If symptoms of histoplasmosis infection occur, they will start within 3 to 17 days after exposure; the average is 12–14 days. Most affected individuals have clinically silent manifestations and show no apparent ill effects. The acute phase of histoplasmosis is characterized by non-specific respiratory symptoms, often cough or flu-like. Chest X-ray findings are normal in 40–70% of cases. Chronic histoplasmosis cases can resemble tuberculosis; disseminated histoplasmosis affects multiple organ systems and is fatal unless treated.

While histoplasmosis is the most common cause of mediastinitis, this remains a relatively rare disease. Severe infections can cause hepatosplenomegaly, lymphadenopathy, and adrenal enlargement. Lesions have a tendency to calcify as they heal.

Presumed ocular histoplasmosis syndrome (POHS) causes chorioretinitis, where the choroid and retina of the eyes are scarred, resulting in a loss of vision not unlike macular degeneration. Despite its name, the relationship to "Histoplasma" is controversial. Distinct from POHS, acute ocular histoplasmosis may rarely occur in immunodeficiency.

In absence of proper treatment and especially in immunocompromised individuals, complications can arise. These include recurrent pneumonia, respiratory failure, fibrosing mediastinitis, superior vena cava syndrome, pulmonary vessel obstruction, progressive fibrosis of lymph nodes. Fibrosing mediastinitis is a serious complication and can be fatal. Smokers with structural lung disease have higher probability of developing chronic cavitary histoplasmosis.

After healing of lesions, hard calcified lymph nodes can erode the walls of airway causing hemoptysis.

African histoplasmosis is an infection caused by "Histoplasma duboisii". Disease has been most often reported in Uganda, Nigeria, Zaire and Senegal. In human disease it manifests differently than histoplasmosis (caused by "Histoplasma capsulatum"), most often involving the skin and bones and rarely involving the lungs.

Progressive disseminated histoplasmosis is an infection caused by Histoplasma capsulatum, and most people who develop this severe form of histoplasmosis are immunocompromised or taking systemic corticosteroids. Skin lesions are present in approximately 6% of patients with dissemination.

As in the majority of paracoccidioidomycosis cases, pulmonary involvement results in shortness of breath, a productive cough and hemoptysis, as well as general symptoms of weight loss, fever and fatigue. Visually, lesions (as pictured) are often present, most commonly on the face.

Paracoccidioidomycosis (PCM) (also known as "Brazilian blastomycosis," "South American blastomycosis,","Lutz-Splendore-de Almeida disease" and "paracoccidioidal granuloma") is a fungal infection caused by the fungus "Paracoccidioides brasiliensis". Sometimes called "South American blastomycosis", paracoccidioidomycosis is caused by a different fungus than that which causes blastomycosis.

The term Winterbottom's sign derives from descriptions of the posterior cervical lymphadenopathy associated with African trypanosomiasis made by a slave trader using the sign to weed out the ill.

The tsetse fly bite erupts into a red chancre sore and within a few weeks, the person can experience fever, swollen lymph glands, blood in urine, aching muscles and joints, headaches and irritability. In the first phase, the patient has only intermittent bouts of fever with lymphadenopathy together with other non-specific signs and symptoms. The second stage of the disease is marked by involvement of the central nervous system with extensive neurological effects like changes in personality, alteration of the biological clock (the circadian rhythm), confusion, slurred speech, seizures and difficulty in walking and talking. These problems can develop over many years and if not treated, the person dies. It is common to the African continent.

Winterbottom's sign is seen in the early phase of African trypanosomiasis, a disease caused by the parasites "Trypanosoma brucei rhodesiense" and "Trypanosoma brucei gambiense" which is more commonly known as African sleeping sickness. Dr. Anthony Martinelli describes Winterbottom's sign as the swelling of lymph nodes (lymphadenopathy) along the back of the neck, in the posterior cervical chain of lymph nodes, as trypanosomes travel in the lymphatic fluid and cause inflammation.

It may be suggestive of cerebral infection.

Trypanosomiasis or trypanosomosis is the name of several diseases in vertebrates caused by parasitic protozoan trypanosomes of the genus "Trypanosoma". In humans this includes African trypanosomiasis and Chagas disease. A number of other diseases occur in other animals.

Approximately 30,000 people in 36 countries of sub-Saharan Africa have African trypanosomiasis, which is caused by either "Trypanosoma brucei gambiense" or "Trypanosoma brucei rhodesiense". Chagas disease causes 21,000 deaths per year mainly in Latin America.

Fungal meningitis refers to meningitis caused by a fungal infection.

Protozoan infections are parasitic diseases caused by organisms formerly classified in the Kingdom Protozoa. They include organisms classified in Amoebozoa, Excavata, and Chromalveolata.

Examples include "Entamoeba histolytica", "Plasmodium" (some of which cause malaria), and "Giardia lamblia". "Trypanosoma brucei", transmitted by the tsetse fly and the cause of African sleeping sickness, is another example.

The species traditionally collectively termed "protozoa" are not closely related to each other, and have only superficial similarities (eukaryotic, unicellular, motile, though with exceptions). The terms "protozoa" (and protist) are usually discouraged in the modern biosciences. However, this terminology is still encountered in medicine. This is partially because of the conservative character of medical classification, and partially due to the necessity of making identifications of organisms based upon appearances and not upon DNA.

Protozoan infections in animals may be caused by organisms in the sub-class Coccidia (disease: Coccidiosis) and species in the genus "Besnoitia" (disease: Besnoitiosis).

Several pathogenic protozoans appear to be capable of sexual processes involving meiosis (or at least a modified form of meiosis). Included among these protozoans are "Plasmodium falciparum" (malaria), "Toxoplasma gondii" (toxoplasmosis), "Leishmania" species (leishmaniases), "Trypanosoma brucei" (African sleeping sickness), "Trypanosoma cruzi" (Chagas disease) and "Giardia intestinalis" (giardiasis).

Animal trypanosomiasis, also known as nagana and nagana pest, or sleeping sickness, is a disease of vertebrates. The disease is caused by trypanosomes of several species in the genus "Trypanosoma" such as "Trypanosoma brucei". "Trypanosoma vivax" causes nagana mainly in West Africa, although it has spread to South America. The trypanosomes infect the blood of the vertebrate host, causing fever, weakness, and lethargy, which lead to weight loss and anemia; in some animals the disease is fatal unless treated. The trypanosomes are transmitted by tsetse flies.

An interesting feature is the remarkable tolerance to nagana pathology shown by some breeds of cattle, notably the N'Dama – a West African "Bos taurus" breed. This contrasts with the susceptibility shown by East African "Bos indicus" cattle such as the zebu.

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.

Symptoms of fungal meningitis are generally similar to those of other types of meningitis, and include: a fever, stiff neck, severe headache, photophobia (sensitivity to light), nausea and vomiting, and altered mental status (drowsiness or confusion).

Besnoitiosis is "a protozoan disease of the skin, subcutis, blood vessels, mucous membranes, and other tissues" of animals. It "is endemic in tropical and sub-tropical regions with high infection rate but low mortality"; however, it is rare in other regions.

The causative organisms of the cutaneous disease, and the affected animals include:

- "Besnoitia besnoiti" in cattle (swelling of the lymph nodes, subcutaneous swellings, diarrhea, abortion and infertility)

- "Besnoitia bennetti" in horses and donkeys (characterized by a widespread, serious dermatitis)

- "Besnoitia jellisoni" and "B. wallacei" in rodents

- "Besnoitia tarandi" in reindeer and caribou

- "Besnoitia darlingi" in lizards, opossums, and snakes

- "Besnoitia sauriana" in lizards

- Viscerotropic strains of "B.besnoiti" in African antelope

- An unidentified "Besnoitia" species in goats in Iran, New Zealand, and Kenya

The incubation period ranges from 4 days to approximately 8 weeks. The infection leads to significant weight loss and anaemia. Various symptoms are observed, including fever, oedema, adenitis, dermatitis and nervous disorders. The disease cannot be diagnosed with certainty except physically detecting parasites by blood microscopic examination or various serological reactions.

Presumptive diagnosis is made by characteristic clinical signs, post mortem lesions, and presence of competent vectors. Laboratory confirmation is by viral isolation, with such techniques as quantitative PCR for detecting viral RNA, antigen capture (ELISA), and immunofluorescence of infected tissues. Serological tests are only useful for detecting recovered animals, as sick animals die before they are able to mount effective immune responses.

They are treated with antiprotozoal agents. Recent papers have also proposed the use of viruses to treat infections caused by protozoa.

African trypanosomiasis symptoms occur in two stages. The first stage, known as the hemolymphatic phase, is characterized by fever, headaches, joint pains, and itching. Fever is intermittent, with attacks lasting from a day to a week, separated by intervals of a few days to a month or longer. Invasion of the circulatory and lymphatic systems by the parasites is associated with severe swelling of lymph nodes, often to tremendous sizes. Winterbottom's sign, the tell-tale swollen lymph nodes along the back of the neck, may appear. Occasionally, a chancre (red sore) will develop at the location of the tsetse fly bite. If left untreated, the disease overcomes the host's defenses and can cause more extensive damage, broadening symptoms to include anemia, endocrine, cardiac, and kidney dysfunctions.

The second phase of the disease, the neurological phase, begins when the parasite invades the central nervous system by passing through the blood–brain barrier. Disruption of the sleep cycle is a leading symptom of this stage and is the one that gave the disease the name 'sleeping sickness.' Infected individuals experience a disorganized and fragmented 24-hour rhythm of the sleep-wake cycle, resulting in daytime sleep episodes and nighttime periods of wakefulness.

Other neurological symptoms include confusion, tremor, general muscle weakness, hemiparesis and paralysis of a limb. Parkinson-like movements might arise due to non-specific movement disorders and speech disorders. Individuals may also exhibit psychiatric symptoms such as irritability, psychotic reactions, aggressive behaviour, or apathy which can sometimes dominate the clinical diagnosis. Without treatment, the disease is invariably fatal, with progressive mental deterioration leading to coma, systemic organ failure, and death. An untreated infection with "T. b. rhodesiense" will cause death within months whereas an untreated infection with "T. b. gambiense" will cause death after several years. Damage caused in the neurological phase is irreversible.

On post-mortem examination (necropsy), the most obvious gross lesion is subcutaneous oedema in the submandibular and pectoral (brisket) regions. Petechial haemorrhages are found subcutaneously and in the thoracic cavity. In addition, congestion and various degrees of consolidation of the lung may occur. Animals that die within 24–36 hours, have only few petechial haemorrhages on the heart and generalised congestion of the lung, while in animals that die after 72 hours, petechial and ecchymotic haemorrhages were more evident and lung consolidation are more extensive.

African trypanosomiasis, also known as sleeping sickness, is an insect-borne parasitic disease of humans and other animals. It is caused by protozoa of the species "Trypanosoma brucei". There are two types that infect humans, "Trypanosoma brucei gambiense" (TbG) and "Trypanosoma brucei rhodesiense" (TbR). TbG causes over 98% of reported cases. Both are usually transmitted by the bite of an infected tsetse fly and are most common in rural areas.

Initially, in the first stage of the disease, there are fevers, headaches, itchiness, and joint pains. This begins one to three weeks after the bite. Weeks to months later the second stage begins with confusion, poor coordination, numbness and trouble sleeping. Diagnosis is via finding the parasite in a blood smear or in the fluid of a lymph node. A lumbar puncture is often needed to tell the difference between first and second stage disease.

Prevention of severe disease involves screening the population at risk with blood tests for TbG. Treatment is easier when the disease is detected early and before neurological symptoms occur. Treatment of the first stage is with the medications pentamidine or suramin. Treatment of the second stage involves eflornithine or a combination of nifurtimox and eflornithine for TbG. While melarsoprol works for both stages, it is typically only used for TbR, due to serious side effects. Without treatment it typically results in death.

The disease occurs regularly in some regions of sub-Saharan Africa with the population at risk being about 70 million in 36 countries. An estimated 11,000 people are currently infected with 2,800 new infections in 2015. In 2015 it caused around 3,500 deaths, down from 34,000 in 1990. More than 80% of these cases are in the Democratic Republic of the Congo. Three major outbreaks have occurred in recent history: one from 1896 to 1906 primarily in Uganda and the Congo Basin and two in 1920 and 1970 in several African countries. It is classified as a neglected tropical disease. Other animals, such as cows, may carry the disease and become infected in which case it is known as animal trypanosomiasis.

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

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

A wide variety of clinical signs have been described for HS in cattle and buffaloes. The incubation periods (the time between exposure and observable disease) for buffalo calves 4–10 months of age varies according to the route of infection. The incubation period is 12–14 hours, approximately 30 hours and 46–80 hours for subcutaneous infection, oral infection and natural exposure, respectively.

There is variability in the duration of the clinical course of the disease. In the case of experimental subcutaneous infection, the clinical course lasted only a few hours, while it persisted for 2–5 days following oral infection and in buffaloes and cattle that had been exposed to naturally-infected animals. It has also been recorded from field observations that the clinical courses of per-acute and acute cases were 4–12 hours and 2–3 days, respectively.

Generally, progression of the disease in buffaloes and cattle is divided into three phases. Phase one is characterised by fever, with a rectal temperature of , loss of appetite and depression. Phase two is typified by increased respiration rate (40–50/minute), laboured breathing, clear nasal discharge (turns opaque and mucopurulent as the disease progresses), salivation and submandibular oedema spreading to the pectoral (brisket) region and even to the forelegs. Finally, in phase three, there is typically recumbency, continued acute respiratory distress and terminal septicaemia. The three phases overlap when the disease course is short. In general, buffaloes have a more acute onset of disease than cattle, with a shorter duration.