A few days after the infective bite, a feeling of lassitude, abdominal distress and chills develop followed by fever of 39 °C to 40 °C, severe frontal headaches, muscle and joint aches, flushing of the face and a fast heart rate. After two days the fever begins to subside and the temperature returns to normal. Fatigue, a slow heart rate and low blood pressure may persist from few days to several weeks but complete recovery is the rule.

Classically, the course of untreated typhoid fever is divided into four distinct stages, each lasting about a week. Over the course of these stages, the patient becomes exhausted and emaciated.

- In the first week, the body temperature rises slowly, and fever fluctuations are seen with relative bradycardia (Faget sign), malaise, headache, and cough. A bloody nose (epistaxis) is seen in a quarter of cases, and abdominal pain is also possible. A decrease in the number of circulating white blood cells (leukopenia) occurs with eosinopenia and relative lymphocytosis; blood cultures are positive for "Salmonella" Typhi or "S. paratyphi". The Widal test is usually negative in the first week.

- In the second week, the person is often too tired to get up, with high fever in plateau around and bradycardia (sphygmothermic dissociation or Faget sign), classically with a dicrotic pulse wave. Delirium is frequent, often calm, but sometimes agitated. This delirium gives to typhoid the nickname of "nervous fever". Rose spots appear on the lower chest and abdomen in around a third of patients. Rhonchi are heard in lung bases.

- The abdomen is distended and painful in the right lower quadrant, where borborygmi can be heard. Diarrhea can occur in this stage: six to eight stools in a day, green, comparable to pea soup, with a characteristic smell. However, constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender, and liver transaminases are elevated. The Widal test is strongly positive, with antiO and antiH antibodies. Blood cultures are sometimes still positive at this stage.

- (The major symptom of this fever is that the fever usually rises in the afternoon up to the first and second week.)

- In the third week of typhoid fever, a number of complications can occur:

- Intestinal haemorrhage due to bleeding in congested Peyer's patches; this can be very serious, but is usually not fatal.

- Intestinal perforation in the distal ileum: this is a very serious complication and is frequently fatal. It may occur without alarming symptoms until septicaemia or diffuse peritonitis sets in.

- Encephalitis

- Respiratory diseases such as pneumonia and acute bronchitis

- Neuropsychiatric symptoms (described as "muttering delirium" or "coma vigil"), with picking at bedclothes or imaginary objects.

- Metastatic abscesses, cholecystitis, endocarditis, and osteitis

- The fever is still very high and oscillates very little over 24 hours. Dehydration ensues, and the patient is delirious (typhoid state). One-third of affected individuals develop a macular rash on the trunk.

- Platelet count goes down slowly and risk of bleeding rises.

- By the end of third week, the fever starts subsiding

Response to infection by "Leishmania donovani" varies a great deal, not only by the strength but also by the type of the patient's immune reaction. People with a history of infection by strains of leishmania that cause visceral leishmaniasis show a continuum of immune responses from protective to non-protective. Those who acquired protective immunity (skin test positive) without ever having visceral leishmaniasis have a strong type 1 CD4+ response to leishmania antigens. Antigen specific interferon-gamma and proliferation, as well as the ability to kill intracellular leishmania, are hallmarks of protective immunity. Because visceral leishmaniasis patients lack these responses to leishmania and other antigens, they usually die of secondary infections if left untreated. In addition, increased interleukin-10 secretion is characteristic of the disease. Addition of interleukin-12, anti-interleukin-10, or anti-interleukin-4 to peripheral blood mononuclear cells from acute patients sometimes increases interferon-gamma secretion and proliferation. Acute patient peripheral blood mononuclear cells include CD8+ T regulatory cells that decrease interferon-gamma secretion and proliferation responses to leishmania and other antigens and increase interleukin-10 secretion when added to autologous peripheral blood mononuclear cells harvested after successful treatment. Thus, the CD8+ T regulatory cells reproduce the immune response characteristic of visceral leishmaniasis. CD8+ T regulatory cells are also associated with post kala azar dermal leishmaniasis. Addition of interleukin-12 or interferon-gamma does not prevent CD8+ T regulatory activity. The dominance of type 1 CD4+ T cells in skin test positive adults maybe explained by their secretion of factors that inhibit and kill CD8+ T regulatory cells. Successfully treated patients rarely develop visceral leishmaniasis a second time. Their peripheral blood mononuclear cells show a mixed T1/T2 CD4+ and CD8+ T suppressor response but do have the ability to kill intracellular leishmania.

When people develop visceral leishmaniasis, the most typical symptoms are fever and the enlargement of the spleen, with enlargement of the liver sometimes being seen as well. The blackening of the skin that gave the disease its common name in India does not appear in most strains of the disease, and the other symptoms are very easy to mistake for those of malaria. Misdiagnosis is dangerous, as without proper treatment the mortality rate for kala-azar is close to 100%. "L. donovani" itself is not usually the direct cause of death in kala-azar sufferers, however. Pneumonia, tuberculosis, and dysentery are omnipresent in the depressed regions where leishmaniasis thrives, and, as with AIDS, it is these opportunistic infections that are more likely to kill, flaring up in a host whose immune system has been weakened by the "L. donovani" infection. Progress of the disease is extremely variable, taking anywhere from one to twenty weeks, but a typical duration for the Sudanese strain of the disease is narrower, between twelve and sixteen weeks.

Even with recovery, kala-azar does not always leave its hosts unmarked. Some time after successful treatment—generally a few months with African kala-azar, or as much as several years with the Indian strain—a secondary form of the disease may set in, called post kala-azar dermal leishmaniasis, or PKDL. This condition manifests first as small, measle-like skin lesions on the face, which gradually increase in size and spread over the body. Eventually the lesions may coalesce to form disfiguring, swollen structures resembling leprosy, and occasionally causing blindness if they spread to the eyes. (This disease is not the same as cutaneous leishmaniasis, a milder disease caused by another protozoan of the Leishmania genus which also causes skin lesions.)

The signs and symptoms of malaria typically begin 8–25 days following infection; however, symptoms may occur later in those who have taken antimalarial medications as prevention. Initial manifestations of the disease—common to all malaria species—are similar to flu-like symptoms, and can resemble other conditions such as sepsis, gastroenteritis, and viral diseases. The presentation may include headache, fever, shivering, joint pain, vomiting, hemolytic anemia, jaundice, hemoglobin in the urine, retinal damage, and convulsions.

The classic symptom of malaria is paroxysm—a cyclical occurrence of sudden coldness followed by shivering and then fever and sweating, occurring every two days (tertian fever) in "P. vivax" and "P. ovale" infections, and every three days (quartan fever) for "P. malariae". "P. falciparum" infection can cause recurrent fever every 36–48 hours, or a less pronounced and almost continuous fever.

Severe malaria is usually caused by "P. falciparum" (often referred to as falciparum malaria). Symptoms of falciparum malaria arise 9–30 days after infection. Individuals with cerebral malaria frequently exhibit neurological symptoms, including abnormal posturing, nystagmus, conjugate gaze palsy (failure of the eyes to turn together in the same direction), opisthotonus, seizures, or coma.

African tick bite fever is often asymptomatic or mild in clinical presentation and complications are rare. The onset of illness is typically 5–7 days after the tick bite, although in some cases it may take up to 10 days for symptoms to occur. Symptoms can persist for several days to up to three weeks. Common presenting symptoms include:

- Fever

- Headache

- Muscle aches

- Inoculation eschar, which is dead, often black, tissue around a bite site (see photo above)

- Eschars may or may not be present. "Amblyomma" ticks actively attack cattle or humans and can bite more than once. In African tick bite fever, unlike what is typically seen with other Rickettsial spotted fevers when only one eschar is identified, multiple eschars may be seen and are considered pathognomonic.

- Swollen lymph nodes near the site of the bite

- Maculopapular and/or vesicular rash

Three serotypes of Phlebovirus are known as the causative agents: Naples virus, Sicilian virus and Toscana virus.

Complications are rare and are not life-threatening. No deaths due to African tick bite fever have been reported. Reported complications include:

- Prolonged fever > 3 weeks in duration

- Reactive arthritis

- Moderate to severe headache

In 80% of cases, the disease is asymptomatic, but in the remaining 20%, it takes a complicated course. The virus is estimated to be responsible for about 5,000 deaths annually. The fever accounts for up to one-third of deaths in hospitals within the affected regions and 10 to 16% of total cases.

After an incubation period of six to 21 days, an acute illness with multiorgan involvement develops. Nonspecific symptoms include fever, facial swelling, and muscle fatigue, as well as conjunctivitis and mucosal bleeding. The other symptoms arising from the affected organs are:

- Gastrointestinal tract

- Nausea

- Vomiting (bloody)

- Diarrhea (bloody)

- Stomach ache

- Constipation

- Dysphagia (difficulty swallowing)

- Hepatitis

- Cardiovascular system

- Pericarditis

- Hypertension

- Hypotension

- Tachycardia (abnormally high heart rate)

- Respiratory tract

- Cough

- Chest pain

- Dyspnoea

- Pharyngitis

- Pleuritis

- Nervous system

- Encephalitis

- Meningitis

- Unilateral or bilateral hearing deficit

- Seizures

Clinically, Lassa fever infections are difficult to distinguish from other viral hemorrhagic fevers such as Ebola and Marburg, and from more common febrile illnesses such as malaria.

The virus is excreted in urine for 3–9 weeks and in semen for three months.

Malaria has several serious complications. Among these is the development of respiratory distress, which occurs in up to 25% of adults and 40% of children with severe "P. falciparum" malaria. Possible causes include respiratory compensation of metabolic acidosis, noncardiogenic pulmonary oedema, concomitant pneumonia, and severe anaemia. Although rare in young children with severe malaria, acute respiratory distress syndrome occurs in 5–25% of adults and up to 29% of pregnant women. Coinfection of HIV with malaria increases mortality. Renal failure is a feature of blackwater fever, where hemoglobin from lysed red blood cells leaks into the urine.

Infection with "P. falciparum" may result in cerebral malaria, a form of severe malaria that involves encephalopathy. It is associated with retinal whitening, which may be a useful clinical sign in distinguishing malaria from other causes of fever. Enlarged spleen, enlarged liver or both of these, severe headache, low blood sugar, and hemoglobin in the urine with renal failure may occur. Complications may include spontaneous bleeding, coagulopathy, and shock.

Malaria in pregnant women is an important cause of stillbirths, infant mortality, abortion and low birth weight, particularly in "P. falciparum" infection, but also with "P. vivax".

Visceral leishmaniasis (VL), also known as kala-azar, black fever, and Dumdum fever, is the most severe form of leishmaniasis and, without proper diagnosis and treatment, is associated with high fatality. Leishmaniasis is a disease caused by protozoan parasites of the "Leishmania" genus.

The parasite migrates to the internal organs such as the liver, spleen (hence "visceral"), and bone marrow, and, if left untreated, will almost always result in the death of the host. Signs and symptoms include fever, weight loss, fatigue, anemia, and substantial swelling of the liver and spleen. Of particular concern, according to the World Health Organization (WHO), is the emerging problem of HIV/VL co-infection.

This disease is the second-largest parasitic killer in the world (after malaria), responsible for an estimated 200,000 to 400,000 infections each year worldwide.

Typhoid fever, also known simply as typhoid, is a bacterial infection due to "Salmonella" typhi that causes symptoms. Symptoms may vary from mild to severe and usually begin six to thirty days after exposure. Often there is a gradual onset of a high fever over several days. Weakness, abdominal pain, constipation, and headaches also commonly occur. Diarrhea is uncommon and vomiting is not usually severe. Some people develop a skin rash with rose colored spots. In severe cases there may be confusion. Without treatment, symptoms may last weeks or months. Other people may carry the bacterium without being affected; however, they are still able to spread the disease to others. Typhoid fever is a type of enteric fever along with paratyphoid fever.

The cause is the bacterium "Salmonella" typhi, also known as "Salmonella enterica" serotype Typhi, growing in the intestines and blood. Typhoid is spread by eating or drinking food or water contaminated with the feces of an infected person. Risk factors include poor sanitation and poor hygiene. Those who travel to the developing world are also at risk and only humans can be infected. Diagnosis is by either culturing the bacteria or detecting the bacterium's DNA in the blood, stool, or bone marrow. Culturing the bacterium can be difficult. Bone marrow testing is the most accurate. Symptoms are similar to that of many other infectious diseases. Typhus is a different disease.

A typhoid vaccine can prevent about 30% to 70% of cases during the first two years. The vaccine may have some effect for up to seven years. It is recommended for those at high risk or people traveling to areas where the disease is common. Other efforts to prevent the disease include providing clean drinking water, better sanitation, and better handwashing. Until it has been confirmed that an individual's infection is cleared, the individual should not prepare food for others. Treatment of disease is with antibiotics such as azithromycin, fluoroquinolones or third generation cephalosporins. Resistance to these antibiotics has been developing, which has made treatment of the disease more difficult.

In 2015, there were 12.5 million new cases worldwide. The disease is most common in India. Children are most commonly affected. Rates of disease decreased in the developed world in the 1940s as a result of improved sanitation and use of antibiotics to treat the disease. Each year in the United States, about 400 cases are reported and it is estimated that the disease occurs in about 6,000 people. In 2015, it resulted in about 149,000 deaths worldwide – down from 181,000 in 1990 (about 0.3% of the global total). The risk of death may be as high as 20% without treatment. With treatment, it is between 1 and 4%. The name typhoid means "resembling typhus" due to the similarity in symptoms.

Yellow fever begins after an incubation period of three to six days. Most cases only cause a mild infection with fever, headache, chills, back pain, fatigue, loss of appetite, muscle pain, nausea, and vomiting. In these cases, the infection lasts only three to four days.

In 15% of cases, however, people enter a second, toxic phase of the disease with recurring fever, this time accompanied by jaundice due to liver damage, as well as abdominal pain. Bleeding in the mouth, the eyes, and the gastrointestinal tract cause vomit containing blood, hence the Spanish name for yellow fever, "vómito negro" ("black vomit"). There may also be kidney failure, hiccups, and delirium.

The toxic phase is fatal in about 20 to 50% of cases, making the overall fatality rate for the disease about 3.0 to 7.5%. However, the fatality rate of those with the toxic phase of the disease may exceed 50%.

Surviving the infection provides lifelong immunity, and normally no permanent organ damage results.

Most people infected with the West Nile virus usually do not develop symptoms. However, some individuals can develop cases of severe fatigue, weakness, headaches, body aches, joint and muscle pain, vomiting, diarrhea, and rash, which can last for weeks or months. More serious symptoms have a greater risk of appearing in people over 60 years of age, or those suffering from cancer, diabetes, hypertension, and kidney disease.

Dengue fever is mostly characterized by high fever, headaches, joint pain, and rash. However, more severe instances can lead to hemorrhagic fever, internal bleeding, and breathing difficulty, which can be fatal.

Symptoms vary on severity, from mild unnoticeable symptoms to more common symptoms like fever, rash, headache, achy muscle and joints, and conjunctivitis. Symptoms can last several days to weeks, but death resulting from this infection is rare.

Most people who are infected develop sickness between five and 15 days after they are bitten. The symptoms may include a sudden fever, chills, headaches, muscle or joint aches, and nausea. A rash may also occur. These symptoms usually continue for two to 9 days, then disappear. This cycle may continue for several weeks if the person is not treated.

Half of all children and a quarter of previously healthy adults are asymptomatic with "Babesia" infection. When people do develop symptoms, the most common are fever and hemolytic anemia, symptoms that are similar to those of malaria. People with symptoms usually become ill 1 to 4 weeks after the bite, or 1 to 9 weeks after transfusion of contaminated blood products. A person infected with babesiosis gradually develops malaise and fatigue, followed by a fever. Hemolytic anemia, in which red blood cells are destroyed and removed from the blood, also develops. Chills, sweats, and thrombocytopenia are also common symptoms. Symptoms may last from several days to several months.

Less common symptoms and physical exam findings of mild-to-moderate babesiosis:

In more severe cases, symptoms similar to malaria occur, with fevers up to 40.5 °C (105 °F), shaking chills, and severe anemia (hemolytic anemia). Organ failure may follow, including adult respiratory distress syndrome. Severe cases occur mostly in people who have had a splenectomy. Severe cases are also more likely to occur in the very young, very old, and persons with immunodeficiency, such as HIV/AIDS patients.

A reported increase in human babesiosis diagnoses in the 2000s is thought to be caused by more widespread testing and higher numbers of people with immunodeficiencies coming in contact with ticks, the disease vector. Little is known about the occurrence of "Babesia" species in malaria-endemic areas, where "Babesia" can easily be misdiagnosed as "Plasmodium". Human patients with repeat babesiosis infection may exhibit premunity.

Women experiencing PAM may exhibit normal symptoms of malaria, but may also be asymptomatic or present with more mild symptoms, including a lack of the characteristic fever. This may prevent a woman from seeking treatment despite the danger to herself and her unborn child.

Yellow fever is a viral disease of typically short duration. In most cases, symptoms include fever, chills, loss of appetite, nausea, muscle pains particularly in the back, and headaches. Symptoms typically improve within five days. In about 15% of people within a day of improving, the fever comes back, abdominal pain occurs, and liver damage begins causing yellow skin. If this occurs, the risk of bleeding and kidney problems is also increased.

The disease is caused by the yellow fever virus and is spread by the bite of an infected female mosquito. It infects only humans, other primates, and several species of mosquitoes. In cities, it is spread primarily by "Aedes aegypti", a type of mosquito found throughout the tropics and subtropics. The virus is an RNA virus of the genus "Flavivirus". The disease may be difficult to tell apart from other illnesses, especially in the early stages. To confirm a suspected case, blood sample testing with polymerase chain reaction is required.

A safe and effective vaccine against yellow fever exists and some countries require vaccinations for travelers. Other efforts to prevent infection include reducing the population of the transmitting mosquito. In areas where yellow fever is common and vaccination is uncommon, early diagnosis of cases and immunization of large parts of the population is important to prevent outbreaks. Once infected, management is symptomatic with no specific measures effective against the virus. Death occurs in up to half of those who get severe disease.

In 2013, yellow fever resulted in about 127,000 severe infections and 45,000 deaths, with nearly 90% of these occurring in Africa. Nearly a billion people live in an area of the world where the disease is common. It is common in tropical areas of South America and Africa, but not in Asia. Since the 1980s, the number of cases of yellow fever has been increasing. This is believed to be due to fewer people being immune, more people living in cities, people moving frequently, and changing climate. The disease originated in Africa, from where it spread to South America through the slave trade in the 17th century. Since the 17th century, several major outbreaks of the disease have occurred in the Americas, Africa, and Europe. In the 18th and 19th centuries, yellow fever was seen as one of the most dangerous infectious diseases. In 1927 yellow fever virus became the first human virus to be isolated.

Pregnancy-associated malaria (PAM) or placental malaria is a presentation of the common illness that is particularly life-threatening to both mother and developing fetus. PAM is caused primarily by infection with "Plasmodium falciparum", the most dangerous of the four species of malaria-causing parasites that infect humans. During pregnancy, a woman faces a much higher risk of contracting malaria and of associated complications. Prevention and treatment of malaria are essential components of prenatal care in areas where the parasite is endemic.

While the average adult citizen of an endemic region possesses some immunity to the parasite, pregnancy causes complications that leave the woman and fetus extremely vulnerable. The parasite interferes with transmission of vital substances through the fetal placenta, often resulting in stillbirth, spontaneous abortion, or dangerously low birth weight. The tragedy of malaria in developing countries receives abundant attention from the international health community, but until recently PAM and its unique complications were not adequately addressed.

A "vaccine-preventable disease" is an infectious disease for which an effective preventive vaccine exists. If a person acquires a vaccine-preventable disease and dies from it, the death is considered a vaccine-preventable death.

The most common and serious vaccine-preventable diseases tracked by the World Health Organization (WHO) are: diphtheria, "Haemophilus influenzae" serotype b infection, hepatitis B, measles, meningitis, mumps, pertussis, poliomyelitis, rubella, tetanus, tuberculosis, and yellow fever. The WHO reports licensed vaccines being available to prevent, or contribute to the prevention and control of, 25 vaccine-preventable infections.

The diagnosis of relapsing fever can be made on blood smear as evidenced by the presence of spirochetes. Other spirochete illnesses (Lyme disease, syphilis, leptospirosis) do not show spirochetes on blood smear. Although considered the gold standard, this method lacks sensitivity and has been replaced by PCR in many settings.

Horses are the most susceptible host with close to 90%

mortality of those affected, followed by mules (50%) and donkeys (10%). African donkeys and zebras very rarely display clinical symptoms, despite high virus titres in blood, and are thought to be the natural reservoir of the virus. AHS manifests itself in four different forms: the pulmonary form, the cardiac form, a mild (horse sickness fever) form, and a mixed form.

Pulmonary form

The peracute form of the disease is characterized by high fever, depression, and respiratory symptoms. The clinically affected animal has trouble breathing, starts coughing frothy fluid from nostril and mouth, and shows signs of pulmonary edema within four days. Serious lung congestion causes respiratory failure and results in death in under 24 hours. This form of the disease has the highest mortality rate.

Cardiac form

This subacute form of the disease has an incubation period longer than that of the pulmonary form. Signs of disease start at day 7–12 after infection. High fever is a common symptom. The disease also manifests as conjunctivitis, with abdominal pain and progressive dyspnea. Additionally, edema is presented under the skin of the head and neck, most notably in swelling of the supra-orbital fossae, palpebral conjunctiva, and intermandibular space. Mortality rate is between 50–70% and survivors recover in 7 days.

Mild or horse sickness fever form

Mild to subclinical disease is seen in zebras and African donkeys. Infected animals may have low grade fever and congested mucous membrane. The survival rate is 100%.

Mixed form

Diagnosis is made at necropsy. Affected horses show signs of both the pulmonary and cardiac forms of AHS.

African horse sickness (AHS) is a highly infectious and deadly disease. It commonly affects horses, mules, and donkeys. It is caused by a virus of the genus Orbivirus belonging to the family Reoviridae. This disease can be caused by any of the nine serotypes of this virus. AHS is not directly contagious, but is known to be spread by insect vectors.

Babesiosis is a malaria-like parasitic disease caused by infection with "Babesia", a genus of Apicomplexa. Human babesiosis is an uncommon but emerging disease in the Northeastern and Midwestern United States and parts of Europe, and sporadic throughout the rest of the world. It occurs in warm weather. Ticks transmit the human strain of babesiosis, so it often presents with other tick-borne illnesses such as Lyme disease. After trypanosomes, "Babesia" is thought to be the second-most common blood parasite of mammals, and they can have a major impact on health of domestic animals in areas without severe winters. In cattle, a major host, the disease is known as Texas cattle fever, redwater, or piroplasmosis.

Congenital malaria is an extremely rare condition which occurs due to transplacental transmission of maternal infection.

Clinical features include fever, irritability, feeding problems, anemia, hepatosplenomegaly and jaundice. Clinical features commence only after 3 weeks due to the protective effect of transplacentally transmitted antibodies.