and are excreted mainly by the kidneys. Average half-lives are about
    170 hours for sulfadoxine and 80-110 hours for pyrimethamine.
    Pyrimethamine-Sulfadoxine is effective against certain strains of falciparum malaria. But,
    quinine must be given concurrently in treatment of seriously ill patients, because fansidar is only
    slowly active. It is not effective in the treatment of vivax malaria.
    Clinical uses<\/strong><\/li>\n\n\n\n
  13. Treatment of Chloroquine-Resistant Falciparum<\/li>\n\n\n\n
  14. Presumptive Treatment of Chloroquine-Resistant Falciparum Malaria
    Adverse Effects: Rare adverse effects to single-dose Fansidar are those associated with
    sulfonamide allergy, including the hematologic, gastrointestinal, central nervous system,
    dermatologic, and renal systems. Fansidar is no longer used in prophylaxis because of severe
    reactions. However, in our situation, it used for prevention of malaria in pregnant women after
    the first trimester.
    Contraindications: Fansidar is contraindicated in patients who have had adverse reactions to
    sulfonamides, in pregnancy at term, in nursing women, or in children less than 2 months of age.
    Fansidar should be used with caution in those with severe allergic disorders, and bronchial
    asthma.
    1.3.7. Mefloquine<\/strong>
    Mefloquine is used in prophylaxis and treatment of chloroquine-resistant and multidrug-resistant
    falciparum malaria. It is also effective in prophylaxis against P. vivax, P. ovale, P. malariae, and
    P. falciparum.
    Mefloquine hydrochloride is chemically related to quinine. It can only be given orally because
    intense local irritation occurs with parenteral use. It is well absorbed. The drug is highly bound
    to plasma proteins, concentrated in red blood cells, and extensively distributed to the tissues,
    including the central nervous system. Mefloquine is cleared in the liver. Its acid metabolites are
    slowly excreted, mainly in the feces. Its elimination half-life, which varies from 13 days to 33
    days, tends to be shortened in patients with acute malaria.
    Mefloquine has blood schizonticidal activity against P falciparum and P vivax. Sporadic and low
    levels of resistance to mefloquine have been reported from Southeast Asia and Africa.
    Resistance to the drug can emerge rapidly, and resistant strains have been found in areas
    where the drug has never been used.
    Clinical uses: Prophylaxis of Chloroquine-Resistant Strains of P falciparum and Treatment of
    Chloroquine-Resistant P falciparum Infection
    Adverse Reactions: The frequency and intensity of reactions are dose-related. In rophylactic
    doses it causes; gastrointestinal disturbances, headache, dizziness, syncope, and extra
    systoles and transient neuropsychiatric events (convulsions, depression, and psychoses). In
    treatment doses; the incidence of neuropsychiatric symptoms (dizziness, headache, visual
    disturbances, tinnitus, insomnia, restlessness, anxiety, depression, confusion, acute psychosis,
    or seizures) may increase.
    Contraindications: A history of epilepsy, psychiatric disorders, arrhythmia, sensitivity to quinine
    and the first trimester of pregnancy.
    1.3.8. Doxycycline<\/strong>
    Doxycycline is generally effective against multidrug-resistant P falciparum. The drug is also
    active against the blood stages of the other Plasmodium species but not against the liver
    stages. In the treatment of acute malaria, it is used in conjunction with quinine.
    1.3.9. Halofantrine<\/strong>
    Halofantrine hydrochloride is an oral schizonticide for all four malarial species. A fatty food
    increases absorption up to six fold. Thus, the drug should not be given from 1 hour before to 3
    hours after a meal. Excretion is mainly in the feces.
    1.3.10. Qinghaosu (Artemisinin)<\/strong>
    These drugs are especially useful in treatment of cerebral falciparum malaria. The drugs
    produce abdominal pain, diarrhea.<\/li>\n\n\n\n
  15. Drugs used in amebiasis<\/strong>
    Amebiasis is infection by the protozoan parasite Entamoeba histolytica. E histolytica infection
    may present as a severe intestinal infection (dysentery), a mild to moderate symptomatic
    intestinal infection, an asymptomatic intestinal infection, ameboma, liver abscess, or other type
    of extraintestinal infection. The choice of drug depends on the clinical presentation and on the
    desired site of drug action, ie, in the intestinal lumen or in the tissues.
    All of the antiamebic drugs act against Entamoeba histolytica trophozoites, but most are not
    effective against the cyst stage. Antiamebic drugs are classified as tissue amebicides and
    luminal amebicides.
    2.1. Tissue amebicides eliminate organisms primarily in the bowel wall, liver, and other
    extraintestinal tissues and are not effective against organisms in the bowel lumen.
    2.1.1. Metronidazole, and tinidazole are highly effective against amebas in the bowel wall and
    other tissues.
    2.1.2. Emetine and dehydroemetine act on organisms in the bowel wall and other tissues but
    not on amebas in the bowel lumen.
    2.1.3. Chloroquine -Active principally against amebas in the liver.
    2.2. Luminal Amebicides act primarily in the bowel lumen.
    2.2.1. Diloxanide furoate
    2.2.2. Iodo-quinol
    2.2.3. Tetracyclines, paromomycin and erythromycin
    2.3. Treatment of Amebiasis
    2.3.1. Asymptomatic Intestinal Infection: The drugs of choice, diloxanide furoate and iodoquinol.
    Alternatives are metronidazole plus iodoquinol or diloxanide.
    2.3.2. Intestinal Infection: The drugs of choice, metronidazole and a luminal amebicide.
    2.3.3. Hepatic Abscess: The treatment of choice is metronidazole. Diloxanide furoate or
    iodoquinol should also be given to eradicate intestinal infection whether or not organisms
    are found in the stools. An advantage of metronidazole is its effectiveness against
    anaerobic bacteria, which are a major cause of bacterial liver abscess. Dehydroemetine
    and emetine are potentially toxic alternative drugs.
    2.3.4. Ameboma or Extraintestinal Forms of Amebiasis: Metronidazole is the drug of choice.
    Dehydroemetine is an alternative drug; chloroquine cannot be used because it does not
    reach high enough tissue concentrations to be effective (except in the liver). A
    simultaneous course of a luminal amebicide should also be given.
    2.4. Antiamoebic drugs<\/strong>
    2.4.1. Metronidazole<\/strong>
    Pharmacokinetics\u001f: Oral metronidazole is readily absorbed and permeates all tissues including
    cerebrospinal fluid, breast milk, alveolar bone, liver abscesses, vaginal secretions, and seminal
    fluid. Intracellular concentrations rapidly approach extracellular levels whether administered
    orally or intravenously. Protein binding is low. The drug and its metabolites are excreted mainly
    in the urine.
    Mechanism of Action:<\/strong> The nitro group of metronidazole is chemically reduced by ferredoxin
    within sensitive organisms. The reduction products appear to be responsible for killing the
    organisms by reacting with various intracellular macromolecules.
    Clinical Uses:<\/strong> Metronidazole is active against amebiasis, urogenital trichomoniasis, giardiasis,
    anaerobic infections, acute ulcerative gingivitis, cancrum Oris, decubitus ulcers, and bacterial
    vaginitis and Helicobacter pylori infection.
    Adverse effects: Nausea, headache, dry mouth, or metallic tastes occur commonly. Rare
    adverse effects include vomiting, diarrhea, insomnia, weakness, dizziness, stomatitis, rash,
    urethral burning, vertigo, and paresthesias. It has a disulfiram-like effect.
    2.4.2. Other Nitroimidazoles<\/strong>
    Other nitroimidazole derivatives include tinidazole, and ornidazole. They have similar adverse
    effects Because of its short half-life, metronidazole must be administered every 8 hours; the
    other drugs can be administered at longer intervals. However, with the exception of tinidazole,
    the other nitroimidazoles have produced poorer results than metronidazole in the treatment of
    amebiasis.
    2.4.3. Chloroquine<\/strong>
    Chloroquine reaches high liver concentrations and is highly effective when given with emetine in
    the treatment and prevention of amebic liver abscess. Chloroquine is not active against luminal
    organisms.
    2.4.4. Dehydroemetine\u001f Emetine<\/strong>
    Emetine and dehydroemetine are administered parenterally. They are stored primarily in the
    liver, lungs, spleen, and kidneys. They are eliminated slowly via the kidneys.These drugs act
    only against trophozoites, which they directly eliminate.
    Clinical Uses:<\/strong> Severe Intestinal Disease (Amebic Dysentery): Parenterally administered
    emetine and dehydroemetine rapidly alleviate severe intestinal symptoms but are rarely curative
    even if a full course is given.
    Adverse Effects: Sterile abscesses, pain, tenderness, and muscle weakness in the area of the
    injection are frequent. Emetine and dehydroemetine should not be used in patients with cardiac
    or renal disease, in patients with a history of polyneuritis, or in young children or liver abscess.
    They should not be used during pregnancy.
    2.4.5. Diloxanide Furoate<\/strong>
    Diloxanide furoate is directly amebicidal, but its mechanism of action is not known. In the 2gut,
    diloxanide furoate is split into diloxanide and furoic acid; about 90% of the diloxanide is rapidly
    absorbed and then conjugated to form the glucuronide, which is rapidly excreted in the urine.
    The unabsorbed diloxanide is the active antiamebic substance. Diloxanide furoate is the drug of
    choice for asymptomatic infections. For mild intestinal disease, and other forms of amebiasis it
    is used with another drug.
    2.4.6. Iodoquinol<\/strong>
    Iodoquinol is effective against organisms in the bowel lumen but not against trophozoites in the
    intestinal wall or extraintestinal tissues. The mechanism of action of iodoquinol against
    trophozoites is unknown. Iodoquinol is an alternative drug for the treatment of asymptomatic or
    mild to moderate intestinal amebiasis.
    Adverse Effects: Reversible severe neurotoxicity (optic atrophy, visual loss, and peripheral
    neuropathy). Mild and infrequent adverse effects that can occur at the standard dosage include
    diarrhea, which usually stops after several days, anorexia, nausea and vomiting, gastritis,
    abdominal discomfort, slight enlargement of the thyroid gland, headache, skin rashes, and
    perianal itching.
    2.4.7. Paromomycin Sulfate<\/strong>
    Paromomycin is an alternative drug for the treatment of asymptomatic amebiasis. In mild to
    moderate intestinal disease, it is an alternative luminal drug used concurrently with
    metronidazole. Paromomycin is both directly and indirectly amebicidal; the indirect effect is
    caused by its inhibition of bowel bacteria. It can be used only as a luminal amebicide and has
    no effect in extraintestinal amebic infections.
    187
    2.4.8. Other Antibiotics<\/strong>
    The tetracyclines (oxytetracycline) have very weak direct amebicidal action, and useful with a
    luminal amebicide in the eradication of mild to severe intestinal disease. Erythromycin although
    less effective can be used in the treatment of luminal amebiasis.<\/li>\n\n\n\n
  16. Drugs used in Giardiasis\u001f and Trichomoniasis
    <\/strong>Metronidazole is a drug of choice for gardiasis and trichomoniasis, and the alternate drug is
    tinidazole.<\/li>\n\n\n\n
  17. Treatment of Leishmaniasis<\/strong>
    Kala-azar, cutaneous, and mucocutaneous leishmaniasis are caused by the genus Leishmania.
    Treatment of leishmaniasis is difficult because of drug toxicity, the long courses of treatment,
    treatment failures, and the frequent need for hospitalization. The drug of choice is sodium
    antimony gluconate (sodium stibogluconate). Alternative drugs are amphotericin B and
    pentamidine.
    4.1. Amphotericin B<\/strong>
    Amphotericin B is injected slowly intravenously. Patients must be closely monitored in hospital,
    because adverse effects may be severe.<\/li>\n\n\n\n
  18. Treatment of Pneumocystis Carinii Pneumonia, Trypanosomiasis<\/strong>\u001f
    5.1. Pentamidine<\/strong>
    Pentamidine is administered parenterally because it is not well absorbed from the
    gastrointestinal tract. The drug leaves the circulation rapidly and is bound avidly by the tissues,
    especially the liver, spleen, and kidneys. The drug is excreted slowly and unchanged in the
    urine. Pentamidine does not cross the blood-brain barrier.
    Antiparasitic Action: The mechanisms of pentamidine’s antiparasitic action are not well known.
    The drug may interfere with the synthesis of DNA, RNA, phospholipids, and proteins.
    Clinical Uses<\/strong><\/li>\n\n\n\n
  19. Leishmaniasis<\/li>\n\n\n\n
  20. Trypanosomiasis: In African trypanosomiasis, pentamidine is an alternative in the
    hemolymphatic stage of the disease to (1) suramin in Trypanosoma brucei gambiense and T
    b rhodesiense infections or to (2) eflornithine in T b gambiense infection.<\/li>\n\n\n\n
  21. Pneumocystosis
    Adverse Effects: Pain at the injection site is common; infrequently, a sterile abscess develops
    and ulcerates. Occasional reactions include rash, gastrointestinal symptoms, neutropenia,
    abnormal liver function tests, serum folate depression, hyperkalemia, and hypocalcemia.
    Severe hypotension, hypoglycemia, hyperglycemia, hyponatremia, and delayed nephrotoxicity.<\/li>\n<\/ol>\n","protected":false},"excerpt":{"rendered":"","protected":false},"author":1,"featured_media":6511,"comment_status":"open","ping_status":"open","sticky":false,"template":"","format":"standard","meta":{"footnotes":""},"categories":[684],"tags":[],"class_list":["post-6658","post","type-post","status-publish","format-standard","has-post-thumbnail","hentry","category-chemotherapeutic-agents"],"jetpack_featured_media_url":"https:\/\/workhouse.sweetdishy.com\/wp-content\/uploads\/2024\/11\/3755529.png","_links":{"self":[{"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/posts\/6658","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/posts"}],"about":[{"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/types\/post"}],"author":[{"embeddable":true,"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/users\/1"}],"replies":[{"embeddable":true,"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/comments?post=6658"}],"version-history":[{"count":1,"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/posts\/6658\/revisions"}],"predecessor-version":[{"id":6659,"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/posts\/6658\/revisions\/6659"}],"wp:featuredmedia":[{"embeddable":true,"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/media\/6511"}],"wp:attachment":[{"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/media?parent=6658"}],"wp:term":[{"taxonomy":"category","embeddable":true,"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/categories?post=6658"},{"taxonomy":"post_tag","embeddable":true,"href":"https:\/\/workhouse.sweetdishy.com\/index.php\/wp-json\/wp\/v2\/tags?post=6658"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}